Citations

Mitral Valve Injury with Catheter AblationIntroductionAn increasing number of catheter ablations involve the mitral annular region and valve apparatus, increasing the risk of catheter interaction with the mitral valve (MV) complex. We review our experience with catheter ablation‐related MV injury resulting in severe mitral regurgitation (MR) to delineate mechanisms of injury and outcomes.MethodsWe searched the Mayo Clinic MV surgical database over a 19‐year period (1993–2012) and the electrophysiologic procedures database over a 23‐year period (1990–2013) and identified 9 patients with catheter ablation related MV injury requiring clinical intervention.ResultsIndications for ablation included atrial fibrillation (AF) [n = 4], ventricular tachycardia (VT) [n = 3], and left‐sided accessory pathways [n = 2]. In all 4 AF patients, a circular mapping catheter entrapped in the MV apparatus was responsible for severe MR. In all 3 VT patients, radiofrequency energy delivery led to direct injury to the MV apparatus. In the 2 patients with accessory pathways, both mechanisms were involved (1 per patient). Six patients required surgical intervention (5 MV repair, 1 catheter removal). One patient developed severe functional MR upon successful endovascular catheter disentanglement that improved spontaneously. Two VT patients with persistent severe postablation MR were managed nonsurgically, 1 of whom died 3 months postprocedure.ConclusionCircular mapping catheter entrapment and ablation at the mitral annulus are the most common etiologies of MV injury during catheter ablation. Close surveillance of the MV is needed during such procedures and early surgical repair is important for successful salvage if significant injury occurs.

The traditional route for teaching cardiac anatomy involves didactic instruction, cadaver dissections, and familiarization with the main structure and relationships of the cardiac chambers, valves, and vasculature. In contemporary cardiac electrophysiology, however, a very different view of anatomy is required including details rarely appreciated with a general overview. In this review, we discuss the critical advances in cardiac electrophysiology that were possible only because of understanding detailed anatomic relationships. While we briefly discuss the clinical relevance, we explain in depth the necessary structural information for the student of clinical anatomy. Interspersed through the text are boxes that highlight and summarize the critical pieces of knowledge to be borne in mind while studying the fascinating structural anatomy of the human heart. Clin. Anat. 27:885–893, 2014. © 2014 Wiley Periodicals, Inc.

ECG Lead I and Outflow Tract ArrhythmiaIntroductionOutflow tract ventricular arrhythmia (OTVA) can be complicated to target for ablation when originating from either the periaortic or pulmonary valve (PV) region. Both sites may present with a small R wave in lead V1. However, the utility of lead I in distinguishing these arrhythmia locations is unknown.Methods and ResultsThirty‐six consecutive patients (mean age 41 ± 14 years, 13 male) underwent catheter ablation for OTVA. OTVA origin was determined from intracardiac electrogram tracings and electroanatomic maps. Observers blinded to results measured QRS waveform amplitude and duration from standard 12‐lead ECG tracings. Measurements with highest diagnostic performance were modeled into an algorithm. Sites of successful ablation were anterior right ventricular outflow tract (RVOT; n = 6), posterior RVOT (n = 4), PV (n = 18), and right coronary cusp (RCC; n = 8). Highest performing surface ECG discriminators were from lead I to V1 vectors: RCC, lead I R wave ≥ 1.5 mV, and V1 R wave ≥2.0 mV (sensitivity 87%, specificity 93%); PV, V1 R wave > 0 mV, and lead I R/(R+S) ≤ 0.75 (sensitivity 78%, specificity 72%); anterior RVOT, V1 R wave = 0 mV, and lead I R/(R+S) <0.4 (sensitivity 67%, specificity 97%); posterior RVOT, V1 R wave > 0 mV, and lead I R/(R+S) > 0.75 (sensitivity 75%, specificity 84%). Sequential algorithmic application of these criteria resulted in an overall accuracy of 72% in predicting site of OTVA origin.ConclusionsA relatively large R wave in lead I is seen with RCC origin but not PV origin. A sequential algorithm has limited but potentially significant value beyond assessment of lead I in approaching OTVA.

