Podcasts about Dabigatran

Play Episode Listen Later Oct 7, 2019 9:56

Commentary by Dr. Valentin Fuster

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Dabigatran Reversal with Idarucizumab in Patients with Renal Impairment

Play Episode Listen Later Sep 30, 2019 12:20

Commentary by Dr. Valentin Fuster

patients commentary reversal renal impairment dabigatran valentin fuster idarucizumab

Episode 31 – Emergency Department Management of Patients Taking Direct Oral Anticoagulant Agents (Pharmacology CME)

EMplify by EB Medicine

Play Episode Listen Later Aug 6, 2019

Show Notes Jeff: Welcome back to EMplify the podcast corollary to EB Medicine's Emergency medicine Practice. I'm Jeff Nusbaum and I'm back with Nachi Gupta. This month, we are tackling a topic for which the literature continues to rapidly change - we're talking about the ED management of patients taking direct oral anticoagulants or DOACs, previously called novel oral anticoagulants or NOACs. Nachi: Specifically, we'll be focusing on the use of DOACs for the indications of stroke prevention in atrial fibrillation and the treatment and prevention of recurrent venous thromboembolisms. Jeff: This month's article was authored by Dr. Patrick Maher and Dr. Emily Taub of the Icahn School of Medicine at Mount Sinai, and it was peer reviewed by Dr. Dowin Boatright from Yale, Dr. Natalie Kreitzer from the University of Cincinnati, and Dr. Isaac Tawil from the University of New Mexico. Nachi: In their quest to update the last Emergency Medicine Practice issue on this topic which was published in 2013, they reviewed over 200 articles from 2000 to present in addition to 5 systematic reviews in the cochrane database, as well as guidelines from the American Heart Association, European society of cardiology, and the american college of cardiology. Jeff: Thanks to a strong literature base, Dr's Maher and Taub found good quality evidence regarding safety and efficacy of the DOACs in relation to warfarin and the heparin-based anticoagulants. Nachi: But do note that the literature directly comparing the DOACs is far more limited and mostly of poor quality. Show More v Jeff: Fair enough, we'll take what we can get. Nachi: Well, I'm sure more of those studies are still coming. Jeff: Agree. Let's get started with some basics. Not surprisingly, DOACs now account for a similar proportion of office visits for anticoagulant use as warfarin. Nachi: With huge benefits including reduced need for monitoring and a potential for reduced bleeding complications, this certainly isn't surprising. Jeff: Though those benefits are not without challenges - most notably the lack of an effective reversal agent and the risk of unintentional overdose in patients with altered drug metabolism. Nachi: Like all things in medicine, it's about balancing and finding an acceptable risk/benefit profile. Jeff: True. Let's talk pathophysiology for a minute - the control of coagulation in the human body is a balance between hemorrhage and thrombosis, mediated by an extensive number of procoagulant and anticoagulant proteins. Nachi: Before the development of the DOACs, vitamin K antagonists controlled the brunt of the market. As their name suggests, they work by inhibiting the action of vitamin K, and thus reducing the production of clotting factors 2, 7, 9, and 10, and the anticoagulant proteins C and S. Jeff: Unfortunately, these agents have a narrow therapeutic window and many drug-drug interactions, and they require frequent monitoring - making them less desirable to many. Nachi: However, in 2010, the FDA approved the first DOAC, a real game-changer. The DOACs currently on the market work by one of two mechanisms - direct thrombin inhibition or factor Xa inhibition. Jeff: DOACs are currently approved for stroke prevention in nonvalvular afib, treatment of VTE, VTE prophylaxis, and reduction of major cardiovascular events in stable cardiovascular disease. Studies are underway to test their safety and efficacy in arterial and venous thromboembolism, prevention of embolic stroke in afib, ACS, cancer-associated thrombosis, upper extremity DVT, and mesenteric thrombosis. Nachi: Direct thrombin inhibitors like Dabigatran, tradename Pradaxa, was the first FDA approved DOAC. It works by directly inhibiting thrombin, or factor IIa, which is a serine protease that converts soluble fibrinogen into fibrin for clot formation. Jeff: Dabigatran comes in doses of 75 and 150 mg. The dose depends on your renal function, and, with a half-life of 12-15 hours,

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Episode 31 - Emergency Department Management of Patients Taking Direct Oral Anticoagulant Agents (Pharmacology CME)

