Search

Background Patients with atrial fibrillation are increasingly prescribed a direct oral anticoagulant (DOAC) over warfarin and seek to avoid anticoagulation even without a history of major bleeding. This study explores the outcomes of patients implanted with a Watchman device in relation to anticoagulation choice (warfarin versus DOAC) in the post-procedure period and a history of bleeding. Methods Patients implanted with a Watchman device at a single center were retrospectively analyzed. Characteristics including anticoagulation in the first 45 days and history of major bleed were assessed and efficacy (thromboembolism) and safety (bleeding) outcomes compared by Kaplan-Meier analysis. Results 209 patients were implanted (57% male, age 74.6  7.8 years) and followed for 23.5 ± 7.1 months. In the first half of patients, 98% were prescribed warfarin, which dropped to 51% in the second half (p

Coronavirus disease (COVID-19) is a serious illness caused by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2). The symptoms of the disease range from asymptomatic to mild respiratory symptoms and even potentially life-threatening cardiovascular and pulmonary complications. Cardiac complications include acute myocardial injury, arrhythmias, cardiogenic shock and even sudden death. Furthermore, drug interactions with COVID-19 therapies may place the patient at risk for arrhythmias, cardiomyopathy and sudden death. In this review, we summarise the cardiac manifestations of COVID-19 infection and propose a simplified algorithm for patient management during the COVID-19 pandemic.

Previous reports indicate that IL18 is a novel candidate gene for diastolic dysfunction in sickle cell disease (SCD)–related cardiomyopathy. We hypothesize that interleukin-18 (IL-18) mediates the development of cardiomyopathy and ventricular tachycardia (VT) in SCD. Compared with control mice, a humanized mouse model of SCD exhibited increased cardiac fibrosis, prolonged duration of action potential, higher VT inducibility in vivo, higher cardiac NF-κB phosphorylation, and higher circulating IL-18 levels, as well as reduced voltage-gated potassium channel expression, which translates to reduced transient outward potassium current (Ito) in isolated cardiomyocytes. Administering IL-18 to isolated mouse hearts resulted in VT originating from the right ventricle and further reduced Ito in SCD mouse cardiomyocytes. Sustained IL-18 inhibition via IL-18–binding protein resulted in decreased cardiac fibrosis and NF-κB phosphorylation, improved diastolic function, normalized electrical remodeling, and attenuated IL-18–mediated VT in SCD mice. Patients with SCD and either myocardial fibrosis or increased QTc displayed greater IL18 gene expression in peripheral blood mononuclear cells (PBMCs), and QTc was strongly correlated with plasma IL-18 levels. PBMC-derived IL18 gene expression was increased in patients who did not survive compared with those who did. IL-18 is a mediator of sickle cell cardiomyopathy and VT in mice and a novel therapeutic target in patients at risk for sudden death.

International audience; Arrhythmogenic cardiomyopathy (ACM) is an arrhythmogenic disorder of the myocardium not secondary to ischemic, hypertensive, or valvular heart disease. ACM incorporates a broad spectrum of genetic, systemic, infectious, and inflammatory disorders. This designation includes, but is not limited to, arrhythmogenic right/left ventricular cardiomyopathy, cardiac amyloidosis, sarcoidosis, Chagas disease, and left ventricular noncompaction. The ACM phenotype overlaps with other cardiomyopathies, particularly dilated cardiomyopathy with arrhythmia presentation that may be associated with ventricular dilatation and/or impaired systolic function. This expert consensus statement provides the clinician with guidance on evaluation and management of ACM and includes clinically relevant information on genetics and disease mechanisms. PICO questions were utilized to evaluate contemporary evidence and provide clinical guidance related to exercise in arrhythmogenic right ventricular cardiomyopathy. Recommendations were developed and approved by an expert writing group, after a systematic literature search with evidence tables, and discussion of their own clinical experience, to present the current knowledge in the field. Each recommendation is presented using the Class of Recommendation and Level of Evidence system formulated by the American College of Cardiology and the American Heart Association and is accompanied by references and explanatory text to provide essential context. The ongoing recognition of the genetic basis of ACM provides the opportunity to examine the diverse triggers and potential common pathway for the development of disease and arrhythmia.

International audience; Arrhythmogenic cardiomyopathy (ACM) is an arrhythmogenic disorder of the myocardium not secondary to ischemic, hypertensive, or valvular heart disease. ACM incorporates a broad spectrum of genetic, systemic, infectious, and inflammatory disorders. This designation includes, but is not limited to, arrhythmogenic right/left ventricular cardiomyopathy, cardiac amyloidosis, sarcoidosis, Chagas disease, and left ventricular noncompaction. The ACM phenotype overlaps with other cardiomyopathies, particularly dilated cardiomyopathy with arrhythmia presentation that may be associated with ventricular dilatation and/or impaired systolic function. This expert consensus statement provides the clinician with guidance on evaluation and management of ACM and includes clinically relevant information on genetics and disease mechanisms. PICO questions were utilized to evaluate contemporary evidence and provide clinical guidance related to exercise in arrhythmogenic right ventricular cardiomyopathy. Recommendations were developed and approved by an expert writing group, after a systematic literature search with evidence tables, and discussion of their own clinical experience, to present the current knowledge in the field. Each recommendation is presented using the Class of Recommendation and Level of Evidence system formulated by the American College of Cardiology and the American Heart Association and is accompanied by references and explanatory text to provide essential context. The ongoing recognition of the genetic basis of ACM provides the opportunity to examine the diverse triggers and potential common pathway for the development of disease and arrhythmia.

A sudden cardiac arrest in school or at a school event is potentially devastating to families and communities. An appropriate response to such an event—as promoted by developing, implementing, and practicing a cardiac emergency response plan (CERP)—can increase survival rates. Understanding that a trained lay-responder team within the school can make a difference in the crucial minutes between the time when the victim collapses and when emergency medical services arrive empowers school staff and can save lives. In 2015, the American Heart Association convened a group of stakeholders to develop tools to assist schools in developing CERPs. This article reviews the critical components of a CERP and a CERP team, the factors that should be taken into account when implementing the CERP, and recommendations for policy makers to support CERPs in schools.