Objective The prevalence, predictors and outcome of myopericarditis in patients with tuberculous (TB) pericarditis are unknown. Methods Eighty-one patients (mean age±SD, 36.1±13.3 years; 54 (66.7%) men; 58 (71.6%) HIV seropositive) with TB pericarditis were recruited between January 2006 and September 2008. Myopericarditis was defined as echocardiographic LV systolic dysfunction (immediately after pericardiocentesis), elevated peripheral blood troponin T (>0.03 ng/mL), or elevated peripheral blood creatine kinase (CK >174 IU/L) with a CK:CK-myocardial band (MB) mass ratio of >6%. The outcome measure was case fatality rate at 6 months of follow-up. Results Myopericarditis was present in 43 (53.1%) patients. Patients with myopericarditis, as compared with those without, were more likely to be HIV seropositive (35 (81.4%) vs 23 (60.5%) respectively, p=0.038) and have lower peripheral CD4 count (median (IQR) 98 (54–290) vs 177 (104–429), p=0.026). Electrocardiographic ST segment elevation was more common in myopericarditis (15 (36.6%) vs 4 (10.8%), p=0.008) and predicted myopericarditis independently of CD4 count on multiple logistic regression analysis (OR 4.36, 95% CI 1.34 to 17.34, p=0.0132). At 6 months, 14 (18%) patients had died with no significant difference between those with or without myopericarditis (6/42 (14%) vs 8/36 (22%), respectively (p=0.363)). Conclusions Myopericarditis is common in TB pericardial effusion and associated with HIV-related immunosuppression. It can be identified by electrocardiographic ST-elevation, particularly when peripheral CD4 count is low. There was no significant difference in case fatality rate in those with or without myopericarditis.

Coronary Artery Ventricular Tachycardia. Background The coronary cusps have been well described as a successful site for ablation in patients with symptomatic outflow tract ventricular tachycardia. The earliest site of activation is rarely found at the ostia or into the main coronary arteries. The exact anatomic substrate, diagnostic characteristics, and therapeutic approaches for such instances are poorly understood. Methods We retrospectively reviewed outflow tract ventricular arrhythmia (OTVA) ablations done at Mayo Clinic Rochester from 2003 to 2011 (total VT: 414; outflow tract VT: 106). Three cases were identified where the earliest site of activation was not within the cusp but rather at or within the coronary ostia (3/414 for all VT: 0.7%; 3/106 for all OTVT: 2.8%). Results In 1 patient, the left main coronary artery (LMCA) was found to have electrograms (EGMs) recorded with bipolar mapping that preceded activation in the cusps or the left ventricular outflow tract. In 2 cases, the right coronary ostium and proximal right coronary artery recorded the earliest signals. Intracardiac echocardiographic guidance was used to successfully ablate these arrhythmias targeting the aortic route (1 patient) or the right coronary cusp (2 patients), and essentially isolated the focus of origin from the ventricular outflow tracts. Detailed mapping of surrounding structures, including the atrial appendages, the contralateral outflow tract, and the coronary venous system excluded far‐field mapping in the artery as a cause for early activation at the ostial location. Local EGM characteristics suggested an unusually lengthy supravalvar myocardial extension as the likely arrhythmogenic substrate. Ablation was successful without coronary arterial or valvular injury and without valvular or root stenosis. Conclusions Endocardial ablation isolating foci of origin in the vicinity of the coronary ostia is a challenging procedure but can be performed safely with appropriate visualization and is effective in the treatment of OTVA.

The last decade has witnessed major advances in our understanding of the epidemiology and pathophysiology of HIV-related cardiovascular disease in sub-Saharan Africa. In this review, we summarise these and discuss clinically relevant advances in diagnosis and treatment. In the Heart of Soweto Study, 10% of patients with newly diagnosed cardiovascular disease were HIV positive, and the most common HIV-related presentations were cardiomyopathy (38%), pericardial disease (13%) and pulmonary arterial hypertension (8%). HIV-related cardiomyopathy is more common with increased immunosuppression and HIV viraemia. With adequate antiretroviral therapy, the prevalence is low. Contributing factors such as malnutrition and genetic predisposition are under investigation. In other settings, pericardial disease is the most common presentation of HIV-related cardiovascular disease (over 40%), and over 90% of pericardial effusions are due to Mycobacterium tuberculosis (TB) pericarditis. HIV-associated TB pericarditis is associated with a greater prevalence of myopericarditis, a lower rate of progression to constriction, and markedly increased mortality. The role of steroids is currently under investigation in the form of a randomised controlled trial. HIV-associated pulmonary hypertension is significantly more common in sub-Saharan Africa than in developed countries, possibly as a result of interactions between HIV and other infectious agents, with very limited treatment options. It has recently been recognised that patients with HIV are at increased risk of sudden death. Infection with HIV is independently associated with QT prolongation, which is more marked with hepatitis C co-infection and associated with a 4.5-fold higher than expected rate of sudden death. The contribution of coronary disease to the overall burden of HIV-associated cardiovascular disease is still low in sub-Saharan Africa.