EMplify by EB Medicine

Play Episode Listen Later Aug 6, 2019

Show Notes Jeff: Welcome back to EMplify the podcast corollary to EB Medicine’s Emergency medicine Practice. I’m Jeff Nusbaum and I’m back with Nachi Gupta. This month, we are tackling a topic for which the literature continues to rapidly change - we’re talking about the ED management of patients taking direct oral anticoagulants or DOACs, previously called novel oral anticoagulants or NOACs. Nachi: Specifically, we’ll be focusing on the use of DOACs for the indications of stroke prevention in atrial fibrillation and the treatment and prevention of recurrent venous thromboembolisms. Jeff: This month’s article was authored by Dr. Patrick Maher and Dr. Emily Taub of the Icahn School of Medicine at Mount Sinai, and it was peer reviewed by Dr. Dowin Boatright from Yale, Dr. Natalie Kreitzer from the University of Cincinnati, and Dr. Isaac Tawil from the University of New Mexico. Nachi: In their quest to update the last Emergency Medicine Practice issue on this topic which was published in 2013, they reviewed over 200 articles from 2000 to present in addition to 5 systematic reviews in the cochrane database, as well as guidelines from the American Heart Association, European society of cardiology, and the american college of cardiology. Jeff: Thanks to a strong literature base, Dr’s Maher and Taub found good quality evidence regarding safety and efficacy of the DOACs in relation to warfarin and the heparin-based anticoagulants. Nachi: But do note that the literature directly comparing the DOACs is far more limited and mostly of poor quality. Show More v Jeff: Fair enough, we’ll take what we can get. Nachi: Well, I’m sure more of those studies are still coming. Jeff: Agree. Let’s get started with some basics. Not surprisingly, DOACs now account for a similar proportion of office visits for anticoagulant use as warfarin. Nachi: With huge benefits including reduced need for monitoring and a potential for reduced bleeding complications, this certainly isn’t surprising. Jeff: Though those benefits are not without challenges - most notably the lack of an effective reversal agent and the risk of unintentional overdose in patients with altered drug metabolism. Nachi: Like all things in medicine, it’s about balancing and finding an acceptable risk/benefit profile. Jeff: True. Let’s talk pathophysiology for a minute - the control of coagulation in the human body is a balance between hemorrhage and thrombosis, mediated by an extensive number of procoagulant and anticoagulant proteins. Nachi: Before the development of the DOACs, vitamin K antagonists controlled the brunt of the market. As their name suggests, they work by inhibiting the action of vitamin K, and thus reducing the production of clotting factors 2, 7, 9, and 10, and the anticoagulant proteins C and S. Jeff: Unfortunately, these agents have a narrow therapeutic window and many drug-drug interactions, and they require frequent monitoring - making them less desirable to many. Nachi: However, in 2010, the FDA approved the first DOAC, a real game-changer. The DOACs currently on the market work by one of two mechanisms - direct thrombin inhibition or factor Xa inhibition. Jeff: DOACs are currently approved for stroke prevention in nonvalvular afib, treatment of VTE, VTE prophylaxis, and reduction of major cardiovascular events in stable cardiovascular disease. Studies are underway to test their safety and efficacy in arterial and venous thromboembolism, prevention of embolic stroke in afib, ACS, cancer-associated thrombosis, upper extremity DVT, and mesenteric thrombosis. Nachi: Direct thrombin inhibitors like Dabigatran, tradename Pradaxa, was the first FDA approved DOAC. It works by directly inhibiting thrombin, or factor IIa, which is a serine protease that converts soluble fibrinogen into fibrin for clot formation. Jeff: Dabigatran comes in doses of 75 and 150 mg. The dose depends on your renal function, and, with a half-life of 12-15 hours, is taken twice daily. Note the drastically reduced half-life as compared to warfarin, which has a half-life of up to 60 hours. Nachi: The RE-LY trial for afib found that taking 150 mg of Dabigatran BID had a lower rate of stroke and systemic embolism than warfarin with a similar rate of major hemorrhage. Dabigatran also had lower rates of fatal and traumatic intracerebral hemorrhage than warfarin. Jeff: A separate RCT found similar efficacy in treating acute VTE and preventing recurrence compared with warfarin, with reduced rates of hemorrhage! Nachi: Less monitoring, less hemorrhage, similar efficacy, I’m sold!!! Jeff: Slow down, there’s lots of other great agents out there, let’s get through them all first... Nachi: Ok, so next up we have the Factor Xa inhibitors, Rivaroxaban, apixaban, edoxaban, and betrixaban.As the name suggests, these medications work by directly inhibiting the clotting of factor Xa, which works in the clotting cascade to convert prothrombin to thrombin. Jeff: Rivaroxaban, trade name Xarelto, the second FDA approved DOAC, is used for stroke prevention in those with nonvalvular afib and VTE treatment. After taking 15 mg BID for the first 21 days, rivaroxaban is typically dosed at 20 mg daily with adjustments for reduced renal function. Nachi: The Rocket AF trial found that rivaroxaban is noninferior to warfarin for stroke and systemic embolism prevention without a significant difference in risk of major bleeding. Interestingly, GI bleeding may be higher in the rivaroxaban group, though the overall incidence was very low in both groups at about 0.4% of patients per year. Jeff: In the Einstein trial, patients with VTE were randomized to rivaroxaban or standard therapy. In the end, they reported similar rates of recurrence and bleeding outcomes for acute treatment. Continuing therapy beyond the acute period resulted in similar rates of VTE recurrence and bleeding episodes to treatment with aspirin alone. Nachi: Next we have apixaban, tradename Eliquis. Apixaban is approved for afib and the treatment of venous thromboembolism. It’s typically dosed as 10 mg BID for 7 days followed by 5 mg BID with dose reductions for the elderly and those with renal failure. Jeff: In the Aristotle trial, when compared to warfarin, apixaban was superior in preventing stroke and systemic embolism with lower mortality and bleeding. Rates of major hemorrhage-related mortality were also nearly cut in half at 30 days when compared to warfarin. Nachi: For the treatment of venous thromboembolism, the literature shows that apixaban has a similar efficacy to warfarin in preventing recurrence with less bleeding complications. Jeff: Unfortunately, with polypharmacy, there is increased risk of thromboembolic and hemorrhage risks, but this risk is similar to what is seen with warfarin. Nachi: And as compared to low molecular weight heparin, apixaban had higher bleeding rates without reducing venous thromboembolism events when used for thromboprophylaxis. It’s also been studied in acute ACS, with increased bleeding and no decrease in ischemic events. Jeff: Edoxaban is up next, approved by the FDA in 2015 for similar indications as the other Factor Xa inhibitors. It’s recommended that edoxaban be given parenterally for 5-10 days prior to starting oral treatment for VTE, which is actually similar to dabigatran. It has similar levels of VTE recurrence with fewer major bleeding episodes compared to warfarin. It has also been used with similar effects and less major bleeding for stroke prevention in afib. In the setting of cancer related DVTs specifically, as compared to low molecular weight heparin, one RCT showed lower rates of VTE but higher rates of major bleeding when compared to dalteparin. Nachi: Next we have Betrixaban, the latest Factor Xa inhibitor to be approved, back in 2017. Because it’s utility is limited to venous thromboembolism prophylaxis in mostly medically ill inpatients, it’s unlikely to be encountered by emergency physicians very frequently. Jeff: As a one sentence FYI though - note that in recent trials, betrixaban reduced the rate of VTE with equivalent rates of bleeding and reduced the rate of stroke with an increased rate of major and clinically relevant non-major bleeding as compared to enoxaparin. Nachi: Well that was a ton of information and background on the DOACs. Let’s move on to your favorite section - prehospital medicine. Jeff: Not a ton to add here this month. Perhaps, most importantly, prehospital providers should specifically ask about DOAC usage, especially in trauma, given increased rates of complications and potential need for surgery. This can help with destination selection when relevant. Interestingly, one retrospective study found limited agreement between EMS records and hospital documentation on current DOAC usage. Nachi: Extremely important to identify DOAC use early. Once the patient arrives in the ED, you can begin your focused history and physical. Make sure to get the name, dose, and time of last administration of any DOAC. Pay particular attention to the med list and the presence of CKD which could point to altered DOAC metabolism. Jeff: In terms of the physical and initial work up - let the sites of bleeding or potential sites of bleeding guide your work up. And don’t forget about the rectal exam, which potentially has some added value here - since DOACs increase the risk of GI bleeding. Nachi: Pretty straight forward history and physical, let’s talk diagnostic studies. Jeff: First up is CT. There are no clear cut guidelines here, so Drs. Maher and Taub had to rely on observational studies and expert opinion. Remember, most standard guidelines and tools, like the canadian and nexus criteria, are less accurate in anticoagulated patients, so they shouldn’t be applied. Instead, most studies recommend a low threshold for head imaging, even with minor trauma, in the setting of DOAC use. Nachi: That is so important that it’s worth repeating. Definitely have a low threshold to CT the head for even minor head trauma patients on DOACs. Basically, if you’re on anticoagulation, and you made it to the ED for anything remotely related to your head, you probably win a spin. Jeff: I suspect you are not alone with that stance... There is, however, much more debate about the utility of follow up imaging and admission after a NEGATIVE scan. Nachi: Wait, is that a thing I should routinely be doing? Jeff: Well there’s not great data here, but in one observational study of 1180 patients on either antiplatelet or anticoagulant therapy, a half a percent of them had positive findings 12 hours later, and importantly none required surgical intervention. Nachi: Certainly reassuring. And for those with positive initial imaging, the authors recommend repeat imaging within 4-6 hours in consultation with neurosurgical services or even earlier in cases of unexpected clinical decline. Jeff: Interestingly, though only a small retrospective study of 156 patients, one study found markedly reduced mortality, 4.9% vs 20.8% in those on DOACs vs warfarin with traumatic intracranial hemorrhage. Nachi: Hmm that actually surprises me a bit with the ease of reversibility of warfarin. Jeff: And we’ll get to that in a few minutes. But next we should talk about ultrasound. As always with trauma, guidelines recommend a FAST exam in the setting of blunt abdominal trauma. The only thing to be aware of here is that you should have an increased index of suspicion for bleeding, especially in hidden sites like the retroperitoneum. Nachi: And just as with traumatic head bleeds, a small observational study of those with blunt abdominal trauma found 8% vs 30% mortality for those on DOACs vs warfarin, respectively. Jeff: That is simply shocking! Let’s also talk lab studies. Hemoglobin and platelet counts should be obtained as part of the standard trauma work up. Assessing renal function via creatinine is also important, especially for those on agents which are renally excreted. Nachi: Though you can, in theory, test for plasma DOAC concentrations, such tests are not routinely indicated as levels don’t correspond to bleeding outcomes. DOAC levels may be indicated in certain specific situations, such as while treating life-threatening bleeding, development of venous thromboembolism despite compliance with DOAC therapy, and treating patients at risk for bleeding because of an overdose. Jeff: In terms of those who require surgery while on a DOAC - if urgent or emergent, the DOAC will need to be empirically reversed. For all others, the recommendation is to wait a half life or even multiple half-lives, if possible, in lieu of level testing. Nachi: Coagulation tests are up next. Routine PT and PTT levels do not help assess DOACs, as abnormalities on either test can suggest the presence of a DOAC, but the values should not be interpreted as reliable measures of either therapeutic or supratherapeutic clinical anticoagulant effect. Jeff: Dabigatran may cause prolongation of both the PT and the PTT, but the overall correlation is poor. In addition, FXa inhibitors may elevate PT in a weakly concentration dependent manner, but this may only be helpful if anti-fXa levels are unavailable. Nachi: Which is a perfect segway into our next test - anti-factor Xa level activity. Direct measurements of the anti-Fxa effect demonstrates a strong linear correlation with plasma concentrations of these agents, but the anticoagulant effect does not necessarily follow the same linear fashion. Jeff: Some labs may even have an anti-FXa effect measurement calibrated specifically to the factor 10a inhibitors. Nachi: While measuring thrombin time is not routinely recommended, the result of thrombin time or dilute thrombin time does correlate well with dabigatran concentrations across normal ranges. Jeff: And lastly, we have the Ecarin clotting time. Ecarin is an enzyme that cleaves prothrombin to an active intermediate that can be inhibited by dabigatran in the same way as thrombin. The ECT is useful for measuring dabigatran concentration - it’s not useful for testing for FXa inhibitors. A normal ECT value could be used to exclude the presence of dabigatran. Nachi: So I think that rounds out testing. Let’s move into the treatment section. Jeff: For all agents, regardless of the DOAC, the initial resuscitation follows the standard principles of hemorrhage control and trauma resuscitation. Tourniquet application, direct pressure, endoscopy for GI bleeds, etc... should all be used as needed. And most importantly, for airway bleeding, pericardial bleeding, CNS bleeding, and those with hemodynamic instability or overt bleeding, those with a 2 point drop in their hemoglobin, and those requiring 2 or more units of pRBC - they all should be considered to have serious, life threatening bleeds. This patient population definitely requires reversal agents, which we’re getting to in a minute. Nachi: A type and screen should also be sent with the plan to follow standard transfusion guidelines, with the goal of a hemoglobin level of 7, understanding that in the setting of an active bleed, the hemoglobin level will not truly be representative. Jeff: Interestingly, in the overdose literature that’s out there, bleeding episodes appear to be rare - occurring in just 5% of DOAC overdose cases. Nachi: Finally, onto the section we’ve all been waiting for. Let’s talk specific reversal agents. Praxbind is up first. Jeff: Idarucizumab or Praxbind, is the reversal agent of choice for dabigatran (which is also called pradaxa). According to data from the RE-LY trial, it reverses dabigatran up to the 99th percentile of levels measured in the trial. Nachi: And praxbind should be given in two 2.5 g IV boluses 15 minutes apart to completely reverse the effects of dabigatran. Jeff: As you would expect given this data, guidelines for DOAC reversal recommend it in major life-threatening bleeding events for patients on dabigatran. Nachi: Next up is recombinant coagulation factor Xa (brand name Andexxa), which was approved in 2018 for the FXa inhibitors. This recombinant factor has a decoy receptor for the FXa agents, thus eliminating their anticoagulant effects. Jeff: Recombinant factor Xa is given in either high or low dose infusions. High dose infusions for those on rivaroxaban doses of >10 mg or apixaban doses >5 mg within the last 8 hours and for unknown doses and unknown time of administration. Low dose infusions should be used for those with smaller doses within the last 8 hours or for last doses taken beyond 8 hours. Nachi: In one trial of 352 patients, recombinant factor Xa given as an IV bolus and 2 hour infusion was highly effective at normalizing anti-FXa levels. 82% of the assessed patients at 12 hours achieved hemostasis, but there were also thrombotic events in 10% of the patients at 30 days. Jeff: And reported thrombotic events aren’t the only downside. Though the literature isn’t clear, there may be limited use of recombinant factor Xa outside of the time of the continuous infusion, and even worse, there may be rebound of anti-Fxa levels and anticoagulant effect. And lastly, the cost is SUBSTANTIAL. Nachi: Is there really a cost threshold for stopping life threatening bleeding…? Jeff: Touche, but that means we need to save it for specific times and consider other options out there. Since this has only been around for a year or so, let’s let the literature play out on this too... Nachi: And that perfectly takes us into our next topic, which is nonspecific reversal agents, starting with prothrombin complex concentrate, also called PCC. Jeff: PCC is FDA approved for rapid reversal of vitamin K antagonist-related hemorrhagic events and is now being used off label for DOAC reversal. Nachi: PCC comes in 3 and 4 factor varieties. 3-factor PCC contains factors 2, 9, 10 and trace amounts of factor 7. 4 factor PCC contains factors 2, 9 10, as well as purified factor 7 and proteins C and S. Jeff: Both also contain trace amounts of heparin so can’t be given to someone with a history of HIT. Nachi: PCC works by overwhelming the inhibitor agent by increasing the concentration of upstream clotting factors. It has been shown, in healthy volunteers, to normalize PT abnormalities and bleeding times, and to achieve effective bleeding control in patients on rivaroxaban, apixaban, and edoxaban with major bleeding events. Jeff: In small studies looking at various end points, 4 factor PCC has been shown to be superior to 3 factor PCC. Nachi: Currently it’s given via weight-based dosing, but there is interest in studying a fixed-dose to decrease both time to medication administration and cost of reversal. Jeff: Guidelines currently recommend 4F PCC over 3F PCC, if available, for the management of factor Xa inhibitor induced bleeding, with studies showing an effectiveness of nearly 70%. As a result, 4F PCC has become an agent of choice for rapid reversal of FXa inhibitors during major bleeding events. Nachi: Next we have activated PCC (trade name FEIBA). This is essentially 4Factor PCC with a modified factor 7. Though traditionally saved for bleeding reversal in hemophiliacs, aPCC is now being studied in DOAC induced bleeding. Though early studies are promising, aPCC should not be used over 4factor PCC routinely as of now but may be used if 4Factor PCC is not available. Jeff: Next we have recombinant factor 7a (trade name novoseven). This works by activating factors 9 and 10 resulting in rapid increase in thrombin. Studies have shown that it may reverse the effect of dabigatran, at the expense of increased risk of thrombosis. As such, it should not be used as long as other agents are available. Nachi: Fresh Frozen Plasma is the last agent to discuss in this section. Not a lot to say here - FFP is not recommended for reversal of any of the DOACs. It may be given as a part of of a balanced massive transfusion resuscitation, but otherwise, at this time, there doesn’t seem to be a clear role. Jeff: Let’s move on to adjunct therapies, of which we have 3 to discuss. Nachi: First is activated charcoal. Only weak evidence exists here - but, according to expert recommendations, there may be a role for DOAC ingestions within 2 hours of presentations. Jeff: Perhaps more useful than charcoal is our next adjunct - tranexamic acid or TXA. TXA is a synthetic lysine analogue with antifibrinolytic activity through reversible binding of plasmin. CRASH-2 is the main trial to know here. CRASH-2 demonstrated reduced mortality if given within 3 hours in trauma patients. There is very limited data with respect to TXA and DOACs specifically, so continue to administer TXA as part of your standard trauma protocol without modification if the patient is on a DOAC, as it’s likely helpful based on what data we have. Nachi: Next is vitamin K - there is no data to support routine use of vitamin K in those taking DOACs - save that for those on vitamin K antagonists. Jeff: Also, worth mentioning here is the importance of hematology input in developing hospital-wide protocols for reversal agents, especially if availability of certain agents is limited. Nachi: Let’s talk about some special circumstances and populations as they relate to DOACs. Patients with mechanical heart valves were excluded from the major DOAC trials. And of note, a trial of dabigatran in mechanical valve patients was stopped early because of bleeding and thromboembolic events. As such, the American College of Cardiology state that DOACs are reasonable for afib with native valve disease. Jeff: DOACs should be used with caution for pregnant, breastfeeding, and pediatric patients. A case series of 233 pregnancies that occurred among patients on a DOAC reported high rates of miscarriage. Nachi: Patients with renal impairment are particularly concerning as all DOACs are dependent to some degree on renal elimination. Current guidelines from the Anticoagulation Forum recommend avoiding dabigatran and rivaroxaban for patients with CrCL < 30 and avoiding edoxaban and betrixaban for patients with CrCl < 15. Jeff: A 2017 Cochrane review noted similar efficacy without increased risk of major bleeding when using DOACs in those with egfr > 30 (that’s ckd3b or better) when compared to patients with normal renal function and limited evidence for safety below this estimated GFR. Nachi: Of course, dosing with renal impairment will be different. We won’t go into the details of that here as you will probably discuss this directly with your pharmacist. Jeff: We should mention, however, that reversal of the anticoagulant in the setting of renal impairment for your major bleeding patient is exactly the same as we already outlined. Nachi: Let’s move on to some controversies and cutting-edge topics. The first one is a pretty big topic and that is treatment for ischemic stroke patients taking DOACs. Jeff: Safety and efficacy of tPA or endovascular therapy for patients on DOACs continues to be debated. Current guidelines do not recommend tPA if the last DOAC dose was within the past 48 hours, unless lab testing specific to these agents shows normal results. Nachi: Specifically, the American Heart Association suggests that INR and PTT be normal in all cases. ECT and TT should be tested for dabigatran. And calibrated anti-FXa level testing be normal for FXa inhibitors. Jeff: The AHA registry actually included 251 patients who received tpa while on DOACs, which along with cohort analysis of 26 ROCKET-AF trial patients, suggest the risk of intracranial hemorrhage is similar to patients on warfarin with INR < 1.7 and to patients not on any anticoagulation who received tpa. However, given the retrospective nature of this data, we cannot exclude the possibility of increased risk of adverse events with tpa given to patients on DOACs. Nachi: Endovascular thrombectomy also has not been studied in large numbers for patients on DOACs. Current recommendations are to discuss with your stroke team. IV lysis or endovascular thrombectomy may be considered for select patients on DOACs. Always include the patient and family in shared decision making here. Jeff: There are also some scoring systems for bleeding risk to discuss briefly. The HAS-BLED has been used to determine bleeding risk in afib patients taking warfarin. The ORBIT score was validated in a cohort that included patients on DOACs and is similarly easy to use, and notably does not require INR values. Nachi: There is also the ABC score which has demonstrated slightly better prediction characteristics for bleeding risk, but it requires high-sensitivity troponin, limiting its practical use. Jeff: We won’t say more about the scoring tools here, but would recommend that you head over to MD Calc, where you can find them and use them in your practice. Nachi: Let’s also comment on the practicality of hemodialysis for removal of the DOACs. Multiple small case series have shown successful removal of dabigatran, given its small size and low protein binding. On the other hand, the FXa inhibitors are less amenable to removal in this way because of their higher protein binding. Jeff: Worth mentioning here also - dialysis catheters if placed should be in compressible areas in case bleeding occurs. The role of hemodialysis for overdose may be limited now that the specific reversal agent, praxbind, exists. Nachi: In terms of cutting-edge tests, we have viscoelastic testing like thromboelastography and rotational thromboelastometry. Several studies have examined the utility of viscoelastic testing to detect presence of DOACs with varying results. Prolongation of clotting times here does appear to correlate with concentration, but these tests haven’t emerged as a gold standard yet. Jeff: Also, for cutting edge, we should mention ciraparantag. And if you’ve been listening patiently and just thinking to yourself why can’t there be one reversal agent to reverse everything, this may be the solution. Ciraparantag (or aripazine) is a universal anticoagulant reversal agent that may have a role in all DOACs and heparins. It binds and inactivates all of these agents and it doesn’t appear to have a procoagulant effect. Nachi: Clinical trials for ciraparantag have shown rapid and durable reversal of edoxaban, but further trials and FDA approval are still needed. Jeff: We’ve covered a ton of material so far. As we near the end of this episode, let’s talk disposition. Nachi: First, we have those already on DOACs - I think it goes without saying that any patient who receives pharmacological reversal of coagulopathy for major bleeding needs to be admitted, likely to the ICU. Jeff: Next we have those that we are considering starting a DOAC, for example in someone with newly diagnosed VTE, or patients with an appropriate CHADS-VASC with newly diagnosed non-valvular afib. Nachi: With respect to venous thromboembolism, both dabigatran and edoxaban require a 5 day bridge with heparin, whereas apixaban and rivaroxaban do not. The latter is not only easier on the patient but also offers potential cost savings with low risk of hemorrhagic complications. Jeff: For patients with newly diagnosed DVT / PE, both the American and British Thoracic Society, as well as ACEP, recommend using either the pulmonary embolism severity index, aka PESI, or the simplified PESI or the Hestia criteria to risk stratify patients with PE. The low risk group is potentially appropriate for discharge home on anticoagulation. This strategy reduces hospital days and costs with otherwise similar outcomes - total win all around. Nachi: Definitely a great opportunity for some shared decision making since data here is fairly sparse. This is also a great place to have institutional policies, which could support this practice and also ensure rapid outpatient follow up. Jeff: If you are going to consider ED discharge after starting a DOAC - there isn’t great data supporting one over another. You’ll have to consider patient insurance, cost, dosing schedules, and patient / caregiver preferences. Vitamin K antagonists should also be discussed as there is lots of data to support their safety outcomes, not to mention that they are often far cheaper…. As an interesting aside - I recently diagnosed a DVT/PE in an Amish gentleman who came to the ED by horse - that was some complicated decision making with respect to balancing the potentially prohibitive cost of DOACs with the massive inconvenience of frequently checking INRs after a 5 mile horseback ride into town... Nachi: Nice opportunity for shared decision making… Jeff: Lastly, we have those patients who are higher risk for bleeding. Though I’d personally be quite uneasy in this population, if you are to start a DOAC, consider apixaban or edoxaban, which likely have lower risk of major bleeding. Nachi: So that’s it for the new material for this month’s issue. Certainly, an important topic as the frequency of DOAC use continues to rise given their clear advantages for both patients and providers. However, despite their outpatient ease of use, it definitely complicates our lives in the ED with no easy way to evaluate their anticoagulant effect and costly reversal options. Hopefully all our hospitals have developed or will soon develop guidelines for both managing ongoing bleeding with reversal agents and for collaborative discharges with appropriate follow up resources for those we send home on a DOAC. Jeff: Absolutely. Let’s wrap up with some the highest yield points and clinical pearls Nachi: Dabigatran works by direct thrombin inhibition, whereas rivaroxaban, apixaban, edoxaban, and betrixaban all work by Factor Xa inhibition. Jeff: The DOACs have a much shorter half-life than warfarin. Nachi: Prehospital care providers should ask all patients about their use of anticoagulants. Jeff: Have a low threshold to order a head CT in patients with mild head trauma if they are on DOACs. Nachi: For positive head CT findings or high suspicion of significant injury, order a repeat head CT in 4 to 6 hours and discuss with neurosurgery. Jeff: Have a lower threshold to conduct a FAST exam for blunt abdominal trauma patients on DOACs. Nachi: Assessment of renal function is important with regards to all DOACs. Jeff: While actual plasma concentrations of DOACs can be measured, these do not correspond to bleeding outcomes and should not be ordered routinely. Nachi: The DOACs may cause mild prolongation of PT and PTT. Jeff: Idarucizumab (Praxbind®) is an antibody to dabigatran. For dabigatran reversal, administer two 2.5g IV boluses 15 minutes apart. Reversal is rapid and does not cause prothrombotic effects. Nachi: Recombinant FXa can be used to reverse the FXa inhibitors. This works as a decoy receptor for the FXa agents. Jeff: Vitamin K and FFP are not recommended for reversal of DOACs. Nachi: Consider activated charcoal to remove DOACs ingested within the last two hours in the setting of life-threatening hemorrhages in patient’s on DOACs. Jeff: Hemodialysis can effectively remove dabigatran, but this is not true for the FXa inhibitors. Nachi: 4F-PCC has been shown to be effective in reversing the effects of the FXa inhibitors. This is thought to be due to overwhelming the inhibitor agent by increased concentrations of upstream clotting factors. Jeff: tPA is contraindicated in acute ischemic stroke if a DOAC dose was administered within the last 48 hours, unless certain laboratory testing criteria are met. Nachi: Emergency clinicians should consider initiating DOACs in the ED for patients with new onset nonvalvular atrial fibrillation, DVT, or PE that is in a low-risk group. Jeff: So that wraps up Episode 31! Nachi: As always, additional materials are available on our website for Emergency Medicine Practice subscribers. If you’re not a subscriber, consider joining today. You can find out more at ebmedicine.net/subscribe. Subscribers get in-depth articles on hundreds of emergency medicine topics, concise summaries of the articles, calculators and risk scores, and CME credit. You’ll also get enhanced access to the podcast, including any images and tables mentioned. PA’s and NP’s - make sure to use the code APP4 at checkout to save 50%. Jeff: And the address for this month’s cme credit is www.ebmedicine.net/E0819, so head over there to get your CME credit. As always, the [DING SOUND] you heard throughout the episode corresponds to the answers to the CME questions. Lastly, be sure to find us on iTunes and rate us or leave comments there. You can also email us directly at EMplify@ebmedicine.net with any comments or suggestions. Talk to you next month!

