Podcasts about septal

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 my co-host, Nachi Gupta. This month, after a few months of primarily medical topics, we’re talking trauma, specifically Blunt Cardiac Injury: Emergency Department Diagnosis and Management. Nachi: With no gold standard diagnostic test and with complications ranging from simple ectopic beats to fulminant cardiac failure and death, this isn’t an episode you’ll want to miss. Jeff: Before we begin, let me give a quick shout out to our incredible group of authors from New York -- Dr. Eric Morley, Dr. Bryan English, and Dr. David Cohen of Stony Brook Medicine and Dr. William Paolo, residency program director at SUNY Upstate. I should also mention their peer reviewers Drs. Jennifer Maccagnano and Ashley Norse of the NY institute of technology college of osteopathic medicine and UF Health Jacksonville, respectively. Nachi: This month’s team parsed through roughly 1200 articles as well as guidelines from the eastern association for surgery in trauma also known as EAST. Jeff: Clearly a large undertaking for a difficult topic to come up with solid evidence based recommendations. Nachi: For sure. Let’s begin with some epidemiology, which is admittedly quite difficult without universally accepted diagnostic criteria. Jeff: As you likely know, despite advances in motor vehicle safety, trauma remains a leading cause of death for young adults. In the US alone, each year, there are about 900,000 cases of cardiac injury secondary to trauma. Most of these occur in the setting of vehicular trauma. Nachi: And keep in mind, that those injuries don’t occur in isolation as 70-80% of patients with blunt cardiac injury sustain other injuries. This idea of concomitant trauma will be a major theme in today’s episode. Jeff: It certainly will. But before we get there, we have some more definitions to review - cardiac concussion and contusion, both of which were defined in a 1989 study. In this study, cardiac concussion was defined as an elevated CKMB with a normal echo, while a cardiac contusion was defined as an elevated CKMB and abnormal echo. Nachi: Much to my surprise, though, abnormal echo and elevated ck-mb have not been shown to be predictive of adverse outcomes, but conduction abnormalities on ekgs have been predictive of development of serious dysrhythmia Jeff: More on complications in a bit, but first, returning to the idea of concomitant injuries, in one autopsy study of nearly 1600 patients with blunt trauma - cardiac injuries were reported in 11.9% of cases and contributed to the death of 45.2% of those patients. Nachi: Looking more broadly at the data, according to one retrospective review, blunt cardiac injury may carry a mortality of up to 44%. Jeff: That’s scary high, though I guess not terribly surprising, given that we are discussing heart injuries due to major trauma... Nachi: The force may be direct or indirect, involve rapid deceleration, be bidirectional, compressive, concussive, or even involve a combination of these. In general, the right ventricle is the most frequently injured area due to the proximity to the chest wall. Jeff: Perfect, so that's enough background, let’s talk differential. As you likely expected, the differential is broad and includes cardiovascular injuries, pulmonary injuries, and other mediastinal injuries like pneumomediastinum and esophageal injuries. Nachi: Among the most devastating injuries on the differential is cardiac wall rupture, which not surprisingly has an extremely high mortality rate. In terms of location of rupture, both ventricles are far more likely to rupture than the atria with the right atria being more likely to rupture than the left atria. Atrial ruptures are more survivable, whereas complete free wall rupture is nearly universally fatal. Jeff: Septal injuries are also on the ddx. Septal injuries occur immediately, either from direct impact or when the heart becomes compressed between the sternum and the spine. Delayed rupture can occur secondary to an inflammatory reaction. This is more likely in patients with a prior healed or repaired septal defects. Nachi: Valvular injuries, like septal injuries, are rare. Left sided valvular damage is more common and carries a higher mortality risk. In order, the aortic valve is more commonly injured followed by the mitral valve then tricuspid valve, and finally the pulmonic valve. Remember that valvular damage can be due to papillary muscle rupture or damage