| Literature DB >> 2076377 |
Abstract
The presence of ventricular arrhythmias mark an individual with underlying structural heart disease as a candidate at high risk for sudden cardiac death. It is still unknown whether suppression of those ventricular arrhythmias by all drugs will in fact prevent sudden cardiac death. Therefore, the efficacy of an antiarrhythmic drug at present must be defined as only its pharmacologic activity that relates to its ability to reduce the frequency of ventricular arrhythmias rather than to a potential beneficial effect on patient outcome. Ventricular arrhythmias can be differentiated using a prognostic classification into those that are benign, potentially lethal, or lethal. Benign and potentially lethal ventricular arrhythmias undergo a high degree of spontaneous variability, and therefore the degree of frequency suppression needed to differentiate drug suppression from spontaneous variability must be carefully considered. It therefore is important to establish the mean ventricular premature complex frequency per hour over at least 24 hours at baseline using quantitative continuous ambulatory electrocardiographic (Holter) monitoring. To eliminate spontaneous variability, a repeat Holter monitoring session after the initiated therapy has reached steady state should show at least a 75% reduction in the mean VPC/hr frequency and at least a 90% suppression in the number of beats in the form of nonsustained ventricular tachycardia (NSVT). Exercise testing is a complementary technique and is best suited for patients with NSVT developing during exercise testing from either a "catecholamine" or an "ischemic" mechanism.(ABSTRACT TRUNCATED AT 250 WORDS)Entities:
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Year: 1990 PMID: 2076377 DOI: 10.1007/BF01856553
Source DB: PubMed Journal: Cardiovasc Drugs Ther ISSN: 0920-3206 Impact factor: 3.727