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Circulation June 18 Issue

Circulation on the Run

Play Episode Listen Later Jun 17, 2019 25:27

Dr Gregory Hundley: Welcome everyone to the June 18th edition of Circulation on the Run. I am Dr Greg Hundley, Professor of Internal Medicine and Director of the Pauley Heart Center at VCU Health in Richmond, Virginia. In today's issue we're deviating from our common format due to some scheduling difficulties. So, rather than our traditional coffee chat in this program I'm going to have a large gulp of coffee and present results from several exciting papers. Then we'll turn over the second half of our program to Dr Carolyn Lam for our feature discussion. Now, I promise this is a one-time deviation and we will return to our common chat format in early July. But, before I launch into my presentations I did want to introduce what will transpire with Carolyn. She will be discussing an exciting paper from the Adelaide Medical School at the University of Adelaide in Australia. Some have wondered whether the persistence of a patent arterial venous fistula post-kidney transplant may contribute to ongoing maladaptive cardiovascular remodeling. To address this issue Carolyn will be discussing with authors whether ligation of this AV fistula may reverse this maladaptive remodeling. And like you, I'm excited to listen to that discussion. But before that let me review several of the other distinctive papers on this issue. The first one is entitled “Individual Treatment Effect Estimation of Two Doses of Dabigatran on Stroke and Major Bleeding in Atrial Fibrillation.” They are the results from the RE-LY trial. The corresponding author is Professor Frank Visseren from the University Medical Center of Utrecht in Utrecht University. The study emanates from the randomized evaluation of long-term anticoagulation therapy or the RE-LY trial. In which high dose dabigatran, that's 150 milligrams twice daily, was found more effective in prevention of ischemic stroke and systemic embolism than low dose dabigatran which is 110 milligrams twice daily. But this occurred at that expense of an increased risk of gastrointestinal bleeds. Importantly however, the absolute treatment effect of dabigatran in both doses, likely differs between individuals. And therefore, individual treatment effect estimation has the potential to identify patients who have a favorable trade off and absolute benefit and harm from dabigatran compared with no treatment, and to select the optimal dose for each individual patient. So in this study, the investigative team derived and validated a prediction model for ischemic stroke and systemic embolism and major bleeding in patients with atrial fibrillation from three treatment arms of the RE-LY study. They had 11,955 individuals in the derivation cohort and 6,158 in the validation cohort. And they evaluated the patient characteristics of sex, age, smoking, anti-platelet drugs, prior vascular disease, diabetes, blood pressure, estimated glomerular filtration rate, and hemoglobin. Dr Gregory Hundley: Well, what were the results? Well the five-year absolute risk reduction, for ischemic stroke and systemic embolus minus the five-year absolute risk increase for major bleeding, when comparing the high to the low dose of dabigatran yielded a net benefit in 46% of patients. And therefore, the authors conclude that the absolute treatment benefits and harms of dabigatran in atrial fibrillation can be estimated based on readily available patient characteristics. And perhaps down the road such treatment effect estimations can be used for shared decision making before starting dabigatran treatment and to determine its optimal dose of administration. Well, how 'bout that? And let's go on to the second paper entitled “Empagliflozin and the Risk of Heart Failure Hospitalization in Routine Clinical Care: A First Analysis from the Empagliflozin Comparative Effectiveness and Safety, or EMPRISE Study. And the corresponding author for this study is Elisabetta Patorno from Brigham and Women's Hospital in the Harvard Medical School. So, as a background in a different study to this, the EMPA-REG OUTCOME trial showed that Empagliflozin an SGLT2 inhibitor was found to reduce the risk of hospitalization for heart failure by 35% on top of standard of care in patients with Type 2 diabetes and established cardiovascular disease. Well, the current study, The Empagliflozin Comparative Effective and Safety or EMPRISE Study was designed to assess empagliflozin's effectiveness, safety, and health care utilization in routine care from the period of time between August of 2014 through September of 2019. And the author's report on the first interim analysis in which they investigated the risk of hospitalization for heart failure among Type 2 diabetic patients initiating empagliflozin vs. sitagliptin. The investigators used two commercial and one federal Medicare claims data source from the U.S. and identified a one-to-one propensity score matched cohort of 16,443 pairs of Type 2 diabetes patients that were greater than 18 years of age initiating empagliflozin or sitagliptin. The average age of the participants was approximately 59 years. And almost 54% of the participants were males and approximately 25% had records of existing cardiovascular disease. So compared to sitagliptin the initiation of empagliflozin decreased the hospitalization for heart failure risk by 50% over a mean follow-up of 5.3 months. And the results were consistent in patients with and without baseline cardiovascular disease for both the empagliflozin 10 milligram or 25 milligram daily dose. Or analysis comparing empagliflozin vs. dipeptidyl peptidase-4 inhibitor class all comers. Thus, in conclusion, in this first interim analysis from EMPRISE, the investigative team showed that compared with sitagliptin the initiation of empagliflozin was associated with a decreased risk of hospitalization for heart failure among patients with Type 2 diabetes as treated in routine care with and without a history of cardiovascular disease. Dr Gregory Hundley: Well, now we're going to turn our attention to red meat. And this next study was entitled, The Consumption of Meat, Fish, Dairy Products, Eggs, and Risk of Ischemic Heart Disease. It's a Perspective study of 7,198 incident cases among 409,885 participants in the Pan European Epic Cohort. And the corresponding author is Professor Timothy Key from The University of Oxford. Some of the background here, met analysis of previous prospective studies have suggested that intake of processed meat maybe associated with a higher risk of ischemia heart disease whereas, unprocessed red meat might not. For dairy products and eggs, systematic reviews of prospective studies have reported no consistent evidence that higher intakes are associated with a higher risk of ischemic heart disease. Other studies have shown that fatty fish consumption may reduce the risk of ischemic heart disease, it is a rich source of long chain N3 fatty acids. And meta-analysis has suggested even an inverse association between overall fish consumption and mortality from ischemic heart disease. So, hear in this cohort: we're going to evaluate all of these. Accordingly Key, and his co-authors report the relationships of these foods with risk of ischemic heart disease in the European prospective investigation into cancer and nutrition, the EPIC study, and that again is a cohort of a half million men and women from nine European countries followed for 12 years to examine the association between the intake of animal foods and the occurrence of ischemic heart disease. The author's found that higher consumption of red, unprocessed and processed meat was positively associated with the risk of ischemic heart disease. None of the other animal foods examined were positively associated with this risk. And intakes of fatty fish, yogurt, cheese and eggs were modestly, inversely associated with the risk. In addition, the red and processed meat were associated with plasma non-HDL cholesterol and systolic blood pressure. And this finding is of interest as possibly these other variables could serve as mediator of the association between red or processed meat and future ischemic heart disease. It is important to note that while these results are of interest to those concerned with the future adverse cardiovascular effects related to the consumption of red meat, one cannot infer causality and other studies would need to be designed to address causal relationships. The last paper that I'm going to present during the coffee gulp, emanates from the basic science arena. And it is entitled The “Shear-Induced CCN1 Promotion of Atheroprone Endothelial Phenotypes and Arthrosclerosis. And the corresponding author is Dr Fan-E Mo from the National Cheng Kung University College of Medicine. Dr Gregory Hundley: The matricellular protein CCN1 has been implicated in arthrosclerosis based on its expression in arterial segments with evidence of arthrosclerosis. And this study evaluated the relationship between sheer stress, both laminar and oscillatory at the site of atherosclerotic liaisons and molecular markers of pathophysiologic process involved in the progression of arthrosclerosis. The authors found that sheer induced CCN1 and its receptor integrin, alpha six, beta one, instigate atheroprone phenotypic changes in endothelial cells via activating NF kappa beta. Because the activation of NF kappa beta further up regulates the expression of CCN1, alpha six, and beta one, atheroprone flow creates a positive feedback to sustain atherogenesis. In addition, disrupting CCN1, alpha 6 beta one engagement by a specific CCN1 mutation, or by a peptide antagonist unhindered atherogenesis in mice. So what are the clinical implications of these findings? That's something Carolyn would ask me. Well, it appears that CCN1 alpha 6 beta one engagement represents a novel therapeutic target for arthrosclerosis. These data demonstrate a causative role of CCN1 in atherosclerosis via modulating endothelial phenotypes. And CCN1 binds to its receptor integrin alpha 6 beta one to activate NF kappa beta, thereby instigating a vicious cycle to persistently promote atherogenesis. Perhaps in the future T1 me medics may further be optimized to treat arthrosclerosis. Well everyone, that concludes the first portion of this June 18 edition of Circulation on the Run and now it's time to move on to Carolyn's discussion of our featured paper. Dr Carolyn Lam: Cardiovascular disease remains the major cause of death in kidney transplant recipients. And today's featured paper has important implications for the management of this cardiovascular risk following kidney transplantation. I'm so excited to be discussing it, and I'm going to let the corresponding author Dr Toby Coates from Royal Adelaide Hospital tell us all about it, and so happy to also welcome our editorialist Dr Patrick Mark from University of Glasgow. Toby, could you please tell us what inspired you to do this remarkable study? Dr Toby Coates: We're very interested in obviously our patients surviving as long as they possible can after kidney transplantation. And we noticed that many of them having had a successful kidney transplant, still had functioning AV fistulas. Now of course the AV fistula, is a connection between the artery and the vein that enabled us to access the circulation after hemodialysis. Which around the world is probably the most, is the most common form of dialysis practice performed. So many of these patients sustained 20 years down the track after successful transplants still had these very large functioning left to right shunts, on the basis of their dialysis history. So we had a couple of patients who developed quite severe cardiac failure and we noticed that when we ligated the AV fistula, their back got dramatically better. So, as a consequence of that, we went to look at the ligature and we couldn't find any randomized control trial that told us what the best thing was to do, post-transplant with these fistulas. So we decided that what we would do be use the state of the art cardiac magnetic resonance imaging, or cardiac MRI to assist the cardiac function with myocardium thickness in our patients and then randomize a group of stable transplant patients to ligation or not. And then follow that up with cardiac MRI six months down the track to see what happened. And so that was the basis of the study that we performed. The first randomized controlled trial of the effect of ligation of the AV fistula on the left ventricular mass, that was the prominent one for trial. Dr Carolyn Lam: You know, Toby, just to let you know right there, I thought it was so incredibly novel. So I'm a heart failure specialist and we know that shunts are associated with high output cardiac failure, and yet, I personally had never questioned this, so I thought this is incredibly novel and it's important. But please, tell us all about the results. Dr Toby Coates: We were delighted to say that there was a very significant reduction in the left ventricle mass. In fact, the main decrease was 22.1 grams compared to the control arm in whom the cardiac mass actually went up 1.2 grams. So, then we mobilized the body surface area, the reduction of the left ventricular mass index dropped by 11.8 grams per metered square. Now, this is quite remarkable for me doing the study because I've never seen an intervention, I've never seen an intervention where every single patient improved with the ligation, every single patient there was an improvement in the cardiac parameters. Never seen anything like it in the pre and post of the ventricular mass it really came down. So that was quite remarkable. And the second thing that really impressed me at the time, was the improvement in the BMP's, and we measured the brain maturated peptide, and being a methodologist that's clearly something that's of interest to us and we saw a substantial reduction. It's statistically significant reduction in BMP as well. The patient themselves, some of them recorded quite significant improvement in exercise tolerance afterwards. And we had, as I mentioned before in a couple of patients, not in the study but outside of the study, subsequently when they're presented with profound right heart failure, the ligation of the AV fistula made a huge difference to them symptomatically. So that was sort of confirming all of the things that we thought along the way. Pleasingly we didn't see any change in kidney function. So, we were concerned that there might have been on the basis of some non-controlled studies in the past, that there might have been a deterioration in the estimated glomerular filtration rate, or eGFR. We didn't see that. And we didn't see any significant change in the blood pressure either. Which is some of us have previously reported. Closing the fistula itself, is a very trivial procedure. It's usually done as an outpatient, so a day procedure. So it's not resulting in coming to the hospital. And the only complications, really were lots of local redness and some pain, potentially from the fistula where in the ligated. So, we thought this was remarkable. An outpatient procedure that could significantly reduce the left ventricular mass by 22.1 grams over the six month period that was associated with minimal side effects and complications. And when you think about that, that's sort of equivalent really to taking an anti-hypertensive medication for six months. That magnitude of reduction with ventricular mass which clearly from the patient's point of view is much preferable to adding more medication to an already over-burdened tablet loading in your patients with kidney transplants. So we were very pleased with that result altogether. Dr Carolyn Lam: Thank you Toby, and we in turn were very pleased to be publishing this in Circulation. Likewise, Patty, if I may, I love your editorial. First, let me tell everybody who's listening out there. Go pick up the editorial and look at the figure. It is so cool. It shows pros and cons of arterial venous fistula ligation in these patients. But could you please share some thoughts Patty? I mean you covered the perspective just so well. Patrick Marks: I must give the credit to my co-author who actually drew the figure himself. So Chris Eaves rather myself. We were really impressed with the study and we're really delighted to write an editorial for it. It's just one of those studies that I have to say, you know, you kick yourself and you wish you'd done it. With all the world of observational data showing that creation of a fistula appears to be associated with an increase in LV mass obstruction by echo and angio and bicartic MR in smalls studies. But it's taken a long stat to move from that to actually doing a randomized control of ligating the fistula in people with you know, stable functioning transplants. We were really, really impressed with Toby and his team for undertaking this study. And until we'd gone through the results, they're really very impressive. The magnitude of reduction LV mass is very impressive and also the changing BMP was really nice to see. One of my comments of the study were, was interesting because as methodologists we are aware of the idea arteriovenous fistula as being the axis for dialysis. And we sometimes feel uncomfortable by ligating this because we know if the transplant was to fail, how much patients need a functioning fistula. And that's the one thing I'm still curious, like and I still offered some comments in the editorial were, that while there's doubt that the cardiovascular benefits demonstrated by Toby's study are really very impressive. I wondered about the implications out with the study came down the line, you know would there be some of these patients whose kidney transplant function would decline? And there may be regret of losing the access. We mentioned there is some inconvenience, it is an operative procedure to loosen the fistula. So there are some things to think about in the study, but overall, I can't help saying just how impressed I am that they managed to do this trial in a proper randomized, controlled trial form. It's really, really impressive in using the cardiac MR endpoint is it seems quite a secure way of assessing this. Dr Carolyn Lam: Those are great points, Patty. Toby, any response to that. Dr Toby Coates: Look it's really very interesting as a transplant pathologist for the last 20 years, one of the biggest, I guess it's a bit of a misconception. When a fistula has been present for 10 or 15 years and still there to come back and try and reuse it for dialysis access after that period of time, in my experience anyway, also very difficult to reuse those fistulas and the surgeons end up having to create a new one anyway. They frequently become quite aneurismal, they get very large and unsightly and the volume of the shunt is significant and often we find that as an access they don't work as well. So I personally don't have a huge concern about closing them. Now I agree with you, these patients were stable, longstanding and we assessed that the risk is, we need to go back onto hemodialysis was small. But you are absolutely right, I mean, it is possible that something could have come out of the blue and maybe a patient would be disappointed that that access that they'd had for so many years was no longer available. So that is, the caveat on the study, but thankfully so far out, some of these patients five or six years down the track, we haven't had anybody need to go back on dialysis, so it's been good. Dr Carolyn Lam: Yeah, it really says to me as well, that patient selection is important exactly like you emphasized, and you, in the editorial Patty. But from a cardiology standpoint, too, are there plans to perhaps do studies with hard, clinical endpoints? What do you think are the next steps? Maybe I'll let Toby go first, then Patty. Dr Toby Coates: We think now with this study done, the next thing is to have a larger study with significant cardiovascular endpoints. Which I obviously would be cardiac failure and acute coronary events. So the two things that would seem in my mind, and I think that needs to be multi-centered, preferable international if we can. And one of the really positive things about the highlight from the American Heart Association is that we've had people reach out to us from France and all around the globe saying that they'd be interested in participating, you know in a multi-centered trial. So, I think that's what we need to do, and clearly you don't it’ll have to be a constant endpoint, or not. I'd be interested in Patty's thoughts about that, right if you had some guidelines and some suggestions. And then obviously would be randomized, controlled trial looking at those hard endpoints with probably some sidearms doing cardiac MRI as well, and potentially more heart functioning tests. So yes, I think this is just the beginning, we do need a hard endpoint trial to really nail this completely. Patrick Marks: Yeah, I'll just come in there and just come on to that Toby. I completely concur with what you said. I think there's been quite a provocative editorial a few years back, and suggesting that while there's lots of studies in chronic kidney disease, end stage renal disease, kidney transplant patients avoid LV mass, really it hasn't yet been translated into actually leading studies in the integration of LV mass and end stage renal failure haven't really yet translated into mortality benefits. And I think we need to move to a bigger study. It's really beautiful that you've been able to demonstrate LV mass falls naturally with ligation. And it's impressive that it just happens so consistently across your population in the intervention arm. But we need to move on to a longer trial with hard clinical endpoints. Certainly heart failure, certainly cardiovascular mortality, [be]cause there's plenty of reasons to believe that producing LV mass in these patients might have benefit both for heart failure, whether that's heart failure, heart injection fraction, or whatever, I'll leave that to Carolyn's judgment to help us with that. But also, if we can reduce LV mass and then we may be able to reduce arrhythmia burden which again is when these things we worry about in end stage renal disease, again, your answer for that is, that in addition to the heart endpoints you should be able to also add in some patient afforded outcomes in a larger study. Or something like an exercise tolerance quota of quality of life. All this has started has journey from the surrogate endpoint of left ventricular mass into a bigger outcome study and I can't wait to see how you get on with it. Dr Carolyn Lam: I can't wait either. And I'm sure the audience is sharing all our enthusiasm as well. Thank you so much Toby and Patty. I really learned so much. You heard it right here on Circulation on the Run. Thank you for joining us this week. Don't forget to turn in again next week. This program is copyright American Heart Association 2019.