to the chordae tendineae. Consider valvular injury in any patient who appears to be in cardiogenic shock, has hypotension without obvious hemorrhage, or has pulmonary edema. Jeff: Next on the ddx are coronary artery injuries, which include lacerations, dissections, aneurysms, thrombosis, and even MI secondary to increased sympathetic activity and platelet activity after trauma. In one review, dissection was the most commonly uncovered pathology, occurring 71% of the time, followed by thrombosis, which occured only 7% of the time. The LAD is the most commonly injured artery followed by the RCA. Nachi: Pericardial injury, including pericarditis, effusion, tamponade, and rarely rupture, is also certainly on the differential. Jeff: In terms of dysrhythmias, sinus tachycardia is the most common dysrhythmia, with other rhythms, including PVC / PAC / and afib being found only 1-6% of the time. Nachi: And while conduction blocks are rare, a RBBB is the most commonly noted, followed by a 1st degree AVB. Jeff: Though also rare, commotio cordis deserves it’s own section as its the second most common cause of death in athletes < 18 who are victims of blunt trauma. Though only studied in swine models, it’s hypothesized that the impact to the chest wall during T-wave upstroke can precipitate v-fib. Nachi: Aortic root injuries usually occur at the insertion of the ligamentum arteriosum and isthmus. Such injuries typically result in aortic insufficiency. Jeff: And the last pathology on the differential requiring special attention is a myocardial contusion. Again, no standard definition exists, with some diagnostic criteria including simply chest pain and increasing cardiac enzymes, and others including cardiac dysfunction, ecg abnormalities, wall motion abnormalities, and an elevation of cardiac enzymes. Nachi: Certainly a pretty broad differential… before moving on to the work up, Jeff why don’t you get us started with prehospital care? Jeff: Prehospital management should focus on rapid identification and stabilization of life threatening injuries with expeditious transport as longer prehospital times have been associated with increased mortality in trauma. Immediate transport to a Level I trauma center should be the highest priority for those with suspected blunt cardiac injury. Nachi: In terms of who specifically should be transporting the patient, a Cochrane review evaluated the utility of ALS vs BLS transport in trauma. There is reasonably good data to support BLS over ALS, even when controlling for trauma severity. Moreover, when airway management is needed, advanced airway techniques by ALS crews were associated with decreased odds of survival. Regardless of who is there, the message is the same: focus not on interventions, but instead on rapid transport. Jeff: And if it does happen to be an ALS transport crew, without delaying transport, pain management with fentanyl is both safe and reasonable and preferred over morphine. Post opiate hypotension in prehospital trauma patients is a rare but documented complication. Nachi: And if the prehospital team is lucky enough, or maybe unlucky enough, i don’t know, to have a credentialed provider who can perform ultrasound for those suspected of having a blunt cardiac injury, the general prehospital data on ultrasound is sparse. As of now, it’s difficult to conclude if prehospital US improves care for trauma patients. Jeff: Interestingly, the system I work in has prehospital physicians, who do carry US, but I can’t think of a major trauma where ultrasound changed any of the decisions we made. Nachi: Right, and I think that just reinforces the main point here: there may be a role, we just don’t have the data to support it at this time. Jeff: Great, let’s move onto ED care, beginning with the H&P. Nachi: On history, make sure to elucidate if there is any chest pain, and if it’s onset was before or after the traumatic event. In addition, make sure to ask about dyspnea, fatigue, palpitations, and lightheadedness. Jeff: And don’t forget to get the crash details from the EMS crew before they depart! As a side note, for anyone taking oral boards in a few months, don’t forget to ask the EMS crew for the details!!! Nachi: A definite must for oral boards and for your clinical practice. Jeff: In terms of the physical, tachycardia is the most common abnormality in blunt cardiac injury. In those with severe injury, you may note refractory hypotension secondary to cardiogenic shock. But