Patterns of left ventricular adaptation in borderline and mild essential hypertension. Echocardiographic findings

To assess patterns of left ventricular adaptation, 38 patients with borderline and 38 with sustained mild essential hypertension, all lacking electrocardiographic and roentgenographic criteria for left ventricular hypertrophy, were compared using systemic hemodynamic values and M-mode echocardiograms. All patients had normal left ventricular function and measurements of wall thickness. Those with borderline hypertension showed no asymmetric increase in the ratio of septal to posterior wall thickness. The ratio of the left ventricular radius to wall thickness remained normal in both groups, indicating no disproportionate hypertrophy or dilatation of chambers during the phase of normal left ventricular function. Neither finding substantiates asymmetric septal hypertrophy in early hypertension. Those with mild essential hypertension demonstrated an augmented mean circumferential fiber shortening rate compared to those with borderline hypertension (P less than 0.005), suggesting an early stage of left ventricular hyperfunction in the development and elaboration of hypertensive heart disease.     

Antihypertensive therapy and cardiovascular reactivity during isometric stress

The cardiovascular reactivity to isometric stress test before and after antihypertensive therapy was evaluated by invasive haemodynamic techniques in 23 patients with mild to moderate essential hypertension. A beta-blocking agent (atenolol 50 to 100 mg daily) was given to 11 patients; 12 patients received calcium entry blockers (diltiazem 240 to 360 mg daily or verapamil 240 to 480 mg per day). The pressor response to isometric stress before therapy consisted of an increase in systolic, diastolic, and mean arterial pressure (all P less than 0.01) that was similar in both treatment groups. The rise in arterial pressure was mainly due to an increase in cardiac output (P less than 0.01), as total peripheral resistance did not change significantly. After treatment with the beta-blocker, the increase in total peripheral resistance during isometric stress was exaggerated (P less than 0.01), and, conversely, the increase in cardiac output was attenuated (P less than 0.01). In contrast, treatment with calcium entry blockers preserved the haemodynamic reactivity pattern of the untreated state: arterial pressure increased during isometric stress through an increase in cardiac output, while total peripheral resistance remained unchanged. Since the haemodynamic culprit of essential hypertension is an elevated peripheral resistance, a drug that numerically increases this culprit under conditions of resting and isometric stress becomes less attractive than one that lowers peripheral resistance and preserves the physiologic response pattern.