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Peri-Operative Dilemmas: Dabigatran for Myocardial Injury Post-Op and Functional Capacity Assessments

Play Episode Listen Later Sep 7, 2018 34:09

Kieran Quinn and Paxton Bach kick off Season 5 of The Rounds Table with two articles surrounding peri-operative medicine – both relevant to a wide variety of health care practitioners. The first addresses the use of dabigatran in myocardial injury after non-cardiac surgery (MINS) and the second covers assessment of functional capacity before major non-cardiac ... The post Peri-Operative Dilemmas: Dabigatran for Myocardial Injury Post-Op and Functional Capacity Assessments appeared first on Healthy Debate.

injury capacity functional assessments dilemmas mins operative post op myocardial dabigatran kieran quinn

Peri-Operative Dilemmas: Dabigatran for Myocardial Injury Post-Op and Functional Capacity Assessments

BaladoCritique – club de lecture médical

Play Episode Listen Later Sep 7, 2018 34:08

Kieran Quinn and Paxton Bach kick off Season 5 of The Rounds Table with two articles surrounding peri-operative medicine – both relevant to a wide variety of health care practitioners. The first addresses the use of dabigatran in myocardial injury after non-cardiac surgery (MINS) and the second covers assessment of functional capacity before major non-cardiac ...The post Peri-Operative Dilemmas: Dabigatran for Myocardial Injury Post-Op and Functional Capacity Assessments appeared first on Healthy Debate.

injury capacity functional assessments dilemmas mins operative post op myocardial dabigatran kieran quinn

BC 018 – Dabigatran chez les patients avec lésion myocardique post-chirurgie non cardiaque (étude MANAGE)

Play Episode Listen Later Jul 16, 2018 39:36

Dans cette 18e baladodiffusion, le Dr Luc Lanthier discute de l’effet du dabigatran chez les patients avec lésion myocardique post-chirurgie non cardiaque (étude MANAGE), en plus de réviser la littérature médicale de juin 2018. Quiz clinique (2 min 02), étude principale (2 min 22), critique (21 min 30), autres articles (30 min 35), réponse au … Continuer la lecture de « BC 018 – Dabigatran chez les patients avec lésion myocardique post-chirurgie non cardiaque (étude MANAGE) »

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MANAGE Trial: Dabigatran in Patients With MI After Non-Cardiac Surgery

Cardiology Now

Play Episode Listen Later Mar 11, 2018 5:04

Dr. PJ Devereaux and Dr. Gibson Discuss Subscribe on iTunes or Google Play.

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Circulation: Arrhythmia and Electrophysiology On the Beat September 2017