Preamble e472 1. Introduction e473 2. General Principles e475 3. Sinus Tachyarrhythmias e480 4. Nonsinus Focal Atrial Tachycardia and MAT e481 5. Atrioventricular Nodal Reentrant Tachycardia e482 6. Manifest and Concealed Accessory Pathways e483 7. Atrial Flutter e485 8. Junctional Tachycardia e487 9. Special Populations e487

Jonathan L. Halperin, MD, FACC, FAHA, Chair Glenn N. Levine, MD, FACC, FAHA, Chair-Elect Jeffrey L. Anderson, MD, FACC, FAHA, Immediate Past Chair [¶][1] Nancy M. Albert, PhD, RN, FAHA[¶][1] Sana M. Al-Khatib, MD, MHS, FACC, FAHA Kim K. Birtcher, PharmD, AACC Biykem Bozkurt, MD, PhD, FACC

See Article by Orgeron et al Arrhythmogenic right ventricular cardiomyopathy (ARVC) is a progressive disorder characterized by morphological changes in the myocardium that place the patient at risk for lethal ventricular arrhythmias. A genetic mutation involving desmosomes is seen in most patients1 that affects myocyte cell-to-cell adhesion. Athletes are likely to express this disease at an earlier age as exercise promotes progression of the disease. Because either ventricle can be affected, the term arrhythmogenic cardiomyopathy has been proposed.1,2 Diagnosis is based on criteria as set out in the 2010 Task Force document,3 encompassing ventricular structure, histology, electrocardiographic features, arrhythmias, and genetic features. In 2015, an International Task Force published a consensus statement to provide clinical practice guidance based on available evidence and expert opinion.4 For implantable cardioverter defibrillator (ICD) implantation, the Task Force assigned a class I recommendation to patients who had been resuscitated from hemodynamically unstable ventricular tachycardia (VT) or ventricular fibrillation (VF) and for patients with severe right ventricular or left ventricular systolic dysfunction because these patients were felt to have life-threatening arrhythmic events >10% per year.4 The Task Force advised that an ICD should be considered (class IIa) for patients with hemodynamically stable sustained VT, syncope, nonsustained VT, or moderate ventricular dysfunction.4 A class IIb (may be considered) designation was assigned for those with minor risk factors, such as male sex, proband status, inducibility on electrophysiological study, or at least 3 precordial leads with T-wave inversion.4 Finally, class III (not recommended) was assigned to asymptomatic patients with no risk factors or healthy gene carriers.4 Since the publication of the International Task Force consensus statement, larger observational studies have added to our understanding of this disease. In 416 …

Objective In out-of-hospital cardiac arrest (OHCA) with ventricular fibrillation (VF) the frequency-based waveform characteristic, amplitude-spectral area (AMSA) is associated with hospital discharge and good neurological outcome, yet AMSA is also known to increase in response to chest compressions (CC). In addition to rate and depth, well performed CC provides good chest recoil without leaning, reflected in the release velocity (RV). We hypothesized that AMSA is associated with hospital discharge and good neurological outcome independent of CC quality. Methods OHCA patients (age≥18), with initial rhythm of VF from an Utstein-Style database were analyzed. AMSA was measured prior to each shock, and averaged for each subject (AMSA-avg). Primary endpoint was hospital discharge and secondary endpoint was a good neurological outcome. Univariate and stepwise multivariable logistic regression, and receiver–operator–characteristic (ROC) analyses were performed. Factors analyzed were age, sex, witnessed status, time from dispatch to monitor/defibrillator application, number of shocks, first shock AMSA (AMSA 1 ), AMSA-avg, averaged pre-shock pause, CC rate, depth, and RV. Results 140 subjects were analyzed. Hospital discharge was 31% and with good neurological outcome in 24% (77% of those discharged). AMSA-avg ( p p =0.002), and age ( p =0.029) were independently associated with hospital discharge, with a non-significant trend for witnessed status ( p =0.069), with AUC=0.846 for the multivariate model. For good neurological outcome, AMSA-avg ( p =0.001) and RV ( p =0.001) remained independently significant, with AUC=0.782. Conclusion In OHCA with an initial rhythm of VF, AMSA-avg and CC RV are both highly and independently associated with hospital discharge and good neurological outcome.

Since the advent of the non-vitamin K antagonist oral anticoagulant (NOAC) agents, which act as direct thrombin inhibitors or inhibitors of Factor Xa, clinicians are provided with valuable alternatives to vitamin K antagonists (VKAs). At the same time, electrophysiologists frequently perform more invasive procedures, increasingly involving the left chambers of the heart. Thus, they are constantly faced with the dilemma of balancing the risk for thromboembolic events and bleeding complications. These changes in the rapidly evolving field mandate an update of the European Heart Rhythm Association (EHRA) 2008 consensus document on this topic.1 The present document covers the antithrombotic management during different ablation procedures, implantation or exchange of cardiac implantable electronical devices (CIEDs), as well as the management of peri-interventional bleeding complications. The document is not a formal guideline and due to the lack of prospective randomized controlled trials (RCTs) for many of the clinical situations encountered, the recommendations are often ‘expert opinion’. The document strives to be practical for which reason we subdivided it in the three main topics: ablation procedure, CIED implantation or generator change, and issues of peri-interventional bleeding complications on concurrent antiplatelet therapy. For quick reference, every subchapter is followed by a short section on consensus recommendations. Many RCTs are ongoing in this field and it is hoped that this document will help to prompt further well-designed studies. ### Ablation of atrial fibrillation, left atrial arrhythmias and right sided atrial flutter In patients with symptomatic paroxysmal or even persistent atrial fibrillation (AF), catheter ablation is indicated when antiarrhythmic drugs have failed in controlling recurrences or even as a first-line therapy in selected patients.2–4 Patients with AF have an increased risk of thromboembolic events, which varies according to the presence of several risk factors.5,6 Apart from their intrinsic thromboembolic risks, ablation in these patients increases thromboembolic risk due to the introduction and manipulation …

In retrospective swine and human investigations of ventricular fibrillation (VF) cardiac arrest, the amplitude-spectral area (AMSA), determined from the VF waveform, can predict defibrillation and a return of spontaneous circulation (ROSC).We hypothesized that an algorithm using AMSA in real time to direct postshock chest compression (CC) duration would shorten the time to ROSC and improve neurological outcome in a swine model of VF cardiac arrest with acute myocardial infarction (AMI) or nonischemic myocardium.AMI was induced by occlusion of the left anterior descending artery. VF was untreated for 10 min. Animals were randomized to either traditional resuscitation with 2 min of CC after each shock or to an AMSA-guided algorithm where postshock CCs were shortened to 1 min if the preshock AMSA exceeded 20 mV-Hz.A total of 48 animals were studied, 12 in each group (AMI vs. normal, and traditional vs. AMSA-guided). There was a nonsignificant shorter time to ROSC with an AMSA-guided approach in AMI swine (17.2 ± 3.4 vs. 18.5 ± 4.7 min, p = NS), and in normal swine (13.5 ± 1.1 vs. 14.4 ± 1.2, p = NS). Neurological outcome was similar between traditional and AMSA-guided animals. AMSA predicted ROSC (p0.001), and a threshold of 20 mV-Hz gave a sensitivity of 89%, with specificity of 29%.Although AMSA predicts ROSC in a swine model of VF arrest in both AMI and normal swine, a waveform-guided approach that uses AMSA to direct postshock CC duration does not significantly shorten the time to ROSC or alter neurological outcome.

