The important study of Davis et al. (1), published in the June 12, 2012, issue of the Journal, delves into the genetic and hemodynamic underpinnings of pre-hypertension (PH), a precursor of established systemic hypertension with all the morbidity and mortality connotations that are entailed. The cross-sectional twin study of the authors identified a relationship of PH with hereditary influences, rise of norepinephrine secretion, decline in parasympathetic tone, elevation of cardiac contractility (maximal left ventricular dP/dT), increased stroke volume, heart rate, cardiac output and pulse pressure, and failure of the systemic vascular resistance to decline in the face of increased cardiac output, with resultant elevated blood pressure at levels compatible with the definition of PH.

Over 50 years ago, Gorlin et al. ((2),(3),(4),5) described the “hyperkinetic heart syndrome,” a new clinical entity characterized by an unexplained primary (as contrasted with all conceivable known secondary causes) rise in stroke volume, cardiac output, pulse pressure, and left ventricular ejection rate, mild systolic hypertension, positive cold pressor test, and increased oxygen consumption, in a group of young, mainly asymptomatic subjects. The authors attributed the “hyperkinetic heart syndrome” to a “defect in central (neurohumoral) regulation of cardiac output” (4).

One would surmise, on the basis of the aforementioned, that PH and “hyperkinetic heart syndrome” might have something in common, if they do not represent the same pathophysiological entity. Of note is that Gorlin et al. (5) remarked that “the high prevalence of all forms of hypertension, including systolic, labile, and sustained hypertension in these patients suggests a relationship between hypertension and hyperkinetic circulatory states,” with significant support from the published data. Also they found a “benign short-term and 20-year prognosis in the majority of patients with the idiopathic hyperkinetic heart syndrome” with occasions of regression, although they recommended beta-blockade particularly for patients with hypertension (5). Because Gorlin et al. found a high rate of “flow” murmurs on physical examination of their subjects and electrocardiogram left ventricular hypertrophy ((2),(3),(4),5), it might be useful to evaluate the University of California, San Diego twin/family database (1), with regard to the prevalence of these 2 items. Also in view of the follow-up study of the “hyperkinetic heart syndrome” of Gorlin et al. (5), it might be advisable to have a follow-up study of PH in due time to complement the cross-sectional investigation by Davis et al. (1).