Circulation: Arrhythmia and Electrophysiology On the Beat

Play Episode Listen Later Sep 19, 2017 64:27

Dr. Paul Wang : Welcome to the monthly podcast On the Beat for circulation, arrhythmia and electrophysiology. I’m Dr. Paul Wang editor in chief with some of the key highlights from this month’s issue. We’ll also hear from Dr. Suraj Kapa reporting on new research for the latest journal articles in the field. The first article in this month's issue is by Yoav Michowitz and Associates who examine the morphological ECG characteristics of left posterior fascicular ventricular tachycardia and differentiated from right bundle branch block and left anterior hemiblock aberrancy. 183 ECGs with left posterior fascicular ventricular tachycardia in patients who underwent ablation were identified using a systematic Medline search were examined and compared to 61 ECGs with right bundle branch block in left anterior hemiblock aberrancy with no obvious cardiac pathology by echocardiography. Using four variables including atypical right bundle branch block like V1 morphology, positive QRS in aVR, V6R greater than S ratio of less than one and QRS less than or equal to 140 ms, a prediction model was developed that predicted posterior fascicular ventricular tachycardia with a sensitivity of 82% and a specificity of 78%. Patients with three out of four positive variables had a high probability of having left posterior fascicular ventricular tachycardia whereas patients with less than or equal to one positive variable always had right bundle branch block plus left anterior hemiblock. In the next article, Anna Thøgersen and associates describe a case series of 10 patients in whom implantable cardioverter defibrillators failed to treat ventricular tachyarrhythmias. The authors examine whether consensus derive generic rate threshold cutoffs between 185 and 200 beats per minute were employed in this case series. In nine patients, ventricular fibrillation did not satisfy program detection criteria. Five patients died with untreated ventricular fibrillation, four had cardiac arrest requiring external shocks and one was rescued by a delayed ICD shock. Seven of these patients had slowest detection rates that were consistent with generic recommendations but not tested in a peer review trial for their manufacturer’s ICDs. In the reported cases, manufacturer specific factors interacted with fast detection rates to withhold therapy including strict ventricular fibrillation episode termination rules, enhancements to minimize T-wave over sensing and features that restrict therapy to regularly rhythms in VT zones. Untreated ventricular fibrillation despite recommended programming accounted for 56% of the deaths and 11% of all of deaths. The authors concluded that complex and unanticipated interactions between manufacturer specific features and generic programming can prevent therapy for ventricular fibrillation. In the next article, Miguel Rodrigo and associates describe from 17 simulations of atrial fibrillation, atrial flutter and focal atrial tachycardia the ability to understand signal processing that can affect identification of reentrant activity using electrograms, body surface potential mapping and electrocardiographic imaging ECGI phase maps. Reentrant activity was identified by singularity point recognition and raw signals and in signals after narrow band pass filtering at the highest dominant frequency. Reentrant activity was identified without filtering in 60% of unipolar records but filtering was required to increase reentrant activity detection from 1% to 62% in bipolar recordings. The filtering resulted in residual false reentrant activity in about 30% of bipolar recordings. The authors concluded that rotor identification is accurate and sensitive and does not require additional signal processing in measured or noninvasively computed unipolar electrograms while bipolar electrograms and body surface potential mapping do require highest dominant frequency filtering in order to detect rotors at the expense of a decrease specificity. In the next article, Raymond Yee and associates examine the ability of a new automated antitachycardia pacing algorithm to reduce ICD shocks. The new automated ATP algorithm was based on electrophysiologic first principles and prescribed the ATP sequences in real time using the same settings for all patients. In 144 patients who had dual chamber or CRT ICDs as well as a history of one or more ICD treated VT or VF episodes or a recorded sustained monomorphic ventricular tachycardia episode. Detection was sent to ventricular fibrillation interval detection of 24 out of 32 ventricular tachycardia interval detection of 16 or greater in a fast VT zone of 242 to 320 ms. There were 1,626 treated episodes in 49 patients over 14.5 month’s follow up. Data logs permitted adjudication of 702 episodes including 669 sustained monomorphic ventricular tachycardia episodes, 20 polymorphic ventricular tachycardia episodes, 10 SVT episodes and three mal sensing episodes. The novel automated antitachycardia pacing algorithm terminated 39 out of 69 episodes or adjusted 59% of the sustained monomorphic ventricular tachycardia events in the fast VT zone, but 509 out of 590 or 85% adjusted in the VT zone and 6 out of 10 in the VF zone. No SVTs were converted to VT or VF and no anomalous ATP behavior was observed. The authors concluded that this new automated ATP algorithm could be used safely in all zones without need for individualized programming. In the next study Pablo Ávila and associates studied the incidence and clinical predictors of atrial tachycardias in adults in a cohort of 3,311 patients with congenital heart disease. Prospectively followed in a tertiary center for 37,607 person years. The study patients were divided into three categories; 49% simple, 39% moderate and 12% complex congenital heart disease. In this cohort, 153 or 4.6% of patients presented with atrial tachycardia. The atrial tachycardia burden was highest in complex congenital heart disease such as single ventricle 22.8% or D-TGA 22.1%. The authors found that univentricular physiology, previous intracardiac repair, systemic right ventricle, pulmonary hypertension, pulmonary regurgitation, pulmonary AV valve regurgitation and pulmonary and systemic ventricular dysfunction were independent risk factors for developing atrial tachycardia. At the age of 40 years, atrial tachycardia free survival in patients with zero risk factors was 100%. With one risk factor, it was 94%. With two risk factors was 76% and three or more risk factors was 50%. These authors confirm these findings in a validation cohort. In the next article, Khidir Dalouk and associates compare clinical outcomes between ICD patients followed up in a telemedicine videoconferencing clinic and a conventional in person clinic. In this retrospective study, the authors compared time to first appropriate ICD therapy, time to first inappropriate ICD therapy, time to first shock and overall survival. The authors studied 287 patients in the telemedicine videoconferencing clinic group and 236 patients in the conventional in person clinic over mean follow-up duration of 4.8 years. The authors found that telemedicine videoconferencing clinic was not inferior to in person follow-up for the pre-specified outcomes. In the next article, Elisabeth Mouws and associates studied the epicardial breakthrough waves in sinus rhythm possibly giving insight to the arrhythmogenic substrate in atrial fibrillation. In 381 patients with ischemic or valvular heart disease, intraoperative epicardial mapping with intro electro distance of 2 mm was performed of the right atrium, Bachmann’s bundle, the left atrioventricular groove and the pulmonary vein area. Epicardial breakthrough waves were referred to as sinus node breakthrough waves if they were the earliest right atrial activated site. A total of 218 epicardial breakthrough waves and 57 sinus node breakthrough waves were observed in 168 patients or 44%. Epicardial breakthrough waves mostly occurred at the right atrium and 48% at the left atrioventricular groove and 31% followed by Bachmann’s bundle and 12% and the pulmonary vein area and 9%. Epicardial breakthrough waves occurred most often in ischemic heart disease patients 49% to valvular patient's 17%. Epicardial breakthrough wave electrograms most often consisted of double or fractionated electrograms seen in 63%. Fractionated epicardial breakthrough wave potentials were more often observed at the right atrium or Bachmann's bundle. The authors concluded that epicardial breakthrough waves are present in over a third of patients possibly indicating muscular connections between the endocardium and epicardium that may enhance the occurrence of epicardial breakthrough waves during atrial fibrillation promoting AF persistence. In the next article, Shouvik Haldar and associates compare horizontal and vertical orientation bipolar electrograms with novel omnipolar peak to peak voltages in sinus rhythm and atrial fibrillation using a high density fixed multi-electrode plaque placed on the epicardial surface of the left atrium in dogs. Bipolar orientation had significant impact on bipolar electrogram voltages obtained either in sinus rhythm or atrial fibrillation. Omnipole Vmax values were 99.9% larger than both horizontal or vertical electrograms in sinus rhythm in larger than horizontal or vertical electrograms in atrial fibrillation. Further vector analysis of omnipole electrograms showed that omnipolar electrograms can record electronic voltage unaffected by collision and fractionation. The authors concluded that omnipolar electrograms can attract maximal voltages from AF signals which are not influenced by directional factors, collision or fractionation compared to contemporary bipolar techniques. In our final article for the month, Pauline Quenin and associates examine the efficacy of screening in relatives of subjects who died suddenly. The authors provided clinical screening to 64 families who experienced unexplained sudden cardiac death before age 45 in a prospective multicenter registry. The diagnosis was established in 16 families, 25% including Brugada syndrome, long QT syndromes, dilated cardiomyopathy and hypertrophic cardiomyopathy. The diagnostic yield was mainly dependent on a number of screen relatives with 3.8 screen relatives in the diagnosed family versus 2.0 in the non-diagnosed families rising to 40% with at least three relatives. It additionally increased from 9% to 41% when both parents were screened. Diagnostic performance was also dependent on the exhaustiveness of the screening. 70% of complete screening versus 25% with incomplete screening with 17 Brugada syndrome and 15 long QT syndrome diagnoses based on pharmacologic tests. The authors concluded that even without autopsy, familial screening after sudden death in young patients is effective greatly increasing the likelihood of diagnosis in families. That's it for this month but keep listening. Suraj Kapa will be surveying all journals for the latest articles on topics of interest in our field. Remember to download the podcast On the Beat. Take it away Suraj. Suraj Kapa: Thank you Paul. It is my pleasure to welcome everybody back to our continued series of On the Beat articles from across the electrophysiology literature especially selected to highlight their potential importance in terms of either current or future practice within the realm of cardiac electrophysiology. Again, my name is Suraj Kapa and it is my pleasure to walk us through a variety of hard-hitting articles. Today we’ll be starting within the realm of atrial fibrillation specifically as it relates to cardiac mapping and ablation. The first article was by Iwasawa et al entitled Temperature Controlled Radiofrequency Ablation for Pulmonary Vein Isolation in Patients with Atrial Fibrillation published in volume 70 of the Journal of the American College of Cardiology. In this article, Iwasawa and colleagues discuss the role of novel temperature controlled irrigated ablation catheter to attempt to obtain deeper transmural lesions in cardiac tissue, specifically they tested the utility of a diamond embedded tip for rapid cooling accompanying six surface thermocouples to better reflect tissue temperature. They demonstrated in this first in human series that a temperature controlled irrigated ablation could produce rapid, efficient and durable PV isolation. The importance of this particular article lies in the continued development of novel tools that can achieve pulmonary vein isolation either more safely or more quickly. This was highlighted in the article by Iwasawa et al when they demonstrated that the mean radiofrequency application duration was significantly less by almost a factor of three and those using the novel radiofrequency ablation catheter versus those with older models. They also noted that there was lower acute dormant pulmonary vein re-conduction rates and patients tend to have more frequent durable isolation when remapped after ablation. While the study group only consisted of 35 patients within the treatment group and 35 patients within the control group, the potential of these novel catheters to achieve aims of both shortening procedure duration as well as improving procedure and success need to be taken in consideration. The next article is by Dr. Gopinathannair entitled Atrial Tachycardia after Surgical Atrial Fibrillation Ablation Clinical Characteristics, Electrophysiological Mechanisms and Ablation Outcomes from a large multicenter study published in the August 2017 issue of JACC Clinical Electrophysiology. In this article, Dr. Gopinathannair reviews the outcomes of cardiac mapping and ablation targeted atrial tachycardias occurring after surgical atrial fibrillation ablation. They reviewed a large number of patients nearly 137 undergoing catheter ablation for symptomatic postsurgical atrial fibrillation ablation atrial tachyarrhythmias across three high volume institutions in the United States. They demonstrated that the vast majority had a left atrial origin though up to a third also had a right atrial origin further atrial tachyarrhythmias. The predominant circuits noted were cavotricuspid isthmus but also frequently perimitral roof and left or right pulmonary veins. In addition, most of the patients namely 93% had at least one pulmonary vein reconnection requiring re-isolation. The key point with the article however were the outcomes. They demonstrated that acute termination inducibility could be achieved in as many as 97% of right atrial and 93% of left atrial tachyarrhythmias in the setting of prior surgical ablation. Furthermore, 12 month followup demonstrated an 80% success rate. Traditionally, surgical atrial fibrillation ablation is seen as a complex procedure with the remapping of arrhythmias requiring a lot more complexity. However, these findings cross a large group of patients suggesting that we can have a high rate of success should propose to individuals that perhaps targeted ablation at these postsurgical atrial tachyarrhythmias should be amenable towards ablation especially at high volume complex ablation centers. Next will discuss the article by Pathik et al entitled Epicardial-Endocardial Breakthroughs through Stable Macroreentry: Evidence from ultra-high-resolution three-dimensional mapping published in Heart Rhythm in August 2017. In this article, the group of Pathik et al decided to review whether epicardial-endocardial breakthrough could be discerned during stable right atrial macroreentry using high density and high spatial resolution three-dimensional mapping. Twenty-six patients were studied and they noted that up to 14 patients had evidence of epicardial-endocardial breakthrough. Using systematic entrainment confirmation, stable atrial macroreentry with epicardial-endocardial breakthrough was consistently demonstrated. The principle of epicardial-endocardial breakthrough or dissociation is critically important during cardiac mapping. While widely accepted for ventricular mapping, the tradition because of lack of available tools and atrial mapping has suggested that endocardial only mapping should reveal the entire cardiac circuits. Advances in signal processing as well as cardiac mapping techniques and technologies has allowed for better discernment of potentially deeper manifestations of cardiac tissue involvement in cardiac arrhythmias. As been well recognized that there can be significant epicardial and endocardial dissociation in cases of persistent atrial fibrillation. The article by Pathik et al is important in that it highlights that such events can manifest themselves even in the setting of relatively organized or stable atrial macroreentry. Part of the reason this becomes so critical is that when we consider endocardial only remapping and rely on these signals alone, we may run into situations where we miss a significant chamber of atrial tissue namely the epicardium, thus the focus of this article and the consideration of it in the clinician's repertoire of cardiac mapping and ablation should lie in an understanding of the fact that the entire story of an electrical circuits may not be told by traditional endocardial mapping alone without consideration for epicardial-endocardial breakthrough. The next article we will focus on is by Dr. Chun et al regarding the impact of cryoballoon versus radiofrequency ablation for paroxysmal atrial fibrillation on healthcare utilization and costs and economic analysis. This was from the FIRE and ICE Trial published in the Journal of the American Heart Association this past month. In this study they sought to assess payer cost following cryoballoon or radiofrequency catheter ablation for paroxysmal atrial fibrillation. They demonstrated that there are cost savings of as much as $355,000 related to the use of cryoballoon over traditional radiofrequency catheter ablation. This reduction in resource use and payer costs was consistent across three different national healthcare systems. Furthermore, the reason for the reduced cost was primarily attributable to fewer repeat ablations and a reduction in cardiovascular rehospitalizations with cryoballoon ablation. In this era of cost reduction, it is important to consider the potential implications of use of novel technologies in terms of procedural costs. The ability to identify novel techniques that can actually both reduce costs and either achieve equal or improved outcomes needs to be strongly considered. While the three national healthcare systems reviewed here might not reflect all healthcare systems or all insurance needs, it still brings up an important economic consideration that all novel technology may not necessarily result in increased costs, and utilization must be considered both in the context of the particular system as well as the particular provider. Changing pace, we’ll move on with an atrial fibrillation to the role of anticoagulation. The first major article recently published is by Pollack et al regarding the use of Idarucizumab for dabigatran Reversal, the full cohort analysis published the New England Journal of Medicine. Idarucizumab is a monoclonal antibody fragments developed to reverse the anticoagulant effect with dabigatran and represents the first reversal agent available for reversal of any of the novel oral anticoagulant drugs. In this study which is both multicenter, prospective and open label, patients were enrolled to undergo treatment with this reversal agents. A total 503 patients were included and the median maximum percentage reversal dabigatran was 100% which was measured using the diluted thrombin time or the ecarin clotting time. In those with active bleeding, the median time to cessation of bleeding was around 2.5 hours. Furthermore, in a surgical cohorts who underwent reversal in order to accommodate them going to surgery, the time to initiation of an intended procedures was 1.6 hours with periprocedural hemostasis assessed as normal in 93%, mildly abnormal in 5% and moderately abnormal in 1.5%. Thrombotic events occurred in about 6.3% of patients undergoing reversal because of active bleeding and then 7.4% undergoing reversal for surgical accommodation. Mortality rates were around 18% to 19%. Thus it was demonstrated that in emergency situations Idarucizumab can rapidly, durably and safely reverse the anticoagulant effect of dabigatran. However, it is important to note that there was a signal for thrombotic events and consideration of the risk of rapid reversal of anticoagulation regardless of the type of anticoagulation in combination with the actual need for reversal should be considered in the patient context. The next article we will review is by Jackevicius et al entitled Early Non-persistence with Dabigatran and Rivaroxaban in Patients with Atrial Fibrillation, published in Heart this past month. In this article, the group reviewed how patients manage being on their novel oral anticoagulants over the course of time after initial diagnosis and prescription. One of the concerns regarding novel oral anticoagulants is given the fact that there is no actual tracking or no actual measurements needed to ensure continued adherence to the drug, whether or not there will be higher rates of nonpersistence with use of these novel oral anticoagulants. Amongst 15,857 dabigatran users and 10,119 rivaroxaban users, they noted that at six months about a third of patients were nonpersistent with either drug. In those patients who were nonpersistent with use of the drug, the combined endpoint of stroke, TIA and death was significantly higher with hazard ratios of 1.76 in the dabigatran cohort and 1.89 in the rivaroxaban cohort. Furthermore, the risk of stroke or TIA was markedly higher in nonpersistent patients with about a hazard ratio of 3.75 in dabigatran nonpersistence and 6.25 in rivaroxaban nonpersistence. Given these relatively high rates of nonpersistence in clinical practice and the negative outcomes associated with nonpersistence, this highlights the importance of continued validation of the need for persistence with use of oral anticoagulation in patients prescribed these perceived to be at high risk of stroke associate with atrial fibrillation. In an era of improving drug use or improving drugs that can be used without the need for blood testing, it must also be considered that these drugs may be more easily stopped on the patient's own discretion without any knowledge from a provider as there is no active blood test associated. Thus this further highlights the importance of continued discussion between patients and physicians over the course of therapy and care regarding the need for continuation. Changing paces. We review the article by Godier et al entitled Predictors of Pre-procedural Concentrations of Direct Oral Anticoagulants a prospective multicenter study published at the European Heart Journal. We all know that one of the major issue with a direct oral anticoagulants is that these patients frequently undergo elective invasive procedures and in this setting the management can be very challenging specifically as it relates to when the direct oral anticoagulants should and can be safely stopped. In clinical practice, there is wide variability in the timing by which providers inform patients to stop these new oral anticoagulants prior to invasive procedure. In this prospective multicenter study, 422 patients were evaluated with preprocedural DOAC concentrations and routine hemostasis assays performed to determine those patients who achieved a minimal preprocedural concentration based on the timing of their discontinuation of the drug. They ranged the duration of discontinuation of the oral anticoagulant from 1 to 218 hours. They noted after a 49 to 72 hour discontinuation period, 95% of the concentration of the direct oral anticoagulants in patients had levels that were significantly low suggesting safety and proceeding with any sort of invasive procedure. Thus a 72 hour discontinuation period predicted sufficiently low concentrations of DOACs with 91% specificity. In multivariable analyses, duration of the DOAC discontinuation with creatinine clearances and antiarrhythmics were independent predictors of a minimal preprocedural DOAC concentration, namely better renal function, longer duration of DOAC discontinuation and interestingly the use of antiarrhythmic drugs were all associated with lower DOAC concentrations. The conclusion from this article was a last DOAC intake of three days before a procedure resulted in a minimal preprocedural anticoagulant effect for almost all patients considered. The exception would be in moderate renal impairment especially in dabigatran treated patients and antiarrhythmics in anti-Xa-treated patients could result in the need for longer DOAC interruption. Thus, the key things here to note are that antiarrhythmics can result in the need for longer DOAC interruption to achieve minimal blood concentrations and that similarly moderate renal impairment especially in dabigatran treated patients may result in the same. Another outcome other studies suggested a lack of association between routine assays such as routine hemostasis assays and DOAC concentrations suggesting that in situations where testing is believed to be needed routine assays should not replace DOAC concentration measurement in decision-making regarding whether or not the DOAC has sufficiently gone down in concentration to safely proceed. Along these lines, the final article we will review within the realm of anticoagulation is by Brendel et al entitled the Anticoagulant Effect of Heparin during Radiofrequency Ablation in Patients Taking Apixaban or Rivaroxaban published in the Journal of Interventional Cardiac Electrophysiology this past month. One concern regarding the use of the direct oral anticoagulants is the fact that during procedures where heparin is needed, knowledge of how much heparin to give is unclear. This is both in the setting of understanding what the synergistic effect of the simultaneous and continued use of apixaban or rivaroxaban or other direct oral anticoagulants in combination with heparin might be and also what the effect on actual activated coagulation time might be. As it is felt that be ACT may not necessarily reflect the true anticoagulant activity of drugs. Thus in a prospective study, Brendel et al studied about 90 patients with atrial fibrillation undergoing radiofrequency ablation procedures. During radiofrequency ablation, unfractionated heparin was given to maintain ACT of 250 to 300 ms with