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Israel C.W.,Div. of Cardiology
Indian Heart Journal | Year: 2014

Worldwide, sudden cardiac death (SCD) is a major problem. It is most frequently caused by ventricular tachyarrhythmias: Monomorphic and polymorphic ventricular tachycardia (VT), torsade de pointes (TdP), and ventricular fibrillation (VF). Beta blockade, ACE inhibition, coronary reperfusion and other treatments have reduced the incidence of VT but pulseless electrical activity (PEA) is increasingly seen, particularly in patients with advanced chronic heart disease. From existing data, bradyarrhythmia in the form of asystole (usually complete heart block without escape rhythm) causes only a minor proportion (10-15%) of SCD. In patients aged 50 years and more, coronary artery disease plays a dominant role causing more than 75% of SCD cases, either by acute ischemia and ventricular fibrillation or by chronic scar formation and reentrant VT. In younger patients, SCD may occur in patients with structurally normal hearts. A number of arrhythmogenic disorders with an increased risk of SCD have been detected and better understood recently, such as long and short QT syndrome, Brugada syndrome, catecholaminergic polymorphic ventricular tachycardia, and the early repolarization syndrome. Most importantly, ECG signs and clinical features indicating high risk for SCD have been identified. Knowledge of the exact electrophysiologic mechanisms of ventricular tachyarrhythmias at the cellular level has been improved and mechanisms such as phase 2 reentry and reflection proposed to better understand why and how SCD occurs. © 2014, Cardiological Society of India. All rights reserved. Source

Myers J.,Div. of Cardiology | Dupain M.,Div. of Cardiology | Vu A.,Div. of Cardiology | Jaffe A.,Div. of Cardiology | And 3 more authors.
Journal of Aging and Physical Activity | Year: 2014

As part of a home-based rehabilitation program, 24 older adult patients (71 × 3 years) with abdominal aortic aneurysm (AAA) disease underwent 3 days (12 awake hr/day) of activity monitoring using an accelerometer (ACC), a pedometer, and a heart rate (HR) monitor, and recorded hourly activity logs. Subjects then underwent an interview to complete a 3-day activity recall questionnaire (3-DR). Mean energy expenditure (EE) in kcals/day for HR, ACC, and 3-DR were 1,687 × 458, 2,068 × 529, and 1,974 × 491, respectively. Differences in EE were not significant between 3-DR and ACC, but HR differed from both ACC (p .001) and 3-DR (p .01). ACC and 3-DR had the highest agreement, with a coefficient of variation of 7.9% and r = .86. Thus, ACC provided a reasonably accurate reflection of EE based the criterion measure, an activity recall questionnaire. ACC can be effectively used to monitor EE to achieve an appropriate training stimulus during home-based cardiac rehabilitation © 2014 Human Kinetics, Inc. Source

Yu T.,Div. of Cardiology | Zhu W.,Div. of Cardiology | Gu B.,Div. of Cardiology | Li S.,Div. of Cardiology | And 4 more authors.
Journal of Applied Physiology | Year: 2012

Statin, as a 3-hydroxy-3-methyl-glutaryl-CoA reductase inhibitor, has been shown to prevent atrial fibrillation (AF) due to its anti-inflammatory and antioxidant effects. However, it is still not known whether statin can improve autonomic remodeling to prevent AF. In the present study, using an in vivo rat myocardial infarction (MI) model, we aimed to test whether simvastatin can attenuate nerve sprouting and sympathetic hyperinnervation to prevent AF during the post-MI remodeling process. Our data demonstrate that simvastatin, delivered 3 days after MI for 4 wk, can result in significant decreases in plasma levels of both TNF-α (239 ± 23 pg/ml) and IL-1β (123 ± 11 pg/ml) compared with MI rats without therapy (TNF-α, 728 ± 57 pg/ml; IL-1β, 213 ± 21 pg/ml; P < 0.05), which, however, were still higher than sham-operated rats (TNF-α, 194 ± 20 pg/ml; IL-1β, 75 ± 8 pg/ml; P < 0.05). The similar pattern of changes in inflammation responses was also observed in TNF-α and IL-1β protein expression in the left atrium free wall. The suppressed inflammation responses were associated with reduced superoxide and malondialdehyde generation in the atrium. These changes account for decreases in neural growth factor expression at levels of both mRNA (1.2 ± 0.09 AU vs. MI group, 1.78 ± 0.16 AU) and protein (1.57 ± 0.17 AU vs. MI group, 2.24±0.19 AU; P<0.05), thus resulting in reduced nerve sprouting and sympathetic hyperinnervation. Accordingly, the rate adaptation of the atrial effective refractory period also recovered, leading to the decreased inducibility of AF. These data suggest that simvastatin administration after MI can prevent AF through reduced sympathetic hyperinnervation. Copyright © 2012 the American Physiological Society. Source

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