Verapamil, a calcium antagonist, has been used extensively for treatment of cardiac arrhythmias. Concern persists, however, that it may seriously depress myocardial function in cardiac patients. To investigate this possibility, 20 patients with coronary artery disease (CAD) but no heart failure were given intravenous verapamil (0.1 mg/kg bolus, followed by 0.005 mg/kg/min infusion), and studied hemodynamically and angiographically. Verapamil markedly lowered mean aortic pressure (94 +/- 17 to 82 +/- 13 mm Hg, p less than 0.0005) and systemic vascular resistance (1413 +/- 429 to 1069 +/- 235 dyn-sec-cm5, p less than 0.0005). Simultaneously, all indices of left ventricular (LV) performance greatly improved: cardiac index rose from 2.8 +/- 0.6 to 3.1 +/- 0.7 1/min/m2 (p less than 0.0005), mean velocity of circumferential fiber shortening increased from 0.85 +/- 0.39 to 0.97 +/- 0.46 circ/sec (p less than 0.01), and ejection fraction improved from 55 +/- 16 to 61 +/- 18% (p less than 0.01). No significant changes were noted in the heart rate before and after verapamil administration, and verapamil did not worsen the extent of LV asynergy in the majority of patients. In patients with CAD, the intrinsic negative inotropic effect of verapamil is of negligible importance because its potent vasodilatory properties more than compensate for any intrinsic decrease in LV contractility, and thereby improve the overall cardiac function.
Eighteen patients with hypertension participated in a double-blind, randomized study to evaluate the effect of trimazosin, methyldopa, and placebo on supine and standing blood pressure and heart rate. Of 6 patients on methyldopa, one developed drug fever (and was dropped from the study) and one developed impotence. None of 6 patients on trimazosin and none of 6 patients on placebo developed any adverse effects. The mean supine blood pressure on 900 mg trimazosin daily was 17.0/12.8 mm Hg lower than that on the first placebo trial (p less than 0.01) and 17.0/12.1 mm Hg lower than that on the second placebo trial (p less than 0.01). The mean supine blood pressure on 2,250 mg methyldopa daily was 17.8/12.4 mm Hg lower than that on the first placebo trial (p less than 0.01) and 16.8/13.0 mm Hg lower than that on the second placebo trial (p less than 0.01). The mean supine blood pressure was not significantly affected by placebo. Trimazosin, 900 mg daily, and methyldopa, 2,250 mg daily, were equally effective in lowering supine and standing systolic and diastolic blood pressure and did not affect supine or standing heart rate.
Oxprenolol is an experimental beta adrenergic blocker with intrinsic sympathomimetic activity. To compare the effects of long‐term administration of oxprenolol on hypertension and hemodynamics with the effects of propranolol, 20 patients with essential hypertension were divided in a double‐blind random manner into two 10‐patient groups and given placebo for 2 wk, followed by equipotent doses of oxprenolol or propranolol for 5 wk and by placebo for another 2 wk. Right heart cardiac catheterization was performed at the beginning and at the end of the 5‐wk beta blockade. Heart rates and blood pressures fell markedly with both agents, although standing heart rate was lowered more by propranolol than by oxprenolol. Plasma renin activity was much lower after beta blockade with either drug. There was no correlation between decreases in blood pressure and renin activity. Although during the stress of repeat cardiac catheterization heart rates remained significantly lower than control, the intra‐arterial pressures were not altered significantly by oxprenolol or propranolol, nor was there significant change in pulmonary pressure, vascular resistance, or cardiac output. Thus oxprenolol closely parallels the effects of propranolol in essential hypertension. The negative chronotropic action of both drugs is more marked than their antihypertensive activity. Clinical Pharmacology and Therapeutics (1980) 27, 733–743; doi:
SUMMARY Recent studies indicate that right ventricular performance is impaired even in uncomplicated systemic hypertension. Because ofwidespread use ofbeta-blockade in essential hypertension, it is possible that such treatment often further depresses right ventricular contractility. To test this premise, and to evaluate the changes induced by different beta-adrenoceptor blocking agents on the contractility of right ventricular myocardium, 20 patients with essential hypertension were divided into two groups on a double-blind randomised basis, and maintained on oral oxprenolol or propranolol for five weeks. Cardiac catheterisation and right ventricular cineangiography were performed at the beginning and again at the end of the five week period. Right ventricular end-diastolic volume index did not change significantly in either group. In contrast, right ventricular end-systolic volume index increased, and right ventricular ejection fraction significantly decreased after chronic beta-blockade. Cardiac index decreased in both groups, but these changes were not statistically significant.When the intergroup differences were compared for all measured indices none of the changes between the two groups was statistically significant. Despite its intrinsic sympathomimetic activity, oxprenolol therefore impairs right ventricular performance to an extent nearly equal to that of propranolol. Moreover, right ventricular contractility is clearly diminished after the institution of beta-blockade in hypertensive patients-an effect that has until now been thought to be limited to the left side of the heart. Great caution must therefore be exercised when beta-blockade is initiated in patients with severely abnormal right ventricular function, because frank right ventricular decompensation may result.Recent studies in our laboratory have shown a commonly accepted concept-that right ventricular function is normal in uncomplicated systemic hypertension-to be incorrect. Right ventricular performance diminishes even with early abnormal increases in arterial pressure.' Because systemic hypertension is frequently treated with beta-blockade, it was essential to determine how such treatment affects the integrity of the right heart which is already compromised by the hypertension itself.The effects of beta-blockade on left ventnrcular performance have been extensively investigated.2-6 There is a virtually unanimous agreement that one ofthe most commonly used beta antagonists, propranolol, depresses left ventricular contractility.7-9 More controversy, however, surrounds some of the newer experimental beta-adrenergic blocking agents, especially those that Received for publication 5 September 1980 possess intrinsic sympathomimetic activity. Moreover, the effects on right ventricular performance generated by beta-blockers with or without intrinsic sympathomimetic activity are still completely unknown.Oxprenolol, which is still not approved for general clinical use in the United States, possesses intrinsic sympathominx tic activity. I0-13 When the...
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