don’t be reassured by normal vitals, especially in the young, who may be compensating well despite being quite ill. Nachi: Fully undress the patient to appropriately inspect and percuss the chest wall - looking for signs of previous cardiac surgeries or pacemaker placement, as well as to auscultate for new murmurs which may be a sign of valvular injury. Jeff: Similarly, as concomitant injuries are common, inspect the abdomen, looking for ecchymosis patterns, which often accompany blunt cardiac injury. Nachi: Pretty standard stuff. Let’s move on to diagnostic testing. Jeff: Lab testing should include a CBC, BMP, coags, troponin, lactate, and T&S. In one retrospective analysis, an elevated troponin and a lactate over 2.5 were predictors of mortality. Nachi: Additionally, in patients with chest trauma, a troponin > 1.05 was associated with a greater risk for dysrhythmias and LV dysfunction. Jeff: And it likely goes without saying, but an EKG is a must on all trauma patients with suspicion for blunt cardiac injury in accordance with the EAST guidelines. New EKG findings requires admission for monitoring. Unfortunately, on the flip side, an ECG cannot be used to rule out blunt cardiac injury. Nachi: Diving a bit deeper into the data, in a prospective study of 333 patients with blunt thoracic trauma, serial EKG and troponins at 0, 4, and 8 hours post injury had a sensitivity and specificity of 100% and 71%, respectively. However, of those with abnormal findings, all but one had them on initial testing, leading to a negative predictive value of 98%. Jeff: Well that’s an impressive NPV and has huge implications, especially in the era of heavily monitored lengths of stay... Nachi: Definitely. In terms of radiography, a chest x-ray should be obtained as rib fractures, hemopneumothorax, and mediastinal free air are all things you wouldn't want to miss and are also associated with blunt cardiac injury. Jeff: Keep in mind, however, that the chest x-ray should not be seen as a test for pericardial fluid as up to 200 mL of fluid can be contained in the pericardial space and remain undetectable by chest radiograph. Nachi: Which is why you’ll have to turn to our good friend the ultrasound, for more useful data. The data is strong that in the hands of trained Emergency Clinicians, when parasternal, apical, and subcostal views are obtained, US has an accuracy of 97.5% for pericardial effusion. Jeff: Not only is US accurate, it’s also quick. In one RCT, the FAST exam reduced the time from arrival in the ED to operative care by 64% in the setting of trauma. Nachi: That’s impressive -- for expediting patient care and for managing ED flow. Jeff: Exactly. The authors do note however that hemopericardium is a rare finding, so, while not the focus of this article, the real utility of the FAST exam may be in its expanded form, the eFAST, in which a rapid bedside ultrasonographic lung exam for pneumothorax is included, as this can lead to immediate changes in management. Nachi: And assuming you do your FAST or eFAST and have no management changing findings, CT will often be your next test. Jeff: Yeah, EKG-gated multidetector CT can easily diagnose myocardial rupture, pneumopericardium, pericardial rupture, hemopericardium, coronary artery insult, ventricular septal defects and even valvular dysfunction. Unfortunately, CT does not perform well for the evaluation of myocardial contusions. Nachi: This is all well and good, and certainly accurate, but let’s not forget that hemodynamically unstable trauma patients, like those with myocardial rupture, need to be in the operating room, not the CT scanner. Jeff: An important point that should not be understated. Nachi: And the last major testing modality to discuss is the echocardiogram. Jeff: The echo is a fantastic test for detecting focal cardiac dysfunction often see with cardiac contusions, hemopericardium, and valve disruption. Nachi: And it’s worth noting that transthoracic is enough, as transesophageal, despite the better images, hasn’t been shown to change management. TEE should be saved for those in whom a optimal TTE study isn’t feasible. Jeff: Great point. And one last quick note on echo: in terms of guidelines, the EAST guidelines from 2012 specifically recommend an echo in hemodynamically unstable patients or those with a persistent new dysrhythmia without other sources of ongoing hemorrhage or neurologic etiology of instability. Nachi: Perfect, so that wraps up testing and imaging