Coronary arterial spasm has long been recognized to cause chest pain and myocardial ischemia, with attacks occurring predominantly at rest and during the night. In 1959, Prinzmetal et al. [(1)][1] described a “variant form of angina pectoris” that occurred at rest with ST-segment elevation or

1. Introduction 95 2. Current Guidelines that Address ICD Use 95 3. Randomized Controlled Trials of ICD Therapy for Primary Prevention of Sudden Cardiac Death 96 4. ICD Implantation in the Context of an Abnormal Troponin that Is Not Due to a Myocardial Infarction 100 5. ICD Implantation Within 40 Days of a Myocardial Infarction 101 6. ICD Implantation Within 90 Days of Revascularization 105 7. ICD Implantation < 9 Months from the Initial Diagnosis of Nonischemic Cardiomyopathy 110 8. Dual-Chamber vs Single-Chamber ICD Recommendations 114 9. Documentation of Clinical Decisions 116 10. Future Research and Directions 117 The implantable cardioverter defibrillator (ICD) has emerged as an important treatment option for selected patients who are at risk of sudden cardiac death. Randomized trials have consistently shown that ICD implantation reduces mortality in patients with heart failure and reduced left ventricular function, as well as in patients who have suffered a cardiac arrest.1–3 Recommendations on the use of the ICD in clinical practice have been provided in four important guideline documents sponsored by the American College of Cardiology (ACC), the American Heart Association (AHA), Heart Rhythm Society (HRS), and the European Society of Cardiology (ESC).4–7 For each indication for ICD therapy, both a Class of indication (I, II, or III) and level of evidence for the indication (A, B, or C) are provided. To ensure that recommendations are evidence-based, Class I recommendations are typically based on the results of prospective randomized clinical trials. For example, in the ACC/AHA/HRS 2012 Focused Update of the …

BackgroundPrevious investigations of out-of-hospital cardiac arrest (OHCA) have shown that the waveform characteristic amplitude spectral area (AMSA) can predict successful defibrillation and return of spontaneous circulation (ROSC) but has not been studied previously for survival.ObjectivesTo determine whether AMSA computed from the ventricular fibrillation (VF) waveform is associated with pre-hospital ROSC, hospital admission, and hospital discharge.MethodsAdults with witnessed OHCA and an initial rhythm of VF from an Utstein style database were studied. AMSA was measured prior to each shock and averaged for each subject (AMSA-avg). Factors such as age, sex, number of shocks, time from dispatch to monitor/defibrillator application, first shock AMSA, and AMSA-avg that could predict pre-hospital ROSC, hospital admission, and hospital discharge were analyzed by logistic regression.ResultsEighty-nine subjects (mean age 62 ± 15 years) with a total of 286 shocks were analyzed. AMSA-avg was associated with pre-hospital ROSC (p = 0.003); a threshold of 20.9 mV-Hz had a 95% sensitivity and a 43.4% specificity. Additionally, AMSA-avg was associated with hospital admission (p < 0.001); a threshold of 21 mV-Hz had a 95% sensitivity and a 54% specificity and with hospital discharge (p < 0.001); a threshold of 25.6 mV-Hz had a 95% sensitivity and a 53% specificity. First-shock AMSA was also predictive of pre-hospital ROSC, hospital admission, and discharge. Time from dispatch to monitor/defibrillator application was associated with hospital admission (p = 0.034) but not pre-hospital ROSC or hospital discharge.ConclusionsAMSA is highly associated with pre-hospital ROSC, survival to hospital admission, and hospital discharge in witnessed VF OHCA. Future studies are needed to determine whether AMSA computed during resuscitation can identify patients for whom continuing current resuscitation efforts would likely be futile.

For almost the past decade, recommendations for the use of implantable cardioverter defibrillators (ICDs) for primary prevention of sudden cardiac death have been based upon the left ventricular ejection fraction (LVEF). Current guidelines recommend an ICD for heart failure patients with LVEF ≤35% and NYHA functional class of II or III; however, because the majority of heart failure patients who qualify for ICD implantation based on these criteria will never have an event requiring ICD therapy over several years of follow-up, additional methods of risk stratification for sudden death are clearly needed. Additionally, most of the nearly 300,000 cardiac arrests that occur each year occur in patients without heart failure or significant left ventricular dysfunction. To improve the identification of patients at risk for sudden death, several criteria other than ejection fraction have been proposed and studied. Markers of autonomic tone, including heart rate turbulence and QT dynamicity, have shown some ability to predict total mortality but not arrhythmic events. Microvolt T-wave alternans testing was initially thought to be highly predictive of life-threatening arrhythmias, but prospective large sub-studies of the MADIT II and SCD-HeFT trials have failed to show a predictive value for T-wave alternans testing. Newer markers for risk are based upon the detection of myocardial fibrosis, which forms the substrate for re-entrant and malignant ventricular tachyarrhythmias. Markers of collagen turnover or quantification of myocardial scar by MRI may hold the best promise for identifying patients at highest risk for sudden cardiac death and may also identify patients at high risk but with an ejection fraction above 35%, who are not currently recommended for ICD implantation.

