Long-term follow-up of the primary hyperkinetic heart syndrome. An echocardiographic and hemodynamic study

Anxiety, cardiac overactivity and hypercontractility, favorable response to beta-blockade characterize the primary hyperkinetic heart syndrome. Its natural history is unknown; evolution toward obstructive cardiomyopathy has been postulated. We undertook this study to evaluate the following: (1) the existence of a mutual potential between anxiety and cardiac overactivity and its contribution to the perpetuation of the disorder; (2) the development of hypertrophic subaortic stenosis and whether it represents a complication of the syndrome; and (3) the very prolonged normalization of the circulatory regimen by beta-blockade and whether it promotes an irreversible circulatory adjustment. Fourteen hyperkinetic patients were investigated by intravascular and ultrasound methods at their first admission and at yearly intervals in the subsequent five years. During this period seven of them were maintained untreated (group I) and seven received propranolol (group II). Interventricular septal and left ventricular posterior wall thickness (ultrasounds) and the ratio between the two were within normal limits in the control state and remained so for the duration of the follow-up, both in the treated (persistent circulatory normalization was documented) and in the untreated patients (cardiac hyperkinesis was unchanged or somewhat increased). Substitution of placebo for the active propranolol in group II, at the end of the follow-up, caused a prompt recurrence of the overactivity of the heart. It is concluded that (1) transition toward hypertrophic cardiomyopathy probably is not a feature of the syndrome; (2) propranolol does not produce an irreversible circulatory adjustment; (3) it is unlikely that a reciprocal potentiation between anxiety and cardiac overactivity perpetuate the disorder; if it did, then prolonged circulatory normalization could be expected to extinguish the syndrome.