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E Kassis

Publications and source records attributed to E Kassis.

10 recordsLinked to original sources

Subcutaneous and skeletal muscle vascular responses in human limbs to lower body negative pressure.

Cardiopulmonary baroreceptor unloading in humans comparably increases sympathetic discharge to skeletal muscle in the forearm and calf, but blood flow studies have disclosed differential rather than uniform vasomotor responses in the extremities. The aim of the present study was to address the issue of differential effects of orthostatic stress on forearm and calf vascular adjustment and to extend previous studies by determining changes in vascular responses separately in various vascular beds of the limbs. The local [133Xenon] washout method was used for recording blood flow rates in subcutaneous tissue and skeletal muscle. Simultaneous recordings from the forearm and calf were performed in 11 healthy young males during lower body negative pressure at -10 mmHg. Heart rate, arterial mean and pulse pressures did not change during lower body negative pressure. In the forearm blood flow rates decreased significantly, in subcutaneous tissue by 16 +/- 2% (mean +/- SEM) and in skeletal muscle by 16 +/- 1%. In the calf lower body negative pressure induced a significant decrease in blood flow rates of 17 +/- 3% in subcutaneous tissue and of 30 +/- 2% in skeletal muscle. This vasoconstriction in calf skeletal muscle was consistently disclosed in both legs and was about the same magnitude in each calf when studied with the one leg exposed to lower body negative pressure and the other outside the lower body negative pressure chamber. These findings suggest that during unloading of cardiopulmonary afferents, reflex sympathetic activation as an important autonomic adjustment to orthostatic stress is accompanied by uniform vasoconstriction in subcutaneous and skeletal muscle vascular beds of human limbs.

Adult

[Coronary bypass surgery in patients with decreased function of the left ventricle].

During 1988-1990, 21 patients with poor left ventricular function underwent coronary artery bypass surgery. The median number of previous infarctions was 1.6 (0-4). Three patients had no previous history of myocardial infarction. All patients had ischemic heart disease and significant stenoses or occlusion of the circumflex artery, the left anterior descendent artery and the right coronary artery. Preoperatively the left ventricular ejection fraction (LVEF) was 23% (10-28) judged by echocardiography. The median number of peripheral anastomoses was 4.8 (2-7). The perioperative mortality was 9.5%. One year survival was 90%. Postoperatively the median LVEF increased to 35% (25-50). The working capacity increased in 70% of the patients. This study has shown that coronary arterial bypass surgery in patients with ischemic heart disease and poor left ventricular function may result in symptomatic and functional benefit.

Adult

[Adult Gaucher's disease with pulmonary involvement].

Gaucher's disease is an autosomal recessive disorder caused by deficiency of the enzyme glucocerebrosidase with accumulation of glucocerebroside in the reticuloendothelial system. Affection of the lungs by this disease is extremely rare. When Gaucher cells infiltrate the lung, fibrosis may result. We describe a case with adult type Gaucher's disease who, besides affection of liver, spleen and bone marrow, had severe pulmonary involvement with extensive interstitial fibrosis, increased pulmonary vascular resistance, and pronounced reduction in diffusion capacity.

Bone Marrow

Long-term clinical, hemodynamic, angiographic, and neurohumoral responses to vasodilation with felodipine in patients with chronic congestive heart failure.

Twenty patients on conventional therapy for severe congestive heart failure (CHF) were randomly assigned to adjunctive treatment with felodipine (n = 10) or placebo (n = 10) and followed over a 6-month period. Baseline clinical, hemodynamic, angiographic, and neurohumoral estimates of CHF were comparable in the two treatment groups. These estimates remained virtually unchanged at 6 months in patients on placebo therapy, but circulating noradrenaline levels were further augmented. In patients on felodipine therapy, substantial reductions in left ventricular end-systolic pressure, mean arterial pressure, and systemic vascular resistance were observed at 6 months. This afterload reduction led to a preferential increment in the stroke volume (36%) which increased cardiac output (30%), whereas heart rate tended to decrease. The improved hemodynamics during felodipine treatment were paralleled by marked improvements in the angiographic left ventricular ejection fraction and regional segmental wall motion score. The enhanced contractile state of the left ventricle was accompanied by significant reductions in the augmented plasma levels of catecholamines, and the patient clinical status improved. The 6-month mortality rate in the 20 patients was 40% and indicated a closer relation to baseline noradrenaline plasma levels than to hemodynamic or angiographic estimates of CHF. Despite the limited number of patients, the long-term clinical efficacy of felodipine is thus evidenced in patients with CHF and is related to sustained arteriolar dilatation and improved neurohumoral profile by this vasoselective calcium antagonist.

Adult

[Cor pulmonale].

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Humans

Systemic hypertension, left ventricular hypertrophy and myocardial infarction in patients with chronic obstructive lung disease.

Left ventricular function was evaluated prospectively during 1 year in a controlled clinical study of 73 patients with chronic obstructive lung disease. The control group comprised 68 patients matched for age and sex and with no evidence of airways obstruction. Left ventricular hypertrophy was found in 52% and systemic hypertension in 58% of patients in the study group compared with 6% and 15% respectively in the controls. Left ventricular hypertrophy was diagnosed in 70% of patients with chronic bronchitis and in 19% of those with chronic emphysema. Systemic hypertension was observed in 45% of the bronchitic type patients and in 81% of those with emphysema. The incidence of myocardial infarction in the study group was not lower than in the controls. The high frequency of left ventricular hypertrophy in patients with chronic obstructive lung disease can probably be related to a similar high frequency of systemic hypertension. Hypertension per se does not explain left ventricular hypertrophy in all patients with chronic bronchitis, but hypoxemia and acidosis seem to be of pathogenetic importance in these cases.

Acute Disease