Imaging of the right ventricle (RV) for the diagnosis of arrhythmogenic right ventricular cardiomyopathy/dysplasia (ARVC/D) is commonly performed by echocardiography or magnetic resonance imaging (MRI). Angiography is an alternative modality, particularly when MRI cannot be performed. We hypothesized that RV volume and ejection fraction computed by angiography would correlate with these quantities as computed by MRI. RV volumes and ejection fraction were computed for subjects enrolled in the North American ARVC/D Registry, with both RV angiography and MRI studies. Angiography was performed in the 30° right anterior oblique (RAO) and 60° left anterior oblique (LAO) views. Angiographic volumes were computed by RAO view and two-view (RAO and LAO) formulae. 17 subjects were analyzed (11 men and 6 women), with 15 subjects classified as affected, and two as unaffected by modified Task Force criteria. The correlation coefficient of MRI to the two-view angiographic analysis was 0.72 (P = 0.003) for end-diastolic volume and 0.68 (P = 0.005) for ejection fraction. Angiographically derived volumes were larger than MRI derived volume (P = 0.009) and with the slope in a linear relationship equal to 0.8 for end diastolic volume, and 0.9 for RV ejection fraction (P < 0.001), computed by the two view formula. End-diastolic volumes and ejection fractions of the RV obtained by dual view angiography correlate with these quantities by MRI. RV end-diastolic volumes are larger by RV angiography in comparison with MRI.

Background— In cardiac arrest, the ventricular fibrillation (VF) waveform, particularly amplitude spectral area (AMSA) and slope, predicts the return of spontaneous circulation (ROSC), but it is unknown whether the predictive utility differs in an acute myocardial infarction (MI), prior MI, or normal myocardium and if the waveform can distinguish the underlying myocardial state. We hypothesized that in a swine model of VF cardiac arrest, AMSA and slope predict ROSC after a shock independent of substrate and distinguish an acute from nonacute MI state. Methods and Results— MI was induced by occlusion of the left anterior descending artery. Post MI swine recovered for a 2-week period before induction of VF. VF was untreated for 8 minutes in 10 acute MI, 10 post MI, and 10 control swine. AMSA and slope predicted ROSC after a shock independent of myocardial state. For AMSA >31 mV-Hz, the odds ratio was 62 ( P ≤0.001) compared with AMSA 3.1 mV/s, odds ratio was 52 ( P ≤0.001) compared with slope 33.5 mV-Hz, the sensitivity to identify an acute from nonacute (control or post MI) state was 83%. Conclusions— In a swine model of VF cardiac arrest, AMSA and slope predict ROSC independent of myocardial substrate. Furthermore, with chest compressions, the VF waveform evolves differently and may offer a means to distinguish an acute MI.

We have demonstrated that a return of spontaneous circulation in the first 3 mins of resuscitation in swine is predicted by ventricular fibrillation waveform (amplitude spectral area or slope) when untreated ventricular fibrillation duration or presence of acute myocardial infarction is unknown. We hypothesized that in prolonged resuscitation efforts that return of spontaneous circulation immediately after a second or later shock with postshock chest compression is independently predicted by end-tidal CO2, coronary perfusion pressure, and ventricular fibrillation waveform measured before that shock in a swine model of ischemic and nonischemic ventricular fibrillation arrest.Animal intervention study with comparison to a control group.University animal laboratory.Twenty swine.Myocardial infarction was induced by steel plug occlusion of the left anterior descending coronary artery. Ventricular fibrillation was untreated for 8 mins in normal swine (n=10) and acute myocardial infarction swine (n=10).End-tidal CO2, coronary perfusion pressure, and ventricular fibrillation waveform characteristics of amplitude spectral area and slope were analyzed before second or later shocks. For an amplitude spectral area35 mV-Hz, the odds ratio for achieving return of spontaneous circulation after that shock was 72 (95% confidence interval, 3.8-1300; p=.004) compared with an amplitude spectral area28 mV-Hz and with an area under the receiver operator characteristic curve of 0.86. For slope3.6 mV/s, the odds ratio for achieving return of spontaneous circulation was 36 (95% confidence interval, 2.7-480; p=.007) compared with slope2.72 mV/s with an area under the curve of 0.86. End-tidal CO2 and coronary perfusion pressure were not predictive of return of spontaneous circulation after a shock, although coronary perfusion pressure was significantly related to both amplitude spectral area (p.001) and slope (p.001).: In prolonged untreated ventricular fibrillation arrest, the waveform characteristics of amplitude spectral area and slope predict the attainment of return of spontaneous circulation with a second or later shock. This has implications for the ideal means to customize the timing of shocks and chest compressions when return of spontaneous circulation is not promptly obtained.

Introduction: Changes due to biventricular pacing have been documented by shortening of QRS duration and echocardiography. Compared to normal ventricular activation, the presence of left bundle branch block (LBBB) results in a significant change in cardiac cycle time intervals. Some of these have been used to quantify the underlying cardiac dyssynchrony, assess the effects of biventricular pacing, and guide programming of ventricular pacing devices. This study evaluates a simple noninvasive method using accelerometers attached to the skin to measure cardiac time intervals in biventricularly paced patients. Methods: Ten patients with biventricular pacemakers previously implanted for congestive heart failure were paced in the AAI mode, then in atrioventricular (AV) sequential mode from the right and left ventricles followed by biventricular pacing. Simultaneous recordings were obtained by 2D, Doppler echocardiography as well as by accelerometers. Similar recordings were obtained from 10 gender, aged matched, normal controls during sinus rhythm. Results: Compared to normals, heart failure patients paced in AAI mode had prolonged isovolumetric contraction time (IVCT), shorter ventricular ejection time (LVET), and prolonged isovolumetric relaxation (IVRT). With biventricular pacing the IVCT decreased, but the LVET and IVRT did not change significantly. There was excellent correlation between the echo and accelerometer-measured intervals. Conclusions: Shortening of the IVCT measured by an accelerometer is a consistent time interval change due to biventricular pacing that probably reflects more rapid acceleration of left ventricular ejection. The accelerometer may be useful to assess immediate efficacy of biventricular pacing during device implantation and optimize programmable time intervals such as AV and interventricular (VV) delays. (PACE 2007; 30:1476‐1481)

Objective: Future automated external defibrillators are being designed to direct rescue efforts (chest compressions first vs. defibrillation) by inferring the duration of ventricular fibrillation based on its waveform characteristics such as frequency content. This approach assumes that the ventricular fibrillation waveform is an appropriate surrogate for ventricular fibrillation duration and is not affected by structural heart disease. We hypothesized that an acute myocardial infarction may alter the frequency content of ventricular fibrillation. Design: Animal intervention study with comparison to control group. Setting: University animal laboratory. Subjects: Twenty-seven swine. Interventions: Acute myocardial infarction was induced by occlusion of the mid-left anterior descending artery. Ventricular fibrillation was induced in swine with acute myocardial infarction and control swine. Measurements and Main Results: Ventricular fibrillation was induced in 11 swine with an acute myocardial infarction and in 16 control swine. Ventricular fibrillation waveforms were analyzed for mean, median, and dominant frequency, as well as bandwidth and amplitude. All frequency characteristics were significantly (p

