Low-dose cyclophosphamide enhances helper-to-non-helper ratios.

This study was conducted to analyze the effect of different doses of cyclophosphamide (CY) on the lymphocyte populations in the rat. Monoclonal antibodies against rat determinants were used: W3/13 (T lymphocytes), W3/25 (T helper), OX-8 (non-helper), and OX-33 (B lymphocytes). Blood samples were collected on days 0, 3, 7, and 14 from four groups of F-344 Fisher rats (n = 4): three that received 25, 50, or 75 mg/kg of CY and a control group. The duration and severity of lymphocyte depletion were dose-related and were evident for both helper and non-helper cells (p less than 0.02). The helper-to-non-helper ratio increased for the group that received 25 mg/kg when compared with control and other groups, but was only significantly changed when compared with the 75 mg/kg group (p = 0.004). This effect was transitory and was only seen on day 3. The control and the 25 mg/kg groups gained weight; the other two groups lost weight (p less than 0.05). Lower doses of CY were associated with a transitory immunostimulatory effect and no morbidity when compared with higher doses.

Pulmonary artery banding: analysis of a 25-year experience.

A 25-year experience (May 1962 through April 1987) with pulmonary artery banding in 183 patients was reviewed and analyzed. Pulmonary artery banding was performed in a heterogeneous group of patients aged two days to 60 months (median, 10 weeks; mean, 21.8 weeks) and weighing 1.4 to 13.8 kg (mean, 4.2 kg). Diagnosis was ventricular septal defect in 76 (41.5%) and atrioventricular communis in 41 (22.4%). Pulmonary artery banding was also used in patients with d-transposition of the great vessels with ventricular septal defect, double-outlet right ventricle, univentricular heart, tricuspid atresia, and truncus arteriosus. Early death occurred in 39 of 175 patients who underwent pulmonary artery banding at Ochsner Foundation Hospital (22.3%). Definitive operation has been performed in 37 of the patients who underwent pulmonary artery banding since 1979 with excellent outcome in 32 (86.5%). Pulmonary artery banding is a useful palliative procedure for a diverse group of patients with congenital cardiac anomalies and unrestricted pulmonary blood flow. With improved results of primary repair of intracardiac anomalies in small infants, however, pulmonary artery banding should be reserved for severely ill patients with complex lesions not amenable to early definitive correction. Currently, pulmonary artery banding is indicated in patients with excessive pulmonary blood flow and single ventricle or tricuspid atresia. Pulmonary artery banding is also appropriate in certain patients with atrioventricular communis and in patients with muscular or multiple ventricular septal defects. Pulmonary artery banding is an option in patients with ventricular septal defect and coarctation of the aorta.

Left ventricular aneurysm repair with myocardial revascularization: an analysis of 246 consecutive patients over 15 years.

From 1970 to 1985, 246 consecutive patients with left ventricular (LV) aneurysm underwent repair and concomitant myocardial revascularization at Ochsner Foundation Hospital. The overall incidence of perioperative death was 7.3%. Although the deaths were mainly cardiac related (10/18) with congestive heart failure (CHF) as the leading cause (6/10), 8 deaths were of noncardiac origin. Perioperative mortality increased significantly in patients with mitral regurgitation (MR) (22%; p = 0.0008); perioperative mortality for patients without MR was 4.8%. The overall 5-year survival was 69%. Late deaths were caused most commonly by myocardial infarction (20/32) with only 7 due to CHF. Predictors of long-term survival were related to LV function preoperatively: absence of CHF (p = 0.001); LV end-diastolic pressure less than or equal to 20 mm Hg (p = 0.03); and ejection fraction greater than or equal to 35% (p = 0.02). Factors that did not significantly affect long-term survival were type of aneurysm repair (resection or plication), morphology of left anterior descending coronary artery (occlusion or stenosis), and size of the aneurysm.

Disparate cardiovascular findings in men and women with essential hypertension.

We measured systemic hemodynamic, volume, and endocrine findings in 100 hypertensive women matched to 100 men by mean arterial pressure, age, race, and body surface area. Women had a higher resting heart rate, cardiac index, and pulse pressure and lower total peripheral resistance (all p less than 0.01) than men with the same pressure level. Isometric stress caused an increase in arterial pressure that was almost 50% higher in men than in women. The sexual difference in cardiovascular findings was significant before but not after menopause. For any level of arterial pressure, total peripheral resistance (and therefore the risk of hypertensive cardiovascular disease) was lower in women than in men. We conclude that premenopausal women are hemodynamically younger than men of the same chronologic age. Our study identifies a pathophysiologic mechanism for the clinical and epidemiologic finding that essential hypertension is less lethal in women than in men.

Clinical and hemodynamic determinants of left ventricular dimensions.

