Mohsen Ibrahim

Hemodynamic Characteristics of Primary Aldosteronism

Abstract As compared with 30 matched patients with essential hypertension, 16 with primary aldosteronism had a higher heart rate (p<0.02), cardiac index (p<0.01) and mean rate of left ventricular ejection (p<0.025). A clinically evident hyperkinetic circulatory state was more frequent in primary aldosteronism (six of 16) than in essential hypertension (four of 30). Cardiac index correlated inversely with diastolic pressure in primary aldosteronism (r = -0.661, p<0.01). Better surgical results were obtained in patients who had the higher cardiac output before operation. Plasma volume was 103 per cent of normal ± 2.7 (S.E.) in primary aldosteronism, 111 per cent ± 2.6 in 10 patients with hypervolemic hypertension, and 86 per cent ± 2.1 in 20 with hypovolemic hypertension. In both the hypovolemic group and primary aldosteronism, plasma volume correlated inversely with peripheral resistance (r = -0.531, p<0.05 and r = -0.610, p<0.02, respectively), so that for any level of resistance, plasma volume was higher...

Idiopathic orthostatic hypotension: Circulatory dynamics in chronic autonomic insufficiency

Idiopathic orthostatic hypotension offers a unique opportunity to study the effect of chronic autonomic insufficiency on circulatory dynamics in man. Evidence of abnormal cardiac performance was found in eight patients with idiopathic orthostatic hypotension secondary to efferent adrenergic dysfunction. Compared with normal subjects these patients had a lower cardiac output (2.37 liters/min per m2, P < 0.001), faster heart rate (83 beats/min, P < 0.001), smaller stroke volume (30 ml/ m2, P < 0.001) and slower rate of left ventricular ejection (107 ml/sec per m2, P < 0.001). Intravascular volume was also reduced (90 percent of normal), (P < 0.01), but this reduction could not by itself account for the marked decrease in cardiac output (75 percent of normal) since there was no correlation between the two variables (r − 0.269, not significant). The ratio of stroke volume to cardiopulmonary volume was reduced (P < 0.025), thus suggesting that impaired myocardial contractility might be partly responsible for the defective cardiac performance. Although failure of peripheral resistance is the basic mechanism in idiopathic orthostatic hypotension, our results indicate that impaired cardiac function possibly related to cardiac denervation may also contribute to the poor circulatory adjustments in this disease.

Hyperkinetic heart in severe hypertension: A separate clinical hemodynamic entity☆

A long-term study of established hypertension helped identify a well defined group of 10 patients who differed both clinically and hemodynamically from 59 patients with the more frequent form of this disease. Their cardiac output was significantly increased (P less than 0.001) despite a severe elevation of arterial pressure (average 212/125 mm Hg plus or minus 13.5/7.3[standard error[). All had labile hypertension of long standing (16.2 years average) that was difficult to control and always symptomatic; in all, the diagnosis of pheochromocytoma had to be specifically excluded. Increased myocardial contractility was suggested by (1) significant elevation of the rate of rise of isovolumic pressure (P less than 0.001), and (2) high ratio of cardiac output to cardiopulmonary volume (P less than 0.005). Beta adrenergic blockade with propranolol helped to alleviate symptoms and to control tachycardia but failed by itself to reduce arterial pressure.

Cardioadrenergic factor in essential hypertension

Determination of STI in 54 untreated essential hypertensive subjects and 17 normal subjects revealed marked differences among three groups of patients. Those with borderline hypertension (29) had a short PEP and IVC periods (93 ± 2.1 and 28 ± 0.7 msec., respectively, p < 0.001) (mean ± S.E.) reduced PEPLVET (0.323 ± 0.009, p < 0.05) and increased DPIVC (3,484 ± 257 mm. Hg per second, p < 0.001). Among those with established hypertension, two groups of equal age and diastolic pressure were identified: nine with marked variations in blood pressure and a hyperkinetic heart clinically and 16 with fixed hypertension; none had cardiac or renal decompensation. Those with a hyperkinetic circulation had normal PEP, IVC, and PEPLVET despite a high diastolic pressure (122 ± 7.1 mm. Hg); DPIVC was elevated (3,651 ± 497 mm. Hg per second, p < 0.001) as in those with borderline hypertension. In contrast, the patients with fixed hypertension had longer PEP and IVC (p < 0.001), higher PEPLVET (p < 0.001), and normal DPIVC. Propranolol (10 mg. intravenously) slowed heart rate and prolonged PEP and IVC more in patients with a hyperkinetic circulation and in those with borderline hypertension than in those with fixed hypertension. These results suggest the presence of an increased cardioadrenergic drive not only in borderline hypertension, but also in a subgroup of patients with established hypertension. Left ventricular hypertrophy (ECG) was found in 1 out of 9 patients with hyperkinetic heart but in 6 out of 16 with fixed hypertension; cardiac index was high normal in the first group but reduced in the latter (3.32 vs 2.38 L./min./M.2, p < 0.001). This factor as determined by the systolic time interval might, therefore, be important in determining cardiac prognosis or planning therapy.