Preamble e472 1. Introduction e473 2. General Principles e475 3. Sinus Tachyarrhythmias e480 4. Nonsinus Focal Atrial Tachycardia and MAT e481 5. Atrioventricular Nodal Reentrant Tachycardia e482 6. Manifest and Concealed Accessory Pathways e483 7. Atrial Flutter e485 8. Junctional Tachycardia e487 9. Special Populations e487

Jonathan L. Halperin, MD, FACC, FAHA, Chair Glenn N. Levine, MD, FACC, FAHA, Chair-Elect Jeffrey L. Anderson, MD, FACC, FAHA, Immediate Past Chair [¶][1] Nancy M. Albert, PhD, RN, FAHA[¶][1] Sana M. Al-Khatib, MD, MHS, FACC, FAHA Kim K. Birtcher, PharmD, AACC Biykem Bozkurt, MD, PhD, FACC

The QT interval on the ECG is prolonged by more than 50 marketed drugs, an effect that has been associated with syncope and/or sudden cardiac death due to an arrhythmia. Because changes in heart rate also change the QT interval, it has become standard practice to use a correction formula, such as the Bazett formula, to normalize the QT interval to a heart rate of 60 bpm, that is, the rate-corrected QT or QTc. Numerous other formulas have been devised to make this correction, including the Fridericia, Hodges, and Framingham formulas.The purpose of this study was to investigate how the Bazett formula and three other formulas influence assessment of the QT-prolonging effect of the potassium channel-blocking drug ibutilide.Using a standardized physical activity protocol, the QT interval was assessed over a broad range of heart rates before and after an infusion of ibutilide (4.75 microg/kg) that produced a stable 15- to 20-ms QT prolongation in consenting normal subjects (9 men and 9 women). The QT interval was measured digitally over a range of heart rates from 60 to 120 bpm, and then four correction formulas (Bazett, Fridericia, Framingham, or Hodges) were applied. The uncorrected change in QT interval due to ibutilide was compared with the change using each of the formulas by repeated measures analysis of variance.At heart rates from 60 to 120 bpm, the Bazett and Fridericia correction formulas overestimated the change in QT in both men and women (P.001). However, the Framingham and Hodges formulas did not alter the accuracy of the assessment of QT interval change.Rate correction of QT intervals using the standard Bazett and Fridericia formulas can introduce significant errors in the assessment of drug effects on the QT interval. This has implications for the clinical assessment of drug effects and for the safety assessment of new drugs under development.

Summary Background For prolonged VF, perfusion of the myocardium by pre-shock chest compressions can improve myocardial readiness for successful defibrillation. Characteristics of the VF waveform correlate with the duration of VF when there is no structural heart disease. A "smart" automated external defibrillator (AED) could therefore analyze the VF waveform, determine if VF has been prolonged, and then direct rescuers to either deliver a shock first or chest compressions first. We hypothesized that ischemic heart failure might alter the waveform content of ventricular fibrillation compared with normal hearts, complicating the determination of VF duration. Methods Myocardial infarction was induced by ligating the proximal left coronary artery. Six weeks later, VF was then induced in 10 rats with myocardial infarction and heart failure (MI-CHF) and 9 control rats. Waveforms were analyzed for total signal amplitude, median frequency, dominant frequency and bandwidth (the frequency interval containing 50% of the total amplitude about the median frequency). Results All of these VF waveform characteristics were altered substantially in MI-CHF rats compared to normal controls. In particular, MI-CHF rats had decreased signal amplitude early in VF ( p =0.02), a broader bandwidth ( p =0.001) and different frequency characteristics over time ( p Conclusions VF waveforms vary over time in a typical manner among rats with and without ischemic heart failure. However, the time-course and waveform characteristics of ventricular fibrillation are altered in rats with myocardial infarctions and ischemic heart failure compared to normal controls. These findings have important implications regarding the use of waveform analyses to determine the duration of VF.

We appreciate the thoughtful letter to the editor by Drs Shiyovich, Gerovich, and Katz. We examined whether an association exists between when chest compressions (CC) are resumed after a shock that defibrillates ventricular fibrillation (VF) and when VF may recur after that shock, in a cohort of witnessed cardiac arrest victims in Arizona. We used 2 main statistical analyses. We first used regression analysis to see whether there was a relationship between CC resumption and VF recurrence. This test considered all VF refibrillations (n=166), and no relationship to CC resumption was found, and furthermore, the randomness is visually apparent in the scatter diagrams of Figure 3. Second, we looked at the risk of VF recurrence in the first 30 …

Background/Aim: Patients with ventricular ectopy from the right ventricular (RV) outflow tract (RVOT) are often referred for RV angiography to exclude disorders such as arrhythmogenic RV cardiomyopathy/dysplasia (ARVC/D). This is usually based on a qualitative assessment of the wall motion. We present a method to quantify the wall motion and to apply this method to compare patients with RVOT ectopy to normal subjects. Methods: RV angiograms were analyzed from 19 normal subjects and 11 subjects with RVOT ventricular arrhythmias (RVOT arrhythmia subjects) who had no other clinical or other evidence for ARVC/D. By a newly developed computer-based method, RV contours were first traced from multiple frames spanning the entire cardiac cycle. The fractional change in area between contours was then calculated as a serial function of time and location to determine both total contour area change and timing of contour movement. Contour area strain, defined as the differential change in area between nearby regions, was also computed. Results: The contour area change was greatest in the tricuspid valve region and least in the RVOT and midanterior regions. The onset of contraction was earliest in the RVOT region and latest in the apical, inferior, inferoapical, and subtricuspid valve regions. The contour strain was largest in superior tricuspid valve and inferior wall and near zero within the lateral tricuspid valve region. There were significant pairwise differences in contraction area, timing, and strain in the various regions. There were no significant differences between normal subjects and RVOT arrhythmia subjects. Conclusions: The RV wall motion is nonuniform in contour area change, strain, and timing of motion. Patients with RVOT ventricular ectopy demonstrate wall motion parameters similar to those of normal subjects. This technique should be applicable in analyzing RV wall motion in patients suspected of having ARVC/D.