for our blunt cardiac injury patient. Let’s move on to treatment. Jeff: In terms of initial resuscitation, there is an ever increasing body of literature to support blood transfusion over crystalloid in patients requiring volume expansion in trauma. There are no specific guidelines for transfusion in the setting of blunt cardiac injury, so stick to your standard trauma protocols. Nachi: It is worth noting, though, that there is literature outside of trauma for those with pericardial effusions, suggesting that those with a SBP < 100 have substantial benefit from volume expansion. So keep this in mind if your clinical suspicion is high and your trauma patient has a soft but not truly shocky blood pressure. Jeff: Operative management, specifically ED thoracotomy is a heavily debated topic, and it’s next on our list to discuss. Nachi: The 2015 EAST guidelines conditionally recommend ED thoracotomy for moribund patients with signs of life. The Western Trauma Association broadens the ED thoracotomy window a bit to include anyone with no signs of life but less than 10 minutes of CPR. The latter also recommend ED thoracotomy in those with refractory shock. Jeff: Though few studies exist on the topic, in one study of 187 patients, cardiac motion on US was 100% sensitive for predicting survivors. Nachi: Not great data, but it does support one's decision to stop any further work up should there be no cardiac activity, which is important, because the decision to pursue an ED thoracotomy is not an easy one. Jeff: And lastly, emergent pericardiocentesis may be another option in an unstable patient when definitive operative management is not possible. But do note that pericardiocentesis is only a temporizing measure, and not definitive for cardiac tamponade. Nachi: Treatment for dysrhythmias is standard, treat in accordance with standard ACLS protocols, as formal randomized trials on prophylaxis and treatment in the setting of blunt cardiac injury do not exist. Jeff: Seems reasonable enough. And in the very rare setting of an MI after blunt cardiac injury, you should involve cardiology, cardiothoracic surgery, and trauma to help make important management decisions. Data is, again, lacking, but the patient likely needs percutaneous angiography for appropriate diagnosis and potentially further intervention. Definitely hold off on ASA and likely nitroglycerin, at least until significant bleeding has been ruled out. Nachi: Yup, no style points for giving aspirin to a bleeding trauma patient. Speaking of medications, the last treatment modality to discuss here is pain control. Pain management is essential with chest injuries, as appropriate pain management has been shown to reduce mortality in pulmonary related complications. Jeff: And in line with every acute pain consult note I’ve ever come across, a multimodal approach utilizing opioids and nonopioids is recommended. Nachi: Perfect, so that sums up treatment, next we have one special circumstance to discuss: sternal fractures. Cardiac contusions are found in 1.8-2.4% of patients with sternal fractures, almost all of which were seen on CT and not XR according to the NEXUS chest CT study. Of these patients, only 2 deaths occured, both due to cardiac causes.  Thus, in patients with isolated sternal fractures, negative trops, ekg, and negative cxr - the patient can likely be discharged from the ED, as long as their pain is well-controlled. Jeff: And let’s talk controversies for this issue. We only have one to discuss: MRI. Nachi: The fact that MRI produces awesome images is not controversial, see figure 3. It’s role, however, is. In accordance with EAST guidelines, MRI may be most useful in differentiating acute ischemia from blunt cardiac injury in those with abnormal ECGs, elevated enzymes, or abnormal echos. It’s use in the hyperacute evaluation, however, is limited, in large part owing to the length of time required to complete an MRI Jeff: What a time to be alive that we even have to say that MRIs may not have a hyperacute role in trauma - absolutely crazy... Nachi: Moving on to disposition: any patient with aortic, pericardial, or myocardial injury and hemodynamic instability needs operative evaluation and likely intervention, so do not hesitate to get the consults coming or the helicopter in the air should such a patient arrive at your non-trauma center. Jeff: And in those that are hemodynamically stable, with either a positive ECG or a positive trop, they should be