blood samples taken before and up 360 minutes after heparin administration. They demonstrated that heparin displayed a lower anti-Xa activity in rivaroxaban treated patients compared to apixaban treated patients. In contrast, D-dimer and prothrombin fragment F1+2 plasma levels indicated a higher activation of the coagulation cascade in apixaban/heparin combinations than in rivaroxaban/heparin combinations. While there was clear differences in the level of anticoagulant effect, depending on which DOAC was combined with heparin, they had no clinical impact in terms of bleeding or thromboembolic complications from the procedure. This article is significant in that it highlights that there are clear and different biochemical responses based on which DOAC is used in combination with heparin during radiofrequency ablation. While in the small study, there was no clear effect on clinical impact, precautions should still be considered when monitoring periprocedural hemostasis in DOAC patients to avoid mismanagement especially considering the variability that might occur between DOACs themselves and not just between DOACs and warfarin. Changing paces to risk stratification and management within atrial fibrillation. We’ll review the article by Labombarda et al entitled Increasing Prevalence of Atrial Fibrillation and Permanent Atrial Arrhythmias in Congenital Heart Disease published in this past month's issue of the Journal the American College of Cardiology. In this article, they sought to assess the types and patterns of atrial arrhythmias, associate factors and age-related trends in a multicenter cohort of patients with adult congenital heart disease. What they demonstrated is that by far the most common presenting arrhythmia was intraatrial reentrant tachycardia in almost two-thirds of patients with the remaining including atrial fibrillation in up to 30% of patients and focal atrial tachycardias in up to 10% of patients. The association of intraatrial reentrant tachycardia with congenital heart disease was stronger with higher complexities of congenital heart disease. With those with more complex defects having a higher frequency of IART than those with simple effects. Furthermore, as is commonly seen in the general population, the frequency of atrial fibrillation increased with age to eventually suppress IART as the most common arrhythmia in those greater than equal to 50 years of age. The predominant arrhythmia pattern was paroxysmal in almost two-thirds of patients though almost 30% were persistent. Furthermore, the frequency of permanent atrial arrhythmias increased with age. While it is commonly seen that patients with congenital heart disease were living longer and as a result it is expected that the frequency of arrhythmias in this population will likely increase. The interesting outcome from the study is the high frequency of intraatrial reentrant tachycardia as the presenting atrial arrhythmia in patients with congenital heart disease and also with the predominantly paroxysmal pattern. The finding also that atrial fibrillation increases in prevalence highlights the importance of closely monitoring these patients in order to assess for anticoagulation needs and options for treatment. Changing gears to cellular electrophysiology. We focus on an article by Qiao et al entitled transient Notch activation induces long-term gene expression changes leading to sick sinus syndrome in mice published in this past month's issue of Circulation Research. Notch signaling programs cardiac conduction during development and in the adult ventricle. It is noted that injury can induce notch reactivation resulting in global transcriptional and epigenetic changes. Thus, the group sought to determine whether notch reactivation may alter atrial ion channel gene expression arrhythmia inducibility. They demonstrated that notch signaling regulates transcription factor in ion channel gene expression in adult atrial myocardium. With reactivation inducing electrical changes resulting in sinus bradycardia, sinus pauses and a susceptibility atrial arrhythmias, altogether contributing to a phenotype resembling sick sinus syndrome. The importance of these findings lies in the mechanism underlying sick sinus syndrome. While we search for genetic clues for why patients might develop atrial fibrillation or sick sinus syndrome or sinus bradycardia as they age, the importance of activation of typically quiet signaling patterns in the adult myocardium and their role in arrhythmogenesis is important because it might highlight novel targets for treatment. Understanding how the arrhythmogenic substrate develops and the mechanisms underlying it, may allow for a better understanding of why in certain patients certain drugs may be effective or not or certain invasive therapies may be effective or not. Next with the realm of electrocardiography, we’ll review the article by Christophersen et al entitled 15 Genetic Loci Associated with Electrocardiographic P-wave published in Circulation Genetics this past month. Similar to the previous article by Dr. Qiao et al, the importance of the article by Christophersen et al lies in the identification of a number of genetic underpinnings for what forms the final electrocardiographic P-wave that is seen. Six novel genetic loci associated with P-wave duration and six novel loci associated with P-wave terminal force were identified by the group. Both in the case of the transient Notch activation findings as well as in the findings related to a specific genetic loci associated with electrocardiographic P-wave abnormalities might highlight potential genetic targets either with existing drugs not traditionally used for atrial electrophysiology or potentially future drug targets. Changing gears yet again, we’ll move on to their own sudden death cardiac arrest and specifically to an article published by Fallavollita et al entitled the denervated myocardium is preferentially associate with sudden cardiac arrest in ischemic cardiomyopathy a pilot competing risks analysis of cost specific mortality. Previous studies identify multiple factors associated with total cardiac mortality but we all recognize the ejection fraction has limited value. Thus within this article published in Circulation: Cardiovascular Imaging, the group decided to do a competing risks analysis the National Institutes of Health sponsored prediction of arrhythmic events with positron emission tomography trial. They demonstrated that sudden cardiac arrest was correlated with greater volumes of denervate myocardium based on defects on positron emission tomography using a norepinephrine analog carbon 11 hydroxy ephedrine. However, they also demonstrated that other factors such as lack of angiotensin inhibition therapy, elevated BNP and large left particular end-diastolic volume were further associated with sudden cardiac arrest. The importance of potential modifying factors to better attribute cardiac arrest risk and thus the need for defibrillator or other therapies in patients with myopathy needs to continue to be highlighted especially in light of recently published Danish and other studies suggesting that the mortality benefit conferred by ICD is an ischemic and nonischemic populations may not be equivalent in newer studies. The fact that further risk stratification opportunities can exist underlying the pathophysiologic basis for why these patients develop ventricular arrhythmias is critical. While recognized for a few decades now that myocardial denervation may be associated with sudden cardiac arrest risk, this study highlights the continued need for further study to help further clarify these populations. Moving onto the realm of genetic channelopathies, we review the article by Anderson et al entitled Lidocaine Attenuation Testing: An in vivo Investigation of Putative LQT3-Associated Variants in the SCN5A-encoded sodium channel published in this past month's issue of Heart Rhythm. Long QT syndrome type 3 represents one of the more difficult types of long QT syndrome to adequately diagnose both by genetic testing as well as through traditional means. Approximate 2% of healthy individuals can have rare variance of uncertain significance in the SCN5A channel and thus distinguishing true LQT3 causative mutations for background genetic noise can be quite difficult in this population. Anderson et al decided to assess the utility of lidocaine attenuation testing in evaluating patients with possible LQT3. They gave a loading dose of 1 mg per kg of intravenous lidocaine followed by continuous infusions of 50 micrograms for 20 minutes. If the corrected QT interval shortened by at least 30 ms, the LAT was defined as positive. They demonstrated that use of this test can help distinguish true LQT3 causative mutations from otherwise noncontributory variance of uncertain significance. Thus in this era of increasing genetic testing where one might identify a variant of uncertain significance in either a family member affected with sudden cardiac arrest or in a patient being evaluated for any sort of uncertain significant variant, the use of lidocaine testing in those variance as they apply to LQT type 3 may offer significant clinical use. Next we will review the article by Ishibashi et al published in this past month's edition of Heart entitled Arrhythmia Risk and Beta Blocker Therapy in Pregnant Woman with Long QT Syndrome. One of the biggest concerns of patients with long QT syndrome especially woman is pregnancy. The fact is because of the different hormonal states, it is possible that pregnancy may alter arrhythmic risk and the safety of beta blocker therapy given both the potential fetal effects as well as the continued efficacy at the level those seen previously. Thus Ishibashi et al reviewed 136 pregnancies across 76 long QT pregnant patients. They retrospectively analyzed clinical and electrophysiological characteristics in pregnancy outcomes in both the presence and absence of beta blocker therapy. All of the beta blocker group had prior events while the majority of the nonbeta blocker group had not been diagnosed with pregnancy. Pregnancy was noted to increase heart rate in those not treated with beta blockers, but interestingly, between the two groups there was no significant difference over the course of pregnancy in QT intervals. In the beta blocker group, only two events occurred and these were relegated to the postpartum period. However, 12 events occurred in the nonbeta blocker group either during pregnancy and half or in the postpartum period and the remaining half. There was no difference in this frequency of spontaneous abortion between the two groups, and furthermore, fetal growth rates and proportion of infants with congenital malformation were similar between the two groups. However, premature delivery and low birth weight infants were more common in those taking beta blockers. Given the high risk of events and the relative safety of beta blocker therapy in this population of patients with long QT who become pregnant, it was felt that the use of early diagnosis and beta blocker therapy could be critical both the during pregnancy and during the postpartum period. It was also felt the beta blocker therapy may be tolerated for babies in long QT pregnant patients. This highlights that the continued use of beta blockers throughout the pregnancy and consideration of the introduction of beta blockers in those not already on them during pregnancy may be an important consideration. Finally within the realm of genetic channelopathies, we focus on the article by Roberts et al entitled Loss of Function in KCNE2 Variants: True Monogenic Culprits of Long QT Syndrome or Proarrhythmic Variants Requiring Secondary Provocation published in this past month's issue of Circulation: Arrhythmia Electrophysiology. As we identify more and more genes the baby is associated with long QT syndrome, the understanding of the clinical phenotype associated with that syndrome requires better study. In this particular study, Roberts et al reviewed the role of long QT syndrome type 6 stemming from mutations in the KCNE2 encoded voltage gated channel beta subunits. They reviewed mutations identified during arrhythmia evaluation from either inherited arrhythmia clinics or the Rochester long QT syndrome registry. They demonstrated that the high allelic frequencies of LQT6 mutations in the Exome aggregation consortium database and the absence of previous documentation of genotype phenotype segregation suggest many KCNE2 variants and potentially all were actually erroneously designated as LQT as causative mutations. Instead, it was felt the KCNE2 variants may actually confer proarrhythmic susceptibility when provoked by additional environmental and/or acquired or genetic factors. What they are saying is that identifying the KCNE2 variants as the principal culprits may be over calling the role of the KCNE2 variants and instead it might be a combination of effects such as two hit affect the requires further provocation by either outside or additional genetic factors. Furthermore, complex genetic studies were likely needed to better understand how variants and genes that may not have been previously designated as disease causing play a role in the actual disease process, whether as potentiating other factors that might exist that might also otherwise be relatively benign or as unique singular hits that might by themselves result in the clinical phenotype. Next moving onto the realm of ventricular arrhythmias, we first focus on an article published in this past month's issue of the American Journal of Physiology, Heart and Circulatory Physiology by Howard Quijano et al entitled Spinal Cord Stimulation Reduces Ventricular Arrhythmias during Acute Ischemia by Attenuation of Regional Myocardial Excitability. In this article, they demonstrated in a porcine model ventricular ischemia that spinal cord stimulation decrease sympathetic nerve activation regionally in ischemic myocardium while having no effect on normal myocardium. They demonstrated that the antiarrhythmic effects conferred by spinal cord stimulation were likely secondary to attenuation of some sympathoexcitation locally in ischemic myocardium rather than changes in the global myocardial electrophysiology. This is important because it highlights the mechanisms by which spinal cord stimulation may confer in antiarrhythmic benefits in both animal and human models. As we search for novel interventions that can be used for the treatment of ventricular arrhythmias, understanding the underlying pathophysiologic mechanisms by which they work is critical. The understanding that the use of spinal cord stimulation is primarily conferred in a regional way primarily in terms of its effect on an ischemic myocardium, further study is also needed in terms of how the effect is seen in nonischemic myopathies where there may be more patchy scar in the same role of denervation, nerve sprouting and hyper innervation may play different roles. In the next article we choose to focus on is by Berte et al entitled a New Cryo-energy for Ventricular Tachycardia Ablation a Proof of Concept Study published in this past month's edition of Europace. One of the key problems in ventricular tachycardia ablation is the lack of transmural lesion formation. This is an important determinant of arrhythmia recurrence. Thus the group decided to do a proof of concept study to evaluate the safety and efficacy of a new and more powerful cryoablation system for ventricular ablation. They demonstrated that a novel cryoablation system to create large transmural ventricular lesions, whether it delivered by endocardial or epicardial approach. It was felt that this technology can hold potential for both surgical and catheter-based VT ablation in humans. While primarily studied in sheep models, it nevertheless highlights the importance of novel therapies that might better achieve through and through lesions. There are many different novel products being developed for the hope of achieving transmural lesions partly to target the myocardial circuits and partly to ensure achievement of through and through lesions without leaving residual potential substrate, because of only partial thickness lesions. These include things like needle ablation catheters, the safety of which still has to be fully evaluated, bipolar ablation or the use of technology such as novel cryo-energy approaches. Comparative efficacy of these different approaches however will be critical to determining which one is safest and best in any given clinical situation. Next we’ll review the article by Venlet et al published this past month's issue of Circulation Arrhythmia and Electrophysiology entitled Unipolar Endocardial Voltage Mapping in the Right Ventricle: Optimal Cutoff Values Correcting for Computed Tomography-derived Epicardial Fat Thickness and their clinical value for substrate delineation. The work by [inaudible 00:53:37] and others highlighted the importance of using unipolar and bipolar voltage cutoffs and helping delineate areas of both endocardial as well as potentially more distal such as epicardial scar during endocardial mapping. It is felt the low endocardial unipolar voltage during bipolar voltage mapping endocardially may indicate epicardial scar. However, the primary issues, the additional presence of epicardial fat both in the right ventricle and left ventricle and how this epicardial fat may effect normal unipolar voltage cutoffs. Thus, Venlet et al decided to review using computed tomography data the effective epicardial fat on unipolar voltage cutoffs. They demonstrated that endocardial unipolar voltage cutoff of 3.9 millivolts was more accurate than previously reported cutoff values for right ventricular epicardial scar during endocardial mapping. It was further demonstrated that while epicardial abnormal electrograms may be associated with transmural scar when associated with low endocardial bipolar voltage, the additional use of endocardial unipolar voltage and normal bipolar voltage sites can improve the diagnostic accuracy resulting in identification of all epicardial abnormal electrograms at sites with less than 1 mm of fat. Thus, the unipolar voltage not only assisted in evaluating whether epicardial scar was present, but also in further clarifying epicardial abnormal electrograms in terms of whether or not they truly represented potential transmural scar. Finally, within the realm of electrogram mapping of ventricular arrhythmias, we focus on the article by Magtibay et al entitled Physiological Assessment of Ventricular Myocardial Voltage using Omnipolar Electrograms published in the Journal of the American Heart Association this past month. Bipolar electrograms are traditionally used to characterize myocardial health. However, dependence on these electrograms may reduce the reliability of voltage assessment along different planes of arrhythmic myocardial substrates. Thus, newer catheters rely on evolving tools that might allow for different approaches to bipolar mapping. Using omnipolar electrograms, Magtibay et al studied in healthy rabbits, pigs and diseased humans under paced conditions the role of two bipolar electrode orientations both horizontal and vertical. Voltage maps were created for both bipoles and omnipoles, and they noted that electric orientation affected the bipolar voltage map with an average absolute difference between horizontal and vertical of up to 0.25 millivolts in humans. Thus, they demonstrated omnipoles can provide physiologically relevant and consistent voltages along the maximal bipolar direction and provide an advantage over traditionally obtained bipolar electrograms. When we consider the use of evolving techniques to get an understanding of myocardial health whether for the purpose of cardiac mapping and ablation or even for the purpose of other intervention such as cardiac biopsy, understanding what the voltage abnormalities perceived actually are is critical to understanding what substrate is actually being targeted. However, given directionality issues in terms of assessment of voltage as well as relative orientation of the catheter in understanding the relevance of received voltage, use of novel signal processing and electro designs are important to consider in the light of their effects on substrate mapping compared to traditional techniques. Changing gears yet again, but nevertheless related to cardiac mapping and ventricular arrhythmias, we focus on article by Yalagudri et al published in this past month's issue of the Journal of Cardiovascular Electrophysiology entitled A Tailored Approach for Management of Ventricular Tachycardia in Cardiac Sarcoidosis. While in a small number of patients, nearly 14 patients, they attempt to develop a methodology for approaching patients with cardiac sarcoidosis for management of their ventricular arrhythmias. Patients with either cardiac myocarditis or cardiac sarcoidosis represent a particularly difficult cohort to treat. Prior work by Dr. Roderick Tung and others has demonstrated the high-frequency of perceived inflammatory abnormalities based on cardiac FDG PET scanning amongst patients with ventricular arrhythmias. Whether this reflects cardiac sarcoidosis or other hypermetabolic activity is unclear. However, how to take into account the FDG PET abnormalities when deciding whether or not to take a patient for ablation or how to best treat them in light of their primary disease process is critical. In this study, the group tried to tailor therapy for ventricular tachycardia and cardiac sarcoidosis according to the phase of disease results. Namely based on the degree of inflammation noted on the FDG PET scan. They noted that via their named clinical protocol, that this tailored therapy could result in good clinical outcome and avoid unnecessary immunosuppression in some patients. Whether or not the use of this tailored therapy approach may apply in larger populations remains to be seen. Finally within the realm of other EP concepts that might apply broadly across the electrophysiology landscape, we focus on two articles. The first is by Kudryashova et al entitled Virtual Cardiac Monolayers for Electrical Wave Propagation in Nature Scientific Reports this past month. It is the complex structure of cardiac tissue that is considered to be one the main determinants of whether a substrate becomes arrhythmogenic or not. Multiple mathematical and computational models have been developed in order to recapitulate this complex cardiac structure. However, there been varying degrees of limitations in these approaches. Using a joint in silico-in vitro approach, the group carefully characterized the morphology of cardiac tissue and cultures of neonatal rat ventricular cells and then proposed mathematical models to result in tissue morphology that could be recapitulated for virtual studies of cardiac electrophysiology mainly in order to study wave propagation. They demonstrated in their virtual cardiac monolayers, that the simulated waves had the same anisotropy ratios and wave form complexity as those in in vitro experimental models. Thus, they demonstrated that they could reproduce both the morphological and physiological properties of cardiac tissue in a virtual landscape. These findings are critical to improving the ability to better study the effects of different antiarrhythmic drugs or interventional techniques on overall cardiac electrophysiology. The difficulty in existing techniques using traditional in vitro cultures is the fact that they’re costly and requires sacrifice of animals that adds to the additional cost of routine studies. The ability to recapitulate actual hearts within a virtual landscape to mimic the cardiac electrophysiology and then study it in a more controlled setting that can be reproducible based on the availability of appropriate computing power is important in terms of future studies within the realm of our field. The final article we will review is by Das and Dutta published in Physical Review E this past month entitled Controlling Three-Dimensional Vortices using Multiple and Moving External Fields. One of the key studies over the course of the last several years has been that of the role of the spiral and scroll waves in not just atrial fibrillation but ventricular fibrillation and other arrhythmias. It is well recognized that the spiral or scroll waves depending on whether one thinks in a two dimensional or three dimensional substrate may have significant contribution to arrhythmogenesis. Whether targeting the spiral or scroll waves actually eliminates arrhythmias remains to be fully elucidated. However, it also remains to be elucidated exactly how one should control the spiral or scroll waves. The review by Das and Dutta demonstrated that in fact the spiral or scroll waves could actually be physically moved around and controlled using moving external electric fields and thermal gradients. They show that the scroll rings can be made to trace cyclic trajectories on a rotating electric field or that application of thermal gradients in addition to electric field could deflect the motion and change the nature of a trajectory of a spiral or scroll wave. These findings are important in that they might represent non-ablative techniques that can eventually be used to control spiral or scroll waves in cardiac media, and thus result in either their alteration or termination without the need for additional cardiac injury. One the biggest problems with additional cardiac ablation in cases such as atrial fibrillation is the fact that they often lead to additional regions of scarring that might lead towards further organized atrial arrhythmias. However, the ability to potentially terminate critical sites responsible for arrhythmogenesis in real time without the need for ablation may represent novel interventions or devices in the future. I appreciate everyone's attention to these key and hard-hitting articles that we have just focus on from this past month of cardiac electrophysiology across the literature. Thanks for listening. Now back to Paul. Dr. Paul Wang : Thanks Suraj. You did a terrific job surveying all journals for the latest articles on topics of interest in our field. There is not an easier way to stay in touch with the latest advances. These summaries and a list of all major articles in our field each month could be downloaded from the Circulation: Arrhythmia and Electrophysiology website. We hope that you’ll find the journal to be the go to place for everyone interested in the field. See you next month.