Background:Derived variables of ventricular fibrillation, such as the frequency distribution by fast Fourier transformation and its evolution over time, have been used to determine the optimum timing for defibrillation. We hypothesized that these frequency variables would differ among neonatal, young child and older child populations due to cardiac developmental and size differences. Such differences may have important implications for developing defibrillation algorithms for pediatric patients and for extrapolating adult defibrillation algorithms to children in VF. Methods: Ventricular fibrillation was induced and recorded for 6 min in 4 kg ( n = 11), 14 kg (n = 10), and 24 kg (n = 16) piglets, corresponding to neonatal, young child and older children. Mean, median, and dominant frequencies were computed in 30 s intervals and compared among weight classes. Results: All frequency variables in all weight groups showed first a decline at 1.25–1.75 min, followed by a gradual rise and plateau. There were significant differences for mean, median and dominant frequencies among weight classes. Specifically, 14 kg piglets showed higher frequency variables overall with a time evolution that was different from that of 4 and 24 kg piglets. Mean frequency showed the most stable time evolution with the least moment-to-moment variability. Conclusion: The frequency waveform characteristics and time course are somewhat different in 14 kg piglets compared with 4 and 24 kg piglets. If similar differences are demonstrable among children of different weights and ages, AEDs designed to determine optimal timing of defibrillation shocks in adults by frequency waveform characteristics may require modification for use in children with VF. © 2004 Elsevier Ireland Ltd. All rights reserved.

This report describes a case of syncope with an initial ECG that showed ST-segment elevation in the right precordial leads suggestive of Brugada syndrome. Procainamide infusion induced a significant increase in the ST-segment abnormalities, further increasing the suspicion for this syndrome. Cardiac catheterization showed lesions in the proximal left anterior descending artery and distal right coronary artery. Following percutaneous coronary intervention at these sites, the ST-segment abnormalities resolved and a repeat procainamide challenge was negative. Electrophysiological study did not provoke any ventricular arrhythmias. Silent myocardial ischemia may result in ECG changes that resemble those seen in patients with Brugada syndrome.

Background— Prior investigation of out-of-hospital cardiac arrest has raised the concern that ventricular fibrillation (VF) recurrence may be triggered by chest compression (CC) resumption. We investigated predictors of VF recurrence after defibrillation, including timing of CC resumption. Methods and Results— Patients with witnessed out-of-hospital cardiac arrest and initial rhythm of VF from an Utstein-style database were analyzed. For each shock that defibrillated VF, CC resumption and VF recurrence times were determined. Shocks were classified according to postshock rhythm. Factors (age, sex, time from dispatch to monitor/defibrillator application, and CC resumption) that could predict VF recurrence were analyzed. CC resumption was categorized into groups: CC1, 1 to 5 seconds; CC2, 6 to 10 seconds; CC3, 11 to 30 seconds; and CC4, >30 seconds. Eighty-eight subjects were analyzed, with a total of 285 shocks, with 226 shocks that achieved asystole (n=102), organized rhythm (n=120), or monomorphic ventricular tachycardia (n=4). After a successful shock, CC resumption occurred at a median (interquartile range) of 8 (5–18) seconds. VF recurred after 166 shocks (74%) and recurred within 30 seconds in 69 shocks. There was no significant relationship between VF recurrence and factors analyzed including CC resumption time, nor stratified by postshock rhythm. The hazard ratios (HRs) for VF recurrence within 30 seconds for later CC groups (CC2, CC3, and CC4) relative to early CC resumption (CC1) were as follows: HR(CC2)=1.05 ( P =0.9); HR(CC3)=1.75 ( P =0.1); and HR(CC4)=0.67 ( P =0.4). Conclusions— VF recurrence within 30 seconds of a defibrillatory shock was not dependent on timing of CC resumption in patients with witnessed arrest and initial rhythm of VF.

Post-myocardial infarction pericarditis occurs in approximately 5% to 6% of patients who receive thrombolytic agents. It should be suspected in any patient with pleuropericardial pain. A pericardial friction rub may or may not be present. Differentiation of pericarditis from recurrent angina may be difficult, but a careful history and evaluation of serial electrocardiograms can help distinguish the two entities. Dressler's syndrome, pericarditis that occurs at least 1 week following myocardial infarction, is now exceedingly rare. Most cases of pericarditis have a benign course; however, because pericarditis is associated with larger infarcts, overall long-term mortality rate is increased. Rare complications include hemopericardium, cardiac tamponade, and constrictive pericarditis. Therapy is directed toward relief of pain, which usually responds well to nonsteroidal anti- inflammatory agents (eg, aspirin or ibuprofen).

Arrhythmogenic Right Ventricular Cardiomyopathy/Dysplasia (ARVC/D) is an inherited ­cardiomyopathy characterized clinically by ventricular arrhythmias, sudden death, and structural abnormalities of the right ventricle. Although structural involvement of the right ventricle predominates, a left dominant form (LDAC) has been described. Structural involvement of both ventricles is common in advanced disease. Due to significant heterogeneity in its manifestation, the diagnosis of ARVC/D is challenging and requires a multifaceted approach to patient evaluation. The recently published Revised Task Force Criteria provide clinicians with a validated model to improve the diagnosis of ARVC/D. The management of ARVC/D is primarily aimed at reducing the burden of symptomatic arrhythmias and decreasing the incidence of sudden ­cardiac death. Automatic implantable cardioverter-defibrillators (AICDs) significantly reduce mortality in patients with ARVC/D. However, accurate risk assessment is needed to avoid exposing low-risk patients to the long-term complications of AICDs. Strenuous exertion increases the rate of disease progression and increases the risk of sudden death.

In out-of-hospital cardiac arrest (OHCA) due to ventricular fibrillation (VF), VF may recur during resuscitation (recurrent VF) or fail to defibrillate (shock-resistant VF). While retrospective studies have suggested that amplitude spectral area (AMSA) and slope predict defibrillation, it is unknown whether the predictive power is influenced by VF type. We hypothesized that in witnessed OHCA with initial rhythm of VF that the utility for AMSA and slope to predict defibrillation would differ between shock-resistant and recurrent VF.AMSA and slope were measured immediately prior to each shock. For second or later shocks, VF was classified as recurrent or shock-resistant. Cardiac arrest was classified according to whether the majority of shocks were for recurrent VF or shock-resistant VF.44 patients received 98 shocks for recurrent VF and 96 shocks for shock-resistant VF; 24 patients achieved ROSC in the field. AMSA and slope were higher in recurrent VF compared to shock-resistant VF (AMSA: 28.8±13.1 vs 15.2±8.6 mVHz, P0.001, and slope: 2.9±1.4 vs 1.4±1.0 mVs(-1), P=0.001). Recurrent VF was more likely to defibrillate than shock-resistant VF (P0.001). AMSA and slope predicted defibrillation in shock-resistant VF (P0.001 for both AMSA and slope) but not in recurrent VF. Recurrent VF predominated in 79% of patients that achieved ROSC compared to 55% that did not (P=0.10).In witnessed OHCA with VF as initial rhythm, recurrent VF is associated with higher values of AMSA and slope and is likely to re-defibrillate. However, when VF is shock-resistant, AMSA and slope are highly predictive of defibrillation.