monitored on telemetry. There is no clear answer as to how long, but numerous studies suggest a 24 hour period of observation is sufficient. For those with persistent ekg abnormalities or rising trops - this is precisely when you will want to pursue echocardiography. Nachi: And if there are positive EKG findings AND a rising trop, they should be admitted to a step down unit or ICU as well -- as ⅔ of them will develop myocardial dysfunction. Similarly, those with hemodynamic instability but no active traumatic bleeding source - they too should be admitted to the ICU for a STAT echo and serial enzymes. Jeff: But in the vast majority of patients, those that are hemodynamically stable with negative serial EKGs and serial tropinins, they can effectively be ruled out for significant BCI after an 8 hour ED observation period, as we mentioned earlier with a sensitivity approaching 100%! Nachi: Though there are, of course, exceptions to this rule, like those with low physiologic reserve, mobility or functional issues, or complex social situations, which may need to be assessed on a more case-by-case basis. Jeff: Let’s wrap up this episode with some key points and clinical pearls. Cardiac wall rupture is the most devastating form of Blunt Cardiac Injury. The sealing of a ruptured wall may lead to a pseudoaneurysm and delayed tamponade. Trauma to the coronary arteries may lead to a myocardial infarction. The left anterior descending artery is most commonly affected. The most common arrhythmia associated with blunt cardiac injury is sinus tachycardia. RBBB is the most commonly associated conduction block. Commotio cordis is the second most common cause of death in athletes under the age of 18. Early defibrillation is linked to better outcomes. Antiplatelet agents like aspirin should be avoided in blunt cardiac injury until significant hemorrhage has been ruled out. An EKG should be obtained in all patients with suspected blunt cardiac injury. However, an EKG alone does not rule out blunt cardiac injury. Serial EKG and serial troponin testing at hours 0, 4, and 8 have a sensitivity approaching 100% for blunt cardiac injury. An elevated lactate level or troponin is associated with increased mortality in blunt cardiac injury. Perform a FAST exam to assess for pericardial effusions. FAST exams are associated with a significant reduction in transfer time to an operating room. Obtain a chest X-ray in all patients in whom you have concern for blunt cardiac injury. Note that the pericardium is poorly compliant and pericardial fluid might not be detected on chest X-ray. Transesophageal echocardiogram should be considered when an optimal transthoracic study cannot be achieved. CT is used routinely in evaluating blunt chest trauma but know that it does not evaluate cardiac contusions well. In acute evaluation, MRI is generally a less useful imaging modality given the long imaging time. There is evidence to suggest that a patient with an isolated sternal fracture and negative biomarkers and negative EKG findings can be safely discharged from the ED if pain is well-controlled. Trauma to the aorta, pericardium, or myocardium is associated with severe hemodynamic instability. These patients need surgical evaluation emergently. Hemodynamically stable patients with a positive troponin test or with new EKG abnormalities should be observed for cardiac monitoring. Nachi: So that wraps up Episode 26 on Blunt Cardiac Injury! Jeff: 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. You can find everything you need to know at ebmedicine.net/subscribe. Nachi: It’s also worth mentioning for current subscribers that the website has recently undergone a major rehaul and update. The new site is easier to use on mobile browsers, has better search functionality, mobile-friendly CME testing, and quick access to the digest and podcast. Jeff: And as those of us in the north east say goodbye to the snow for the year, it’s time to start thinking about the summer and maybe start planning for the Clinical Decision Making conference in sunny Ponta Vedra Beach, Fl. The conference will run from June 27th to June 30th this year with a pre-conference workshop on June 26th. Nachi: And the address for this month’s credit is ebmedicine.net/E0319, 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! Most Important References 7.* Clancy K, Velopulos C, Bilaniuk JW, et al. Screening for blunt cardiac injury: an Eastern Association for the Surgery of Trauma practice management guideline. J Trauma Acute Care Surg. 2012;73(5 Suppl 4):S301-S306. (Guideline) 22.