Hauser R.G.,Minneapolis Heart Institute Foundation
Europace : European pacing, arrhythmias, and cardiac electrophysiology : journal of the working groups on cardiac pacing, arrhythmias, and cardiac cellular electrophysiology of the European Society of Cardiology | Year: 2013
The purpose of this study was to determine if Optim™, a unique copolymer of silicone and polyurethane, protects Riata ST Optim and Durata implantable cardioverter-defibrillator (ICD) leads (SJM, St Jude Medical Inc., Sylmar, CA, USA) from abrasions that cause lead failure. We searched the US Food and Drug Administration's (FDA's) Manufacturers and User Device Experience (MAUDE) database on 13 April 2012 using the simple search terms 'Riata ST Optim™ abrasion analysis' and 'Durata abrasion analysis'. Lead implant time was estimated by subtracting 3 months from the reported lead age. The MAUDE search returned 15 reports for Riata ST Optim™ and 37 reports for Durata leads, which were submitted by SJM based on its analyses of returned leads for clinical events that occurred between December 2007 and January 2012. Riata ST Optim™ leads had been implanted 29.1 ± 11.7 months. Eight of 15 leads had can abrasions and three abrasions were caused by friction with another device, most likely another lead. Four of these abrasions resulted in high-voltage failures and one death. One failure was caused by an internal insulation defect. Durata leads had been implanted 22.2 ± 10.6 months. Twelve Durata leads had can abrasions, and six leads had abrasions caused by friction with another device. Of these 18 can and other device abrasions, 13 (72%) had electrical abnormalities. Low impedances identified three internal insulation abrasions. Riata ST Optim™ and Durata ICD leads have failed due to insulation abrasions. Optim™ did not prevent these abrasions, which developed ≤ 4 years after implant. Studies are needed to determine the incidence of these failures and their clinical implications.
Sharkey S.W.,Minneapolis Heart Institute Foundation
Heart Failure Clinics | Year: 2013
This article provides a comprehensive review of the clinical features of takotsubo (stress) cardiomyopathy. The author discusses key features that distinguish this cardiomyopathy from acute coronary syndrome. This review includes detail of characteristic findings on electrocardiogram, biochemical testing, and cardiac imaging, as well as complications including congestive heart failure, arrhythmia, ventricular thrombi, and left ventricular outflow obstruction. The review concludes with a discussion of the proper treatment, long-term survival, and proposed pathophysiology. © 2013 Elsevier Inc.
Maron B.J.,Minneapolis Heart Institute Foundation |
Maron M.S.,Hypertrophic Cardiomyopathy Center |
Semsarian C.,University of Sydney
Journal of the American College of Cardiology | Year: 2012
Hypertrophic cardiomyopathy (HCM) is the most common familial heart disease with vast genetic heterogeneity, demonstrated over the past 20 years. Mutations in 11 or more genes encoding proteins of the cardiac sarcomere (>1,400 variants) are responsible for (or associated with) HCM. Explosive progress achieved in understanding the rapidly evolving science underlying HCM genomics has resulted in fee-for-service testing, making genetic information widely available. The power of HCM mutational analysis, albeit a more limited role than initially envisioned, lies most prominently in screening family members at risk for developing disease and excluding unaffected relatives, which is information not achievable otherwise. Genetic testing also allows expansion of the broad HCM disease spectrum and diagnosis of HCM phenocopies with different natural history and treatment options, but is not a reliable strategy for predicting prognosis. Interfacing a heterogeneous disease such as HCM with the vast genetic variability of the human genome, and high frequency of novel mutations, has created unforeseen difficulties in translating complex science (and language) into the clinical arena. Indeed, proband diagnostic testing is often expressed on a probabilistic scale, which is frequently incompatible with clinical decision making. Major challenges rest with making reliable distinctions between pathogenic mutations and benign variants, and those judged to be of uncertain significance. Genotyping in HCM can be a powerful tool for family screening and diagnosis. However, wider adoption and future success of genetic testing in the practicing cardiovascular community depends on a standardized approach to mutation interpretation, and bridging the communication gap between basic scientists and clinicians. © 2012 American College of Cardiology Foundation.
Maron B.J.,Minneapolis Heart Institute Foundation
Heart rhythm : the official journal of the Heart Rhythm Society | Year: 2013
Commotio cordis events due to precordial blows triggering ventricular fibrillation are a cause of sudden death (SD) during sports and also daily activities. Despite the absence of structural cardiac abnormalities, these events have been considered predominantly fatal with low survival rates. To determine whether expected mortality rates for commotio cordis have changed over time, associated with greater public visibility. US Commotio Cordis Registry was accessed to tabulate frequency of reported SD or resuscitated cardiac arrest over 4 decades. At their commotio cordis event, 216 study patients were 0.2-51 years old (mean age 15±9 years); 95% were males. Death occurred in 156 individuals (72%), while the other 60 (28%) survived. Proportion of survivors increased steadily with concomitant decrease in fatal events. For the initial years (1970-1993), 6 of 59 cases survived (10%), while during 1994-2012, 54 of 157 (34%) survived (P = .001). The most recent 6 years, survival from commotio cordis was 31 of 53 (58%), with survivor and nonsurvivor curves ultimately crossing. Higher survival rates were associated with more prompt resuscitation (40%<3 minutes vs 5%>3 minutes; P<.001) and participation in competitive sports (39%; P<.001), but with lower rates in African Americans (1 of 24; 4%) than in whites (54 of 166; 33%; P = .004). Independent predictors of mortality were black race (P = .045) and participation in noncompetitive sports (P = .002), with an on-site automated external defibrillator use protective against SD (P = .01). Survival from commotio cordis has increased, likely owing to more rapid response times and access to defibrillation, as well as greater public awareness of this condition. Copyright © 2013 Heart Rhythm Society. Published by Elsevier Inc. All rights reserved.
Maron B.J.,Minneapolis Heart Institute Foundation |
Estes III N.A.M.,Tufts University
New England Journal of Medicine | Year: 2010
In the past decade, the general public and the medical community have become more aware of commotio cordis as an important cause of sudden death. Commotio cordis occurs in otherwise healthy and active young people, typically during recreational and competitive sports but in some cases even during normal daily activities. A variety of experimental models indicate that if delivered at a particular moment in the cardiac cycle, even innocent-appearing precordial blows can trigger ventricular fibrillation and result in fatal commotio cordis events. Further efforts are needed to prevent these largely avoidable deaths by providing more education, better-designed athletic equipment (e.g., effective chest-wall protectors), and wider access to AEDs at organized athletic events. These strategies should result in a safer sports environment for our youth. Copyright © 2010 Massachusetts Medical Society. All rights reserved.