Vasopressors administered IV late during resuscitation efforts fail to improve survival. Intraosseous (IO) access can provide a route for earlier administration. We hypothesized that IO epinephrine after 1 minute of cardiopulmonary resuscitation (CPR) (an "optimal" IO scenario) after 10 minutes of untreated ventricular fibrillation (VF) cardiac arrest would improve outcome in comparison with either IV epinephrine after 8 minutes of CPR (a "realistic" IV scenario) or placebo controls with no epinephrine.Thirty swine were randomized to IO epinephrine, IV epinephrine, or placebo. Important outcomes included return of spontaneous circulation (ROSC), 24-hour survival, and 24-hour survival with good neurological outcome (cerebral performance category 1).ROSC after 10 minutes of untreated VF was uncommon without administration of epinephrine (1 of 10), whereas ROSC was nearly universal with IO epinephrine or delayed IV epinephrine (10 of 10 and 9 of 10, respectively; P = 0.001 for either versus placebo). Twenty-four hour survival was substantially more likely after IO epinephrine than after delayed IV epinephrine (10 of 10 vs. 4 of 10, P = 0.001). None of the placebo group survived at 24 hours. Survival with good neurological outcome was more likely after IO epinephrine than after placebo (6 of 10 vs. 0 of 10, P = 0.011), and only 3 of 10 survived with good neurological outcome in the delayed IV epinephrine group (not significant versus either IO or placebo).In this swine model of prolonged VF cardiac arrest, epinephrine administration during CPR improved outcomes. In addition, early IO epinephrine improved outcomes in comparison with delayed IV epinephrine.

Background— Some clinical studies have suggested that chest compressions before defibrillation improve survival in cardiac arrest because of prolonged ventricular fibrillation (VF; ie, within the circulatory phase). Animal data have also supported this conclusion, and we have previously demonstrated that preshock chest compressions increase the VF median frequency and improve the likelihood of a return of spontaneous circulation in normal swine. We hypothesized that chest compressions before defibrillation in a swine model of acute myocardial ischemia would also increase VF median frequency and improve resuscitation outcome. Methods and Results— Twenty-six swine were subjected to balloon occlusion of the left anterior descending coronary artery for 2 hours. The balloon was removed and VF was induced and untreated for 8 minutes. Swine were then treated with up to 3 stacked defibrillation shocks (n=13, shock-first group) or 3 minutes of chest compressions before shock (n=13, preshock cardiopulmonary resuscitation group). In the preshock cardiopulmonary resuscitation group, median frequency was increased from 7.0�0.8 to 13.9�1.6 Hz after chest compressions ( P =0.002). Despite the improved median frequency in the preshock cardiopulmonary resuscitation group, 24-hour survival with favorable neurological status was significantly worse in the preshock cardiopulmonary resuscitation group (1/13) compared with the shock-first group (8/13, P =0.01). Conclusions— In a swine model of prolonged VF in acute myocardial ischemia, 24-hour survival with favorable neurological status was more likely when defibrillation was performed first without preceding chest compressions. Myocardial substrate is an important factor in determining the optimal resuscitation strategy.

OBJECTIVE In cardiac arrest resulting from ventricular fibrillation, the ventricular fibrillation waveform may be a clue to its duration and predict the likelihood of shock success. However, ventricular fibrillation occurs in different myocardial substrates such as ischemia, heart failure, and structurally normal hearts. We hypothesized that ventricular fibrillation is altered by myocardial infarction and varies from the acute to postmyocardial infarction periods. DESIGN An animal intervention study was conducted with comparison to a control group. SETTING This study took place in a university animal laboratory. SUBJECTS Study subjects included 37 swine. INTERVENTIONS Myocardial infarction was induced by occlusion of the midleft anterior descending artery. Ventricular fibrillation was induced in control swine, acute myocardial infarction swine, and in postmyocardial infarction swine after a 2-wk recovery period. MEASUREMENTS AND MAIN RESULTS Ventricular fibrillation was recorded in 11 swine with acute myocardial infarction, ten postmyocardial infarction, and 16 controls. Frequency (mean, median, dominant, and bandwidth) and amplitude-related content (slope, slope-amp [slope divided by amplitude], and amplitude-spectrum area) were analyzed. Frequencies at 5 mins of ventricular fibrillation were altered in both acute myocardial infarction (p < .001 for all frequency characteristics) and postmyocardial infarction swine (p = .015 for mean, .002 for median, .002 for dominant frequency, and

This study was designed to test the hypothesis that immediate post-shock chest compressions improve outcome from prolonged ventricular fibrillation (VF) compared with typical "hands off" period (i.e., delayed post-shock compressions) associated with AED use.After 7.5 min of untreated VF, 36 domestic swine (26+/-1 kg) were treated with 200 J biphasic shocks and randomly assigned to: (1) 1 min of immediate post-shock chest compressions or (2) simulated pre-hospital automated external defibrillator (AED) care with delays in post-shock chest compressions. Return of spontaneous circulation (ROSC) occurred in 7/18 immediate chest compressions animals within 2 min of the first shock versus 0/18 AED animals (P0.01). Ten of 18 immediate chest compressions animals attained ROSC compared with 3/18 AED animals (P0.05). Nine of 18 immediate chest compressions swine were alive at 24 and 48 h compared with 3/18 AED swine (P0.05). All 48-h survivors had good neurologic outcomes. Among the 21 animals that defibrillated with the first shock, ROSC was attained in 7/10 immediate chest compressions animals within 2 min of the first shock compared with 0/11 AED animals (P=0.001), and 48-h survival was attained in 8/10 versus 3/11, respectively (P0.05).Immediate post-shock chest compressions can substantially improve outcome from prolonged VF compared with simulated pre-hospital AED care.