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Therapy Persistence With Dabigatran Over 2 years

Play Episode Listen Later Sep 18, 2017 12:16

Commentary by Dr. Valentin Fuster

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Summer Replay: Big Data – Dabigatran vs. Rivaroxaban for Atrial Fibrillation and Association of Frailty with Post-Operative Mortality

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Play Episode Listen Later Jul 28, 2017 29:19

It's big data week on The Rounds Table! When initiating pharmacotherapy for atrial fibrillation, which drug is best? How does frailty influence surgical outcomes? Kieran and Michael Fralick, General Internist at St. Michael's Hospital, take listeners through two noteworthy studies: When a new medication is developed it is generally compared against standard of care or ...The post Summer Replay: Big Data – Dabigatran vs. Rivaroxaban for Atrial Fibrillation and Association of Frailty with Post-Operative Mortality appeared first on Healthy Debate.

Summer Replay: Big Data – Dabigatran vs. Rivaroxaban for Atrial Fibrillation and Association of Frailty with Post-Operative Mortality

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Play Episode Listen Later Jul 28, 2017 29:20

It's big data week on The Rounds Table! When initiating pharmacotherapy for atrial fibrillation, which drug is best? How does frailty influence surgical outcomes? Kieran and Michael Fralick, General Internist at St. Michael's Hospital, take listeners through two noteworthy studies: When a new medication is developed it is generally compared against standard of care or ... The post Summer Replay: Big Data – Dabigatran vs. Rivaroxaban for Atrial Fibrillation and Association of Frailty with Post-Operative Mortality appeared first on Healthy Debate.

Dabigatran vs Warfarin in Patients Undergoing Catheter Ablation of AFib

Cardiology Now

Play Episode Listen Later Mar 17, 2017 4:58

Dr. Stefan Hohnloser and Dr. Serge Korjian Discuss

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Big Data: Dabigatran vs. Rivaroxaban for Atrial Fibrillation and Association of Frailty with Post-Operative Mortality

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Play Episode Listen Later Dec 16, 2016 29:19

It's big data week on The Rounds Table! When initiating pharmacotherapy for atrial fibrillation, which drug is best? How does frailty influence surgical outcomes? Kieran and Michael Fralick, General Internist at St. Michael's Hospital, take listeners through two noteworthy studies: When a new medication is developed it is generally compared against standard of care or ...The post Big Data: Dabigatran vs. Rivaroxaban for Atrial Fibrillation and Association of Frailty with Post-Operative Mortality appeared first on Healthy Debate.

Big Data: Dabigatran vs. Rivaroxaban for Atrial Fibrillation and Association of Frailty with Post-Operative Mortality

hospitals big data mortality operative frailty atrial fibrillation michael's hospital rivaroxaban dabigatran

Play Episode Listen Later Dec 16, 2016 29:20

It's big data week on The Rounds Table! When initiating pharmacotherapy for atrial fibrillation, which drug is best? How does frailty influence surgical outcomes? Kieran and Michael Fralick, General Internist at St. Michael's Hospital, take listeners through two noteworthy studies: When a new medication is developed it is generally compared against standard of care or ... The post Big Data: Dabigatran vs. Rivaroxaban for Atrial Fibrillation and Association of Frailty with Post-Operative Mortality appeared first on Healthy Debate.

JEM September 2016 Podcast Summary

AAEM: The Journal of Emergency Medicine Audio Summary

Play Episode Listen Later Oct 9, 2016 46:15

Podcast summary of articles from September 2016 edition of Journal of Emergency Medicine from the American Academy of Emergency Medicine. Topics include Bleeding in Dabigatran, Pediatric Pelvic Fractures, Midline Catheters, Adulterated Heroin, CO Toxicity, Lidocaine Toxicity, and Board Review on Alcohol Withdrawal. Guest speaker is Dr. Brian Drummond.

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Rivaroxaban and Dabigatran in Asians with Atrial Fibrillation

BrainWaves: A Neurology Podcast

Play Episode Listen Later Sep 19, 2016 11:12

Commentary by Dr. Valentin Fuster

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#11 Which NOAC is best for secondary stroke prevention?

Play Episode Listen Later Jun 7, 2016 10:55

Long-term anti-thrombotic treatment of embolic stroke sounds like a tricky field to navigate. Aspirin is the drug of choice in the acute setting for most patients, but when cardioembolic stroke is suspected, aspirin is inferior to anticoagulation for preventing recurrent stroke. In the age of novel oral anticoagulants, why choose warfarin and risk drug interactions, dietary restrictions and bleeding risk? In this episode, we discuss the pros and cons of each of the major NOACs for secondary stroke prevention. Enjoy! BrainWaves podcasts and online content are intended for medical education only and should not be used to guide medical decision making in routine clinical practice. Any cases discussed in this episode are fictional and do not contain any patient health identifying information. REFERENCES 1. Connolly SJ, et al. Dabigatran versus warfarin in patients with atrial fibrillation. New Engl J Med 2009; 361:1139-1151. 2. Granger CB, et al. Apixaban versus warfarin in patients with atrial fibrillation. New Engl J Med 2011; 365:981-992. 3. Patel MR, et al. Rivaroxaban versus warfarin in nonvalvular atrial fibrillation. New Engl J Med 2011; 365:883-891. 4. Giugliano RP, et al. Edoxaban versus warfarin in patients with atrial fibrillation. New Engl J Med 2013; 369:2093-2104.

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#10 Cryptogenic stroke: Solving the unsolved

BrainWaves: A Neurology Podcast

Play Episode Listen Later Jun 1, 2016 23:36

Diagnostic dilemmas, cryptogenic infarcts account for almost a third of all stroke subtypes. But if you break it down, it's really not so complicated. Except, it may complicated enough that we had to entirely rewrite and re-produce this episode of the podcast. To ensure the accuracy of the content that is distributed, we have also replaced this original episode with the 2019 update. Produced by James E. Siegler. Music courtesy of Josh Woodward, Julie Maxwell, Dan Lebowitz, and this group called E’s Jammy Jams. Sound effects by Mike Koenig and Daniel Simion. BrainWaves' podcasts and online content are intended for medical education only and should not be used for clinical decision making. Be sure to follow us on Twitter @brainwavesaudio for the latest updates to the podcast. REFERENCES Siegler JE, Swaminathan B, Giruparajah M, Bosch J, Perera KS, Hart RG, Kasner SE and Investigators EGR. Age disparity in diagnostic evaluation of stroke patients: Embolic Stroke of Undetermined Source Global Registry Project. Eur Stroke J. 2016;1:130-138. Jacobs BS, Boden-Albala B, Lin IF and Sacco RL. Stroke in the young in the northern Manhattan stroke study. Stroke; a journal of cerebral circulation. 2002;33:2789-93. Hart RG, Sharma M, Mundl H, Kasner SE, Bangdiwala SI, Berkowitz SD, Swaminathan B, Lavados P, Wang Y, Wang Y, Davalos A, Shamalov N, Mikulik R, Cunha L, Lindgren A, Arauz A, Lang W, Czlonkowska A, Eckstein J, Gagliardi RJ, Amarenco P, Ameriso SF, Tatlisumak T, Veltkamp R, Hankey GJ, Toni D, Bereczki D, Uchiyama S, Ntaios G, Yoon BW, Brouns R, Endres M, Muir KW, Bornstein N, Ozturk S, O'Donnell MJ, De Vries Basson MM, Pare G, Pater C, Kirsch B, Sheridan P, Peters G, Weitz JI, Peacock WF, Shoamanesh A, Benavente OR, Joyner C, Themeles E, Connolly SJ and Investigators NE. Rivaroxaban for Stroke Prevention after Embolic Stroke of Undetermined Source. The New England journal of medicine. 2018;378:2191-2201. Diener HC, Sacco RL, Easton JD, Granger CB, Bernstein RA, Uchiyama S, Kreuzer J, Cronin L, Cotton D, Grauer C, Brueckmann M, Chernyatina M, Donnan G, Ferro JM, Grond M, Kallmunzer B, Krupinski J, Lee BC, Lemmens R, Masjuan J, Odinak M, Saver JL, Schellinger PD, Toni D, Toyoda K, Committee R-SES and Investigators. Dabigatran for Prevention of Stroke after Embolic Stroke of Undetermined Source. The New England journal of medicine. 2019;380:1906-1917. Di Tullio M, Sacco RL, Gopal A, Mohr JP and Homma S. Patent foramen ovale as a risk factor for cryptogenic stroke. Annals of internal medicine. 1992;117:461-5. Overell JR, Bone I and Lees KR. Interatrial septal abnormalities and stroke: a meta-analysis of case-control studies. Neurology. 2000;55:1172-9. Li J, Liu J, Liu M, Zhang S, Hao Z, Zhang J and Zhang C. Closure versus medical therapy for preventing recurrent stroke in patients with patent foramen ovale and a history of cryptogenic stroke or transient ischemic attack. The Cochrane database of systematic reviews. 2015;9:CD009938. Mas JL, Derumeaux G, Guillon B, Massardier E, Hosseini H, Mechtouff L, Arquizan C, Bejot Y, Vuillier F, Detante O, Guidoux C, Canaple S, Vaduva C, Dequatre-Ponchelle N, Sibon I, Garnier P, Ferrier A, Timsit S, Robinet-Borgomano E, Sablot D, Lacour JC, Zuber M, Favrole P, Pinel JF, Apoil M, Reiner P, Lefebvre C, Guerin P, Piot C, Rossi R, Dubois-Rande JL, Eicher JC, Meneveau N, Lusson JR, Bertrand B, Schleich JM, Godart F, Thambo JB, Leborgne L, Michel P, Pierard L, Turc G, Barthelet M, Charles-Nelson A, Weimar C, Moulin T, Juliard JM, Chatellier G and Investigators C. Patent Foramen Ovale Closure or Anticoagulation vs. Antiplatelets after Stroke. The New England journal of medicine. 2017;377:1011-1021. Saver JL, Carroll JD, Thaler DE, Smalling RW, MacDonald LA, Marks DS, Tirschwell DL and Investigators R. Long-Term Outcomes of Patent Foramen Ovale Closure or Medical Therapy after Stroke. The New England journal of medicine. 2017;377:1022-1032. Sondergaard L, Kasner SE, Rhodes JF, Andersen G, Iversen HK, Nielsen-Kudsk JE, Settergren M, Sjostrand C, Roine RO, Hildick-Smith D, Spence JD, Thomassen L and Gore RCSI. Patent Foramen Ovale Closure or Antiplatelet Therapy for Cryptogenic Stroke. The New England journal of medicine. 2017;377:1033-1042. Juul K, Tybjaerg-Hansen A, Steffensen R, Kofoed S, Jensen G and Nordestgaard BG. Factor V Leiden: The Copenhagen City Heart Study and 2 meta-analyses. Blood. 2002;100:3-10. Kaku DA and Lowenstein DH. Emergence of recreational drug abuse as a major risk factor for stroke in young adults. Annals of internal medicine. 1990;113:821-7. Fonseca AC and Ferro JM. Drug abuse and stroke. Current neurology and neuroscience reports. 2013;13:325. Susac JO, Egan RA, Rennebohm RM and Lubow M. Susac's syndrome: 1975-2005 microangiopathy/autoimmune endotheliopathy. Journal of the neurological sciences. 2007;257:270-2. Perera KS, Ng KKH, Nayar S, Catanese L, Dyal L, Sharma M, Connolly SJ, Yusuf S, Bosch J, Eikelboom JW and Hart RG. Association Between Low-Dose Rivaroxaban With or Without Aspirin and Ischemic Stroke Subtypes: A Secondary Analysis of the COMPASS Trial. JAMA Neurol. 2019. Epub ahead of print.

SCCM Pod-313 Idarucizumab for Dabigatran Reversal

iCritical Care: LearnICU

Play Episode Listen Later Mar 10, 2016 24:01

Michael S. Weinstein, MD, FACS, FCCM, speaks with Charles V. Pollack, Jr., MD. Dr. Pollack is Professor and Senior Advisor for Interdisciplinary Research and Clinical Trials in the Department of Emergency Medicine at Sidney Kimmel Medical College of Thomas Jefferson University.

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SCCM Pod-313 Idarucizumab for Dabigatran Reversal

iCritical Care: All Audio

Play Episode Listen Later Mar 10, 2016 24:01

Michael S. Weinstein, MD, FACS, FCCM, speaks with Charles V. Pollack, Jr., MD. Dr. Pollack is Professor and Senior Advisor for Interdisciplinary Research and Clinical Trials in the Department of Emergency Medicine at Sidney Kimmel Medical College of Thomas Jefferson University.

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Neonatal hypoglycemia; Hysteroscopic sterilization; Dabigatran reversal agent

UpToDate Talk

Play Episode Listen Later Jan 19, 2016 29:11

This episode features Dr. Paul Rozance, discussing the management of neonatal hypoglycemia (starts at 01:13); Dr. Howard Sharp, discussing concerns related to hysteroscopic sterilization (starts at 11:55); and Dr. Lawrence Leung, discussing a new reversal agent for the direct oral anticoagulant dabigatran (starts at 21:46). Dr. Nancy Sokol hosts.

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PA Boards 74: First Dabigatran Reversal Agent!

Medgeeks Clinical Review Podcast

Play Episode Listen Later Oct 28, 2015 10:18

physicianassistantboards.com/app - First off I want to let everyone know the app is FINALLY ready! It's available for both apple and android. Go and download the app for free! Find it at physicianassistantboards.com/app Todays episode is about the first dabigatran reversal agent. Officially FDA approved in October 2015. This is definitely a practice changing update!