* Schultz JM, Trunkey DD. Blunt cardiac injury. Crit Care Clin. 2004;20(1):57-70. (Review article) 23.* El-Chami MF, Nicholson W, Helmy T. Blunt cardiac trauma. J Emerg Med. 2008;35(2):127-133. (Review article) 27.* Bock JS, Benitez RM. Blunt cardiac injury. Cardiol Clin. 2012;30(4):545-555. (Review article) 34.* Berk WA. ECG findings in nonpenetrating chest trauma: a review. J Emerg Med. 1987;5(3):209-215. (Review article) 64.* Velmahos GC, Karaiskakis M, Salim A, et al. Normal electrocardiography and serum troponin I levels preclude the presence of clinically significant blunt cardiac injury. J Trauma. 2003;54(1):45-50. (Prospective; 333 patients) 73.* Melniker LA, Leibner E, McKenney MG, et al. Randomized controlled clinical trial of point-of-care, limited ultrasonography for trauma in the emergency department: the first sonography outcomes assessment program trial. Ann Emerg Med. 2006;48(3):227-235. (Randomized controlled trial; 262 patients)

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. In our first paper this month, Shaan Khurshid and associates determine the frequency of rhythm abnormalities in 502,627 adults in the UK Biobank, a national prospective cohort. They found that 2.35% had a baseline rhythm abnormality. The prevalence increased with age, with 4.84% of individuals aged 65 to 73 years having rhythm abnormalities. During over three million person- years of follow up, nearly 16,000 new rhythm abnormalities were detected. Atrial fibrillation was the most frequent with three per thousand person-years. Bradyarrhythmia with almost one per thousand person-years. Conduction system disease is about one per one thousand years. Supraventricular and ventricular arrhythmias, each about one half per one thousand person-years. Older age was associated with a hazard ratio of 2.35 for each 10 year increase. Male sex, hypertension, chronic kidney disease and heart failure were all associated with new rhythm abnormalities. In our next paper, Fabien Squara and associates evaluated a method of determining the septal or free wall positioning of pacemaker or ICD leads during fluoroscopy. They compared in 50 patients a classical approach using posterior anterior, right anterior oblique 30 degrees, and left anterior oblique 40 degrees fluoroscopic imaging’s to 50 patients undergoing an individualized left anterior oblique or LAO approach. This individualized LAO approach view provided a true view of the interventricular septum. This angle was defined by the degree of LAO that allowed the perfect superimposition of the RV apex, using the tip of the right ventricular lead, temporarily placed at the apex, and one of the superior vena cava, inferior vena cava access using a guide wire. Transthoracic echo was used to confirm position of the right ventricular lead. Septal, or free wall, right ventricular lead positioning was correctly identified in 96% of patients in the individualized group, versus 76% in the classical group. P equals 0.004. For septal lead positioning fluoroscopy had 100% sensitivity, and an 89.5 specificity in an individualized group, versus 91.4% sensitivity, and a 40% specificity in the classical group. In our next paper, Elsayed Soliman and associates examined the lifetime risk of atrial fibrillation based on race and socioeconomic status. In the atherosclerosis risk in communities, ARIC, cohort, of 15,343 participants without atrial fibrillation, patients were recruited in 1987 to 1989, when they were 45 to 64 years of age, and followed through 2014. The authors identify 2,760 atrial fibrillation cases during a mean follow up of 21 years. The authors found that the lifetime risk of atrial fibrillation in the ARIC cohort was approximately one in three among whites, and one in five among African Americans. And, the socioeconomic status was inversely associated with cumulative incidents of atrial fibrillation before the last decades of life. In our next paper, Jonathan Steinberg and associates sought to determine the impact of atrial fibrillation episode duration threshold on atrial fibrillation incidents and burden in pacemaker patients in a prospective registry. In 615 pacemaker patients was device detected atrial fibrillation over a mean follow up of 3.7 years, 599 had one or more atrial fibrillation episodes of 30 seconds duration, with a mean number of 22 episodes. At 12 months, freedom from