Arrhythmogenic right ventricular cardiomyopathy/dysplasia (ARVC/D) is characterized by regional or global abnormalities of right ventricular (RV) structure and function and ventricular tachyarrhythmias including sudden death [1, 2]. It is an inheritable cardiomyopathy predominantly affecting the myocardium of the RV free wall. Progressive atrophy and loss of myocytes with subsequent fatty and/or fibrous tissue replacement and interspersed surviving myocyte fibers provide the morphological substrate for re-entrant arrhythmias and regional (segmental) or global (diffuse) abnormalities of RV structure and function. In the advanced stages of ARVC/D, clinical signs of right or global heart failure and left ventricular (LV) involvement may develop [3].

s d a e b t t l f An 18-year-old male is seen in the emergency department fter awakening with palpitations and chest pressure. He has ad episodes of supraventricular tachycardia in the past, and he as learned to terminate these with a Valsalva maneuver. This ime, however, his attempts to end the palpitations have been nsuccessful. The patient has no history of syncope. At resent, he takes the anti-arrhythmic drug sotalol (80 mg BID), nd he also uses albuterol for asthma. An ECG was obtained mmediately (Figure 1). What is the rhythm, and how would ou proceed?

Congestive heart failure (HF) is characterized by inadequate nitric oxide (NO) production in the vasculature. Because NO is degraded by oxygen radicals, we hypothesized that NO is degraded faster in HF from inadequate peripheral arterial antioxidant reserves. HF was induced in male Sprague-Dawley rats by left coronary artery ligation. Vascular endothelial function was evaluated by measuring the NO-mediated vasorelaxation response to acetylcholine (ACh; 10−9–10−4M) in excised aortas. This was repeated with the free radical generator pyrogallol (20 μM) and again with pyrogallol and superoxide dismutase (SOD; 60 U/ml). Aortic and myocardial SOD activity was also determined. ACh-induced vasorelaxation was reduced in HF ( n = 9) compared with normal control rats ( n = 11; P < 0.001). Pyrogallol further reduced vasorelaxation in HF: 74 ± 11% at 10−4M ACh versus 58 ± 10% in normal control rats ( P < 0.004). There was a trend ( P = 0.06) toward reduced SOD activity in HF aortas. In conclusion, altered NO-dependent vasorelaxation in HF is in part due to excessive degradation of NO and is likely related to reduced vascular SOD activity.

Pulmonary embolism (PE) remains difficult to diagnose. Ventilation perfusion lung scan, the standard diagnostic test for PE, has poor overall sensitivity. The gold standard examination, pulmonary angiography, is invasive and has some risk, making clinicians reluctant to refer patients. In recent years, new diagnostic modalities have been investigated, including D-Dimer assays, spiral computed tomography (CT), and magnetic resonance imaging (MRI). The authors reviewed the literature and noted that the D-Dimer assays by ELISA or rapid ELISA design are approximately 90% to 95% sensitive, but are not specific for the diagnosis of pulmonary embolism. Spiral CT has been studied with conflicting results; however, in the largest studies the reported sensitivities are greater than approximately 85%. Electron beam CT is an alternative technique, which has not been as extensively studied. MRI is also useful for imaging the pulmonary arterial vasculature, but remains experimental. Although a more accurate assessment of the sensitivity of these new modalities will need to wait until a large angiographically controlled study, such as the planned PIOPED II, can be done, D-Dimer assay and spiral CT are often useful in the detection of pulmonary embolism. The authors make recommendations for their use in a diagnostic algorithm, as alternatives to the standard ventilation perfusion lung scan.

We describe a case of multiple hepatic pyogenic abscesses with an unusual presentation. The typical signs and symptoms of fever and pain in the right upper quadrant were absent. Instead, the chief complaint was muscle weakness and myalgias accompanied by weight loss. Findings from an ultrasonogram of the abdomen revealed multiple hepatic lesions consistent with metastases. Hence, the initial presumptive diagnosis was metastatic malignancy with unknown primary tumor. It was only when purulent material was unexpectedly encountered when a needle biopsy was performed that the true diagnosis of pyogenic liver abscess was recognized. While liver abscess is rare, it should not be forgotten in the differential diagnosis for multiple hepatic lesions seen on imaging studies.

55-year-old woman presented to the emergency departent with a chief complaint of chest pain. Her discomfort ad started earlier in the morning and soon became more ntense and unrelenting. She had a history of hypertension, ight hemispheric stroke, and hyperlipidemia. An initial electrocardiogram (ECG) showed the classic igns of an acute anterior wall myocardial infarction (Figure ). There is ST segment elevation throughout the precordial eads, reaching a maximum height of about 9 mm in lead 4. The T waves are upright in leads V1 through V4. Q aves in the inferior limb leads (II, III, AVF) suggest an old nferior wall infarction. Left ventricular hypertrophy is resent with increased voltage in AVL (17mm). ST-segent depression with asymmetrically inverted T waves in eads I and AVL imply a strain pattern due to hypertrophy, ut this had already been documented on a prior baseline CG. Left atrial enlargement is also indicated by a broad P ave with a wide negative deflection in V1. The patient was promptly brought to the cardiac catheerization laboratory where a total acute occlusion of the left nterior descending artery was discovered and then opened y balloon angioplasty. Of note, the right coronary artery ad the appearance of a chronic total occlusion filling from ell-developed collateral circulation from the left coronary rtery. The peak troponin level was 47.6 ng/mL. The next orning, the ECG in Figure 2 was obtained. What is hapening here?

The tracing offered no evidence of atrial fibrillation. ather, it documented a regular, narrow complex rhythm ith no discernable P waves at a rate of 31 bpm (Figure 1). his is a junctional escape rhythm due to sinus arrest. Note hat the baseline from the end of the T wave to the begining of the next QRS complex is remarkably flat; the conpicuous absence of P waves indicates that the atria are lectrically silent. In contrast, patients with complete—or hird degree—heart block have atrial activity that cannot be onducted to the ventricles. As a result, an escape rhythm rises below the level of block. For example, when the mpasse is beneath the AV junction, a ventricular focus then aces the heart. In our patient’s case, an escape rhythm ccurred because there was no atrial activity in the first lace. Shortly after the ECG, the patient’s heart rate increased

A patient who had undergone heterotopic heart transplantation and placement of an implantable cardioverter defibrillator in his native heart underwent generator change. Defibrillation testing induced ventricular fibrillation in his donor heart. To prevent this potentially lethal complication, defibrillator shock therapy must be synchronized to the donor heart R wave.