Cardiovascular clinics最新文献

Only antiarrhythmic agents with class I activity prolong QRS duration The most marked QRS prolongation is produced by the IC agents, followed by IA and IB. This is consistent with the kinetics of interaction of each of these three subclasses with the sodium channel. Amiodarone's effect on QRS duration is between that of the IB and IA agents consistent with its tau rec of 1.5 seconds. Moricizine's effects on QRS duration are more marked than would be expected from its tau rec of 2.6 seconds but may be explained by the slow onset of inactivation block. The greatest efficacy in VPC suppression is exhibited by the class IC agents and amiodarone. Although amiodarone and sotalol are included in class III, amiodarone has marked class IB activity and sotalol is a more potent beta-adrenergic blocker. The disparate effects of these two drugs in suppressing VPCs may be explained by the class I action of amiodarone. It is surprising that drugs within each subclass correlate at all in VPC suppression in view of the marked heterogeneity of mechanisms potentially producing VPCs. Antiarrhythmic agents with class III activity seem to be the most effective in patients with inducible sustained ventricular tachyarrhythmias. Except for the class I agents with class III activity, that is, IA agents, all class I agents are effective in only 10% to 15% of patients with inducible ventricular tachycardia. The discordance between sotalol and amiodarone is unexplained. As expected, the most marked prolongation of ventricular tachycardia cycle length occurs with the class IC agents, followed by class IA and IB. At the rapid rates of the ventricular tachycardia, frequency-dependent sodium channel block occurs even with the "fast IB" drugs, and ventricular tachycardia cycle length is prolonged.

Coronary occlusion leading to nearly total absence of myocardial perfusion is the major cause of lethal ischemic arrhythmia in humans. In this setting, intracellular acidosis rapidly develops and leads to accelerated K+ efflux from the myocyte. Other metabolites, including lipid amphiphiles such as LPC, also rapidly accumulate in the ischemic zone. Elevated extracellular K+ and LPC cause membrane depolarization, which leads to slow conduction and increased refractoriness. These electrophysiologic changes contribute to the development of re-entrant rhythms, which predominate during early ischemia (phase 1a). Diffusion of extracellular K+ from the ischemic zone and release of endogenous catecholamines result in improvement in electrophysiologic parameters and are associated with a short arrhythmia-free interval, which occurs approximately 10 minutes after coronary occlusion. A second phase of arrhythmia (1b) then occurs and may be due in part to catecholamine-mediated triggered activity. Irreversible cell injury occurs 15 to 20 minutes after coronary occlusion and is associated with cell Ca++ overload, loss of gap junctions, and impaired cell coupling. This may lead to re-entrant arrhythmias. Reperfusion of ischemic myocardium leads to arrhythmia predominantly mediated by non re-entrant mechanisms. In humans, these reperfusion arrhythmias are usually relatively benign.

The normal aging process is associated with a variety of cardiovascular changes. Recognition of these alterations in cardiovascular structure and function that occur in the aging population is essential for assessment of cardiac disease in older patients. For example, a number of studies show that aging is associated with increasing left ventricular wall thickness and mass. However, these changes are gradual and relatively mild, and absolute wall thickness measurements in individual elderly subjects rarely exceed generally accepted normal values. Parameters of left ventricular systolic function (either under basal conditions or with exercise) change little with aging. In contrast, apparent alterations in left ventricular diastolic filling patterns often accompany advancing age. Investigations in normal elderly subjects have shown that the early filling phase is prolonged, and the rate and volume (as well as flow-velocity) of rapid filling are decreased. These alterations are associated with a compensatory increase in late diastolic filling with atrial systole. The aging changes in left ventricular filling identified by noninvasive tests (such as Doppler echocardiography or radionuclide angiography) may mimic in appearance those observed in a number of cardiovascular diseases, making interpretation of their clinical significance difficult in an elderly population.

Care of the elderly patient with CHD requires an understanding of the prevalence of disease and its variability of presentation. Sound application of the diagnostic and therapeutic maneuvers developed for younger patients remains the predominant basis for the clinical approach to older individuals with heart disease. As more research is directed toward age-related issues in cardiac disease, the approach may be refined with more specific guidelines than are currently available.