atrial fibrillation ranged from 25.5% to 73.1%, based on a duration threshold from 30 seconds up to 24 hours. Of patients with a first episode of 30 seconds to two minutes, 35.8% were free from subsequent episodes greater than two minutes at 180 days. The mean atrial fibrillation burden of 0.2% for patients with first episodes between 30 seconds and 3.8 hours, was significantly less than the 9.5% burden for those with greater than 3.8 hours. The authors concluded that small differences in atrial fibrillation episode duration definition can significantly affect the perceived incidents of atrial fibrillation impact reported outcomes, including atrial fibrillation success. An initial atrial fibrillation episode of 30 seconds does not predict clinically meaningful atrial fibrillation burden. In the next paper, Hongwu Chen and Linsheng Shi and associates examined the distinct electrophysiologic features of bundle branch reentrant ventricular tachycardia in patients without structural heart disease. They described nine patients, mean age 29.6 years, with normal left ventricular function and bundle branch reentrant ventricular tachycardia, with a right bundle branch block pattern in one patient, and left bundle branch block patterns in nine patients. In all left bundle branch block pattern ventricular tachycardia, the mean ventricular tachycardia cycling was 329.3 milliseconds, and the median HV interval during tachycardia was longer than that of baseline, 78 versus 71 milliseconds. The H to right bundle interval during ventricular tachycardia was slightly shorter, however, the right bundle to ventricular interval was markedly longer than that during sinus rhythm, 50 versus 30 milliseconds. In six patients with three dimensional mapping of the left ventricle, a slow anterograde, or retrograde conduction over the left His-Purkinje system with normal myocardial voltage was identified. In addition, Purkinje related ventricular tachycardias were also induced in five patients. Ablation was applied to the distal left bundle branch block in patients with baseline left bundle branch block, and in one narrow QRS patient with sustained Purkinje related ventricular tachycardia, while right bundle branch was targeted in other patients. During a mean follow up at 31.4 months, frequent premature ventricular contractions occurred in one patient, and new ventricular tachycardia developed in the other patient. In the next paper, Michel Haissaguerre and associates examined detailed mapping in 24 patients who survived idiopathic ventricular fibrillation. They used multi-electrode body surface recordings to identify the drivers maintaining ventricular fibrillation, and analyze electrograms in the driver regions, using endocardial and epicardial catheter mapping during sinus rhythm. Ventricular fibrillation occurred spontaneous in three patients, and was induced in 16, while VF was non-inducible in five. Ventricular fibrillation mapping demonstrated reentrant and focal activities, 87% and 13% respectively. The activities were dominant in one ventricle in nine patients, while they were biventricular in the others. During sinus rhythm, areas of abnormal electrograms were identified in 15 out of 24 patients, or 62.5%, revealing localized structural alterations, in the right ventricle in 11, the left ventricle in one, in both in three. They covered a limited surface, 13 centimeters squared, representing 5% of the total surface, and recorded predominantly on the epicardium. 76% of these areas were co-located with ventricular fibrillation drivers. In nine patients without structural alterations, the authors observed a high incidence of Purkinje triggers, seven out of nine, versus four out of 15. Catheter ablation resulted in arrhythmia-free outcomes in 15 out of 18 patients at a 17 month follow up. In our next paper, David Spar and associates describe the effectiveness, safety, and compliance of the wearable cardioverter defibrillator in the identification and treatment of life-threatening ventricular arrhythmias in all US pediatric patients who wore a wearable defibrillator from 2009 to 2016, ages less than 18 years. The 455 patients had a median age of 15 years, median duration of wearable cardioverter defibrillator use of 33 days, and median patient wear time of 20.6 hours per day. The study population was divided into two groups, 63 patients with an ICD problem, or 392 patients without an ICD problem. The wear time was greater than 20 hours