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Bloody Anticoagulants

Intensive Care Network Podcasts

Play Episode Listen Later Sep 2, 2015 18:32

Bloody Oral Anticoagulants – BCC talk 2014 The use of the New Oral Anticoagulant Drugs present unique challenges for the Intensive Care practitioner 1. The NOACs now have PBS approval for non-valvular AF, below knee DVT, DVT prophylaxis and low volume PE 2. There is no specific antidote for NOAC related bleeding but don’t despair there are some things that can help 3. Routine coagulation testing does not reflect drug levels or anticoagulation activity Global sales of Dabigatran topped $1billion in 2012. This talk outlines the pharmacodynamics and pharmacokinetics of the NOACs. Limitations and cautions of use are outlined with a review of the extensive literature. Clinical cases involving the NOACs are presented. The timing of stopping the agents before minor or major surgery, the approach to a patient with intracranial haemorrhage taking oral anticoagulants and the challenges faced when patients have an Acute Kidney Injury whilst taking these

Season Finale: Dabigatran Reversal and Digoxin Mortality

Play Episode Listen Later Jul 3, 2015 25:43

Fahad and Amol want you to recognize that: 1. Idarucizumab as an agent that specifically reverses the hemostatic effects of dabigatran. 2. A post-hoc analysis of the ROCKET-AF study showed that digoxin is associated with increased mortality in patients with atrial fibrillation. The papers Idaracizumab for Dabigatran reversal. Digoxin use and mortality in ROCKET-AF. Good stuff http://www.smacc.net.au/about-us/welcome/ http://emupdates.com/wp-content/uploads/2015/06/Strayer-Opioid-Misuse-SMACC-Slideset.pdf ...The post Season Finale: Dabigatran Reversal and Digoxin Mortality appeared first on Healthy Debate.

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Season Finale: Dabigatran Reversal and Digoxin Mortality

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Play Episode Listen Later Jul 3, 2015 25:13

Fahad and Amol want you to recognize that: 1. Idarucizumab as an agent that specifically reverses the hemostatic effects of dabigatran. 2. A post-hoc analysis of the ROCKET-AF study showed that digoxin is associated with increased mortality in patients with atrial fibrillation. The papers Idaracizumab for Dabigatran reversal. Digoxin use and mortality in ROCKET-AF. Good stuff http://www.smacc.net.au/about-us/welcome/ http://emupdates.com/wp-content/uploads/2015/06/Strayer-Opioid-Misuse-SMACC-Slideset.pdf ... The post Season Finale: Dabigatran Reversal and Digoxin Mortality appeared first on Healthy Debate.

To Monitor Dabigatran or Not: A Matter of Patient Safety

Clinical Chemistry Podcast

Play Episode Listen Later Jun 15, 2015 13:14

Biomarkers are playing increasingly important roles in the detection and management of patients with cancer. Despite an enormous number of publications on cancer biomarkers, few of these biomarkers are in widespread clinical use.

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Maternal diabetes and autism, survival with bioprosthetic vs mechanical mitral valve replacement, dabigatran adherence, treatment of stroke, and more.

JAMA Editors' Summary: On research in medicine, science, & clinical practice. For physicians, researchers, & clinicians.

Play Episode Listen Later Apr 14, 2015 5:52

Editor's Audio Summary by Howard Bauchner, MD, Editor in Chief of JAMA, the Journal of the American Medical Association, for the April 14, 2015 issue

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A Fib 5: Antithrombotics

Family Medicine & Pharmacy Podcast

Play Episode Listen Later Mar 2, 2014 33:50

Antiplatelets: ASA Clopidogrel Anticoagulants: Warfarin Apixaban Dabigatran Rivaroxaban Clotting Cascade: Clotting Factor Song, by Emily Anne Nagler: Twelve, eleven, nine, it’s clotting factor time 8 and 9 to 10a 5, that’s how we stay alive Don’t forget to say: the tissue factor way 7 to 7a helps 10 go to 10a Then 2 to thrombin, […] The post A Fib 5: Antithrombotics appeared first on Family Pharm Podcast.

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February 4 2014 Issue

Neurology® Podcast

Play Episode Listen Later Feb 3, 2014 19:15

1) ASA/clopidogrel combination confers better long term vascular protection in ASA failure and 2) Topic of the month: Review of new oral anticoagulants for stroke. This podcast for the Neurology Journal begins and closes with Dr. Robert Gross, Editor-in-Chief, briefly discussing highlighted articles from the print issue of Neurology. In the second segment Dr. Justin Sattin interviews Dr. Robert Cote about his paper on whether the combination of ASA/clopidogrel confers better long term vascular protection in ASA failure. Dr. James Addington is reading our e-Pearl of the week about hypoglycorrhachia. In the next part of the podcast Dr. Andy Southerland interviews Dr. Seemant Chaturvedi about a brief review of new oral anticoagulant (Dabigatran), reference clinical trial, indication and dosing. The participants had nothing to disclose except Drs. Cote, Addington, Southerland and Chaturvedi.Dr. Cote served on the scientific advisory board for Bayer Schering Pharma, Bristol-Myers Squibb, Boehringer Ingelheim, Pfizer Inc; serves on the scientific advisory board for DSMB for National Institute of Health (Point Study), Steering committee for the National Institute of Health (SPS3 study); is a consultant for Otsuka Pharmaceutical Co., Ltd.; received speaker honoraria from Boehringer Ingelheim, Merck Serono, Sanofi-aventis.Dr. Addington serves on the editorial team for the Neurology® Resident and Fellow Section. Dr. Southerland serves as Podcast Deputy Editor for Neurology®; serves as Clinical Research Advisor for Totier Technologies, Inc.Dr. Chaturvedi serves as an editorial board member for Neurology®, Stroke; serves as contributing editor NEJM Journal Watch Neurology; serves as executive committee member for ACT I study; is a consultant for Genetech, Inc., Boehringer Ingelheim, Abbott Vascular, Thorhill research, WL Gore, Bristol-Myers Squibb; receives research support from Daichi Sankyo, AstraZeneca, Pfizer Inc, NIH; received compensation for expert witness testimony.

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Episode 37: Anticoagulants, PCCs and Platelets

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Play Episode Listen Later Oct 8, 2013 101:03

In the second part of this epic 2-part authoritative episode, Anticoagulants, PCCs & Platelets, we have Dr. Walter Himmel (also known as 'The walking encyclopedia of EM') along with Dr. Katerina Pavenski (Head of Transfusion Medicine at St. Michael's Hospital) & Dr. Jeannie Callum (Head of Transfusion Medicine at Sunnybrook Hospital) who will discuss the latest on comparative efficacy and reversal of Warfarin vs Dabigatran vs Rivaroxiban vs Abixaban, the use of prothrombin complex concentrates (PCCs), the ins and outs of thrombocytopenia & platelet transfusions, ITP, TTP, anti-platelet associated intracranial bleeds, indications for Tranexamic Acid & more... The post Episode 37: Anticoagulants, PCCs and Platelets appeared first on Emergency Medicine Cases.

Episode 37: Anticoagulants, PCCs and Platelets

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Play Episode Listen Later Oct 7, 2013 101:03

In the second part of this epic 2-part authoritative episode, Anticoagulants, PCCs & Platelets, we have Dr. Walter Himmel (also known as 'The walking encyclopedia of EM') along with Dr. Katerina Pavenski (Head of Transfusion Medicine at St. Michael's Hospital) & Dr. Jeannie Callum (Head of Transfusion Medicine at Sunnybrook Hospital) who will discuss the latest on comparative efficacy and reversal of Warfarin vs Dabigatran vs Rivaroxiban vs Abixaban, the use of prothrombin complex concentrates (PCCs), the ins and outs of thrombocytopenia & platelet transfusions, ITP, TTP, anti-platelet associated intracranial bleeds, indications for Tranexamic Acid & more... The post Episode 37: Anticoagulants, PCCs and Platelets appeared first on Emergency Medicine Cases.

Episode 36: Transfusions, Anticoagulants and Bleeding

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Play Episode Listen Later Sep 20, 2013 88:18

In the first part of this epic 2 part must-hear episode, Transfusions, Anticoagulants & Bleeding, we have the triumphant return of Dr. Walter Himmel (also known as 'The walking encyclopedia of EM') along with Dr. Katerina Pavenski (Head of Transfusion Medicine at St. Michael's Hospital) & Dr. Jeannie Callum (Head of Transfusion Medicine at Sunnybrook Hospital) who will update you on the latest in transfusion indications & risks, managing INRs and how Wararin compares to Dabigatran, Rivaroxiban & Apixaban. They give you the authoritative low down on: Indications for red cell transfusions in different clinical scenarios (GI bleed, cardiac disease, vaginal bleeding etc) and how to give them, Risks of red cell transfusions including Host vs Graft Disease, TRALI & TACO and how to manage them, IV Iron as an alternative to red cell transfusions, Managing INRs: indications for Vit K, Prothrombin Complex Concentrates (Octaplex & Beriplex), adjusting Warfarin Dose, liver patients, and much much more......... The post Episode 36: Transfusions, Anticoagulants and Bleeding appeared first on Emergency Medicine Cases.

Episode 36: Transfusions, Anticoagulants and Bleeding

hospitals risks gi taco bleeding indications transfusions anticoagulants transfusion medicine sunnybrook hospital apixaban vit k inrs dabigatran

Play Episode Listen Later Sep 20, 2013 88:18

In the first part of this epic 2 part must-hear episode, Transfusions, Anticoagulants & Bleeding, we have the triumphant return of Dr. Walter Himmel (also known as 'The walking encyclopedia of EM') along with Dr. Katerina Pavenski (Head of Transfusion Medicine at St. Michael's Hospital) & Dr. Jeannie Callum (Head of Transfusion Medicine at Sunnybrook Hospital) who will update you on the latest in transfusion indications & risks, managing INRs and how Wararin compares to Dabigatran, Rivaroxiban & Apixaban. They give you the authoritative low down on: Indications for red cell transfusions in different clinical scenarios (GI bleed, cardiac disease, vaginal bleeding etc) and how to give them, Risks of red cell transfusions including Host vs Graft Disease, TRALI & TACO and how to manage them, IV Iron as an alternative to red cell transfusions, Managing INRs: indications for Vit K, Prothrombin Complex Concentrates (Octaplex & Beriplex), adjusting Warfarin Dose, liver patients, and much much more......... The post Episode 36: Transfusions, Anticoagulants and Bleeding appeared first on Emergency Medicine Cases.

Best Case Ever 18: Anticoagulant Reversal in Trauma

Play Episode Listen Later Sep 4, 2013 5:44

Dr. Katerina Pavenski, on Anticoagulant Reversal in Trauma. A leader in Transfusion Medicine from St. Michael's Hospital, Dr. Pavenski tells us about her Best Case Ever in which a straight forward trauma case turns into a 'bloody disaster', after Prothrombin Complex Concentrates (PCCs) were given in an anticoagulant reversal attempt. In the related two-part epic episode on Antiocagulants, Transfusions & Bleeding, Drs. Pavenski, Dr. Jeannie Callum (Head of Transfusion Medicine at Sunnybrook Hospital & Dr. Walter Himmel (also known as 'The walking encyclopedia of EM') cover: Indications for red cell transfusion in different clinical scenarios (GI bleed, cardiac disease, vaginal bleeding etc), Risks of transfusion including Host vs Graft Disease, TRALI & TACO, Indications for Platelet transfusion in different scenarios (hyporoliferative patients vs ITP, invasive procedures with thrombocytopenia), Managing INRs - indications for Vit K, PCC, adjusting Warfarin Dose, liver patients, Apixaban vs Rivaroxiban vs Dabigatran vs Warfarin and reversal of them, Anti-platelet medication-associated intracranial hemorrhage management, Indications for Tranexamic Acid, and much more........ The post Best Case Ever 18: Anticoagulant Reversal in Trauma appeared first on Emergency Medicine Cases.

Best Case Ever 18: Anticoagulant Reversal in Trauma

Play Episode Listen Later Sep 4, 2013 5:44

Dr. Katerina Pavenski, on Anticoagulant Reversal in Trauma. A leader in Transfusion Medicine from St. Michael's Hospital, Dr. Pavenski tells us about her Best Case Ever in which a straight forward trauma case turns into a 'bloody disaster', after Prothrombin Complex Concentrates (PCCs) were given in an anticoagulant reversal attempt. In the related two-part epic episode on Antiocagulants, Transfusions & Bleeding, Drs. Pavenski, Dr. Jeannie Callum (Head of Transfusion Medicine at Sunnybrook Hospital & Dr. Walter Himmel (also known as 'The walking encyclopedia of EM') cover: Indications for red cell transfusion in different clinical scenarios (GI bleed, cardiac disease, vaginal bleeding etc), Risks of transfusion including Host vs Graft Disease, TRALI & TACO, Indications for Platelet transfusion in different scenarios (hyporoliferative patients vs ITP, invasive procedures with thrombocytopenia), Managing INRs - indications for Vit K, PCC, adjusting Warfarin Dose, liver patients, Apixaban vs Rivaroxiban vs Dabigatran vs Warfarin and reversal of them, Anti-platelet medication-associated intracranial hemorrhage management, Indications for Tranexamic Acid, and much more........ The post Best Case Ever 18: Anticoagulant Reversal in Trauma appeared first on Emergency Medicine Cases.

Episode 20: Atrial Fibrillation

Play Episode Listen Later Feb 10, 2012 89:19

In this episode Dr. Clare Atzema, Dr. Nazanin Meshkat and Dr. Bryan Au discuss the presentation, etiology, precipitants, management and disposition of Atrial Fibrillation in the Emergency Department. The pros and cons of rate and rhythm control are debated, what you need to know about rate and rhythm control medications reviewed, and the strength of the Ottawa Aggressive Protocol discussed. The importance of appropriate anticoagulation is detailed, with a review of the CHADS-VASc score and whether to use Warfarin, Dabigatran or ASA for stroke prevention for patient with Atrial Fibrillation. We end off with a discussion on how to recognize and treat Wolff-Parkinson-White syndrome in the setting of Atrial Fibrillation.

emergency departments atrial fibrillation warfarin wolff parkinson white dabigatran chadsvasc bryan au

Episode 20: Atrial Fibrillation

halloween contributors dabigatran medwatch

Play Episode Listen Later Feb 9, 2012 89:19

In this episode Dr. Clare Atzema, Dr. Nazanin Meshkat and Dr. Bryan Au discuss the presentation, etiology, precipitants, management and disposition of Atrial Fibrillation in the Emergency Department. The pros and cons of rate and rhythm control are debated, what you need to know about rate and rhythm control medications reviewed, and the strength of the Ottawa Aggressive Protocol discussed. The importance of appropriate anticoagulation is detailed, with a review of the CHADS-VASc score and whether to use Warfarin, Dabigatran or ASA for stroke prevention for patient with Atrial Fibrillation. We end off with a discussion on how to recognize and treat Wolff-Parkinson-White syndrome in the setting of Atrial Fibrillation. The post Episode 20: Atrial Fibrillation appeared first on Emergency Medicine Cases.

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Episode 3 Halloween and Dabigatran

ToxNow

Play Episode Listen Later Nov 22, 2011 76:06

On this months episode we talk about spooky Halloween toxicology. What might that be? Listen and find out. Additionally, we cover something even scarier, uncontrollable bleeding. Contributors include Matt Zuckerman, Ed Boyer, Stephanie Weiss, Kavita Babu, and Scott Glazier. As noted in the podcast, here is a link to MedWatch and to the [...]

Episode 17 Part 2: Stroke, Dabigatran and Intracranial Hemorrhage

stroke bp hemorrhage warfarin intracranial dabigatran

Play Episode Listen Later Sep 7, 2011 67:37

In the 2nd part of this episode on Stroke, Dabigitran & Intracranial Hemorrhage Dr. Walter Himmel & Dr. Dan Selchen tell us everything the ED doc needs to know about the oral direct thrombin inhibitor Dabigatran and how to reverse a Dabigatran ICH. The ED treatment of stroke is reviewed including best medications and a simple way to remember BP goals. They review the management of ICH including BP goals, indications for neurosurgery, the role of recombinant Factor Vlla, and how best to reverse Warfarin-associated and platelet-associated ICH.

Episode 17 Part 2: Stroke, Dabigatran and Intracranial Hemorrhage