Although not included in the World Health Organization (WHO)/Inter-national Society and Federation of Cardiology (ISFC) classification, a chronically elevated heart rate due to high-frequen-cy arrhythmia can result in a cardiomyopathy with ventricular dilatation and dysfunction that resolves partially or even totally in response to heart rate control, whether pharmacological or nonpharmaco-logical.
In animal models, experimental tachycardia induces cardiomyopathy with systolic and diastolic myocardial dysfunction, decreased response to catecholamine infusion, and decreased myocardial contractility. Numerous functional and neurohumoral features have been described (Table I). Adrenergic stimulation and the extracellular CaJ+ response are decreased. There are also changes in cell architecture which probably result from decreased sarcolemmal Na+/IC ATPase activity, and changes in enzyme distribution that interfere with Exchange across the sarcolemma. A decrease in myocardial perfusion reserve, unassociated with significant morphological changes during or after tachycardia, has also been observed. The whole pattern is reversible after tachycardia control.
A similar pattern has been observed in humans. A diagnosis of cardiomyopathy due to high-frequency arrhythmia can only be retrospective. It should be suspected in the presence of dilated-hypokinetic cardiomyopathy and frequent or chronic atrial tachyarrhythmia. In addition, atrial flutter and fibrillation, prolonged nodal and junctional automatic tachycardia, accessory pathway tachycardia, and ventricular tachycardia can all precipitate decompensation in stable heart failure.
Tachycardia may be causal the only possible explanation of cardiac dysfunction or contributory, in which case it coexists with concomitant factors. Chronic tachy-
pathophysiology; ventricular rate; cardiomyopathy; neurohumoral activation; arrhythmia
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