in both groups. There were seven deaths, or 1.5%. All patients were not wearing the wearable cardioverter defibrillator at the time of death. Eight patients, 1.8%, received at least one wearable cardioverter defibrillator shock treatment. Of the six patients who had appropriate therapy, there were seven episodes of either polymorphic ventricular tachycardia, or ventricular fibrillation, with a total of 13 treatments delivered. All episodes were successfully converted, and the patient survived. In our next paper, Marc Lemoine and associates used human-induced pluripotential stem cell-derived cardiomyocytes to examine differences in repolarization reserve. The authors compared the contribution of IKs and IKr on action potential durations in human left ventricular tissue, and the human induced pluripotential stem cell derived cardiomyocytes, or IPS-derived engineered heart tissue. They found that the IPS-derived heart tissue showed spontaneous diastolic depolarization in action potential duration, which were sensitive to low concentrations of Ivabradine. IKr block by E-4031 prolonged action potential duration 90 with similar EC50 in both the IPS-derived heart tissue and the human left ventricular tissue. But a larger effect size in the IPS-derived heart tissue, 281 milliseconds versus 110 milliseconds, in the human left ventricular tissue. While IKr block alone evoked early after depolarizations, it triggered activity in 50% of the IPS-derived heart tissue. Slow pacing reduced extracellular potassium blocking of IKr, IKs and IK1 were necessary to induce early after depolarizations in human left ventricular tissue. In accordance with their clinical safety, Moxifloxacin and Verapamil did not induce EADs in IPS-derived heart tissue. In both IPS-derived heart tissue and human left ventricular tissue, IKs block by HMR 1556 prolonged action potential duration 90 slightly in the combined presence of E-4031 and isoprenaline. In our next paper, Elizabeth Saarel and associates sought to obtain contemporary digital ECG measurements in healthy children from North America to evaluate the effects of sex and race, and to compare the results to commonly published data sets, using 2400 digital ECGs, collected for children less than 18 years of age with normal electrocardiograms at 19 centers in the pediatric heart network. The authors found that the QTc in lead II was greater for females compared to males for age groups three years or older, for whites compared to African Americans, for ages 12 years or older. The R wave amplitude in V6 was greater for males compared to females for age groups 12 years and greater; for African Americans compared to white or other race categories for age groups three years or greater; and greater compared to commonly used public data set groups for ages 12 years and greater. In our next paper, Pyotr Platonov and associates examined T-wave morphology as a possible predictor of cardiac events in patients with type 2 long QT syndrome mutation carriers with normal QTc intervals. The authors compared 154 LQT2 mutation carriers with QTc less than 360 milliseconds in men, and less than 470 milliseconds in women, with 1007 unaffected family members. Flat, notched, or negative T-waves in leads II or V5 on baseline ECG were considered abnormal. Using Cox regression analysis, the associations between T-wave morphology, the presence in mutations in the poor region of KCNH2, and the risk of cardiac events defined that syncope aborted cardiac arrest, defibrillator therapy, or sudden cardiac arrests were assessed. The authors found that LQT2 female carriers with abnormal T-wave morphology had a threefold increased risk of cardiac events compared to LQT2 female carriers with normal T-waves, while this association was not seen in males. LQT2 males with poor location of mutations had a six-fold increased risk of cardiac events than non-poor location males, while no such association was found in females. In our last paper, Yaniv Bar-Cohen and associates describe a percutaneous pacemaker entirely implanted in the pericardium, using a sheath for sub-xiphoid access to the pericardial space, and a miniaturized camera with fiber optic illumination, the micro-pacemakers were successfully implanted in six pigs. All animals were studied during follow up, survived without symptoms. That's it for this month. We hope that you'll find the Journal to be the go-to place for everyone interested in the field. See you next time!