This study was designed to quantitate the influence of 20 clinical, hemodynamic, and volume determinants of left ventricular (LV) structure. Systemic hemodynamics, intravascular volume, and LV echocardiographic measurements were collected in a heterogeneous population of 171 patients. Stepwise multiple-regression analysis indicated that body weight and body-surface area were the most powerful determinants of LV chamber size, wall thickness, and muscle mass. Age, a pressure independent determinant of myocardial mass, had no influence on chamber size or LV function. Arterial pressure correlated best with the relative wall thickness and chamber volume. Intravascular volume was a major discriminator for chamber volume, LV mass, and velocity of circumferential fiber shortening. It is concluded that body weight, arterial pressure, intravascular volume, and age are each independent determinants of the LV dimension. Systolic pressure most closely correlated with relative wall thickness and thereby is the best predictor of degree of concentric LV hypertrophy.

Greater renal vascular involvement in the black patient with essential hypertension. A comparison of systemic and renal hemodynamics in black and white patients.

Systemic, splanchnic, and renal hemodynamic data were derived from 60 male and female, black and white, untreated and uncomplicated patients with essential hypertension. The systemic hemodynamic data confirmed our previous findings that at any level of arterial pressure, when black and white patients are matched for age, sex, and mean arterial pressure, cardiac index and total peripheral resistance were similar. This suggests that hypertensive vascular disease is no more severe in the black. This concept was supported further with respect to the splanchnic vasculature; however, renal blood flow was less and renal vascular resistance was higher at any level of mean arterial pressure (or total peripheral resistance) in the black. These physiological findings lend credence to those reports suggesting that at any level of pressure, hypertensive disease and morbidity (e.g., renal impairment) are more severe in the black patient. In addition, these data underscore the importance of understanding regional circulatory characteristics and they do not necessarily follow pari passu measured indices of systemic hemodynamics.

Dimorphic cardiac adaptation to obesity and arterial hypertension.

Cardiovascular function and structure were evaluated by M-mode echocardiography and systemic hemodynamics in paired lean and obese patients, either hypertensive or normotensive. Compared to lean patients, obese patients had greater left atrial (p less than 0.0001), ventricular (p less than 0.001), and aortic root (p less than 0.002) diameters; posterior and septal wall thickness (p less than 0.001); and ventricular mass, cardiac output, stroke volume, and stroke work (all p less than 0.0001). Hypertensive patients had increased posterior wall thickness, end diastolic wall stress, stroke work (p less than 0.01), and a lower radius to posterior wall thickness ratio indicating concentric hypertrophy (p less than 0.001) when compared to normotensive patients. Cardiac adaptation to obesity consists of left ventricular dilatation and hypertrophy (eccentric hypertrophy) irrespective of arterial pressure levels. In contrast, essential hypertension solely produces concentric hypertrophy. Both obesity and hypertension increase left ventricular stroke work by disparate hemodynamic mechanisms; their presence in the same patient will tax the heart and increase the long-term risk of congestive failure.

Essential hypertension in the elderly: haemodynamics, intravascular volume, plasma renin activity, and circulating catecholamine levels.

In an attempt to dissociate the cardiovascular adaptations to high blood pressure from those of ageing, 30 patients with established essential hypertension aged over 65 years were matched for mean arterial pressure, race, sex, height, and weight with 30 patients younger than 42 years. Cardiac output, heart rate, stroke volume, intravascular volume, renal blood flow, and plasma renin activity were significantly lower in the elderly, whereas total peripheral (and renal vascular) resistance, left ventricular posterior wall and septal thicknesses, and left ventricular mass were higher. Intravascular volume correlated inversely with total peripheral resistance in both groups and in all patients. Pathophysiological findings of essential hypertension in the elderly are characterised by a hypertrophied heart of the concentric type with a low cardiac output resulting from a smaller stroke volume and a slower heart rate. Renal blood flow is disproportionally reduced and total peripheral and renal vascular resistance elevated.

Disparate cardiovascular effects of obesity and arterial hypertension.

Since obesity and essential hypertension frequently coexist, a study was designed to analyze some of their cardiovascular effects. Twenty-eight obese patients, half of whom were normotensive and half with established hypertension, were matched for mean arterial pressure with 28 corresponding lean subjects. Systemic and renal hemodynamics, intravascular volume, plasma renin activity, and circulating catecholamine levels were measured. Obese patients had increased cardiac output (p less than 0.001), stroke volume (p less than 0.001), central blood volume (p less than 0.02), plasma and total blood volume (p less than 0.01), and decreased total peripheral resistance (p less than 0.001). In contrast, cardiac output, central blood volume, and stroke volume of hypertensive patients were normal, but they had increased total peripheral (p less than 0.001) and renal vascular resistance (p less than 0.001) and a contracted intravascular volume. Left ventricular stroke work was elevated to a similar level in obesity (p less than 0.001) and hypertension (p less than 0.02), but the increase was caused by an expanded stroke volume in the former and by an increase in systolic pressure in the latter. It is concluded that the disparate effects of obesity and hypertension on total peripheral resistance and intravascular volume counteract and may even offset each other. Thus, obesity may mitigate the effects of chronically elevated total peripheral resistance (and therefore end-organ damage) in essential hypertension. Since both entities affect the heart through different mechanisms, their presence in the same patient results in a double burden to the left ventricle, thereby gently enhancing the long-term risk of congestive failure.