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Biomedical subjects

E Kassis

Publications and source records attributed to E Kassis.

At least 37 records · Page 2Linked to original sources
PubMed1991

[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↗
PubMed1991

[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↗
PubMed1990

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↗
PubMed1989

Baroreflex control of the circulation in patients with congestive heart failure.

Vagal and glossopharyngeal afferents from cardiopulmonary and arterial baroreceptors exert supraspinal tonic restraint on sympathetic efferent outflow. The baroreceptor inhibitory influence is directly related to physiological changes in cardiac filling and arterial pressures. Increased cardiac pressures and dimensions during CHF may provide chronic stimulation that reduces responsiveness of these receptors and thereby influence the neurohumoral control of the circulation. Patients with chronic and severe CHF of ischemic cause were compared with control subjects whose ischemic heart disease did not affect cardiac performance. Orthostatic pooling of blood with use of upright tilt (45 degree), provided an apparently sufficient stimulus to unload baroreceptors in patients like controls. In contrast to peripheral vasoconstriction in controls, the patients dilated their resistance vessels during upright tilt. This abnormal vasodilation was systemic and uniform in skeletal muscle and subcutaneous tissue of the forearm remaining at heart level. Such an inability to vasoconstrict in the patients, could not be attributed to depression of local vasoconstrictor reflex or autoregulatory responsiveness of forearm vascular beds. Neural blockade carried out separately or in combination with blockades of forearm vascular effector receptors revealed; increased neural efferent activity to the forearm during tilting the patients which mediated beta-adrenergic vasodilation in both vascular beds. The patients had augmented circulating catecholamine levels, those for epinephrine increased in venous effluents but were maintained in brachial arterial inflow, and those for norepinephrine increased in arterial rather than venous plasma in the forearm. Following the patients during a course of therapy with a selective vasodilator calcium antagonist, the beta-adrenergic reflex vasodilation became substantially attenuated but was preserved during a placebo course of therapy. The beta-adrenergic reflex effect evidenced in the studied patients is most probably a manifestation of reduced baroreceptor afferent restraint and it could subsequently relate to the severity of depression of baroreceptor sensitivity during the course of CHF.

Adult↗
PubMed1987

Cardiovascular response to orthostatic tilt in patients with severe congestive heart failure.

Baroreflex mediated haemodynamic responses and aortic pulsatile stretch were studied in patients with congestive heart failure due to ischaemia. Seven patients with severe congestive heart failure (baseline angiographic ejection fraction 21(3)% (mean(SEM); left ventricular end diastolic volume and pressure 351(43) ml and 22(3) mmHg respectively) were compared with seven control subjects whose angiographic ejection fraction was 74(3)%. Passive 45 degrees upright tilt was used to unload baroreceptors. Aortic pulsatile stretch (pulsatile distension as percentage of diastolic diameter) was calculated from echocardiographic measurements of aortic diameters. Upright tilt caused a significant decrease in cardiac filling pressures in patients with congestive heart failure, as in control subjects. During tilt control subjects had substantially increased systemic vascular resistance and heart rate and decreased stroke volume, but arterial pressure, cardiac index, and aortic pulsatile stretch were maintained constant. Patients with congestive heart failure developed peripheral vasodilatation, had no increase in heart rate, and failed to maintain arterial mean and systolic pressures in the tilted position. They had, however, maintained a constant pulse pressure and increased cardiac index, stroke volume, and aortic pulsatile stretch. The response to upright tilt in patients with congestive heart failure may be explained by faulty sympathetic reflexes, causing vasodilatation and hypotension rather than vasoconstriction, and a rise in stroke volume due to the decrease in afterload.

Aorta↗
PubMed1987

Efficacy of felodipine in chronic congestive heart failure: a placebo controlled haemodynamic study at rest and during exercise and orthostatic stress.

A vascular selective calcium antagonist, felodipine, was evaluated in a randomised, double blind, crossover trial in 18 patients with chronic congestive heart failure of ischaemic cause. Felodipine (10 mg twice daily) or a corresponding placebo was added to conventional treatment. After three weeks haemodynamic function was assessed at rest, during a standard supine leg exercise, and during 45 degrees passive upright tilt. In patients in the supine resting position, felodipine reduced the mean arterial pressure (9%) and systemic vascular resistance (24%) and increased the stroke volume (25%) and cardiac index (23%). The heart rate and right and left ventricular filling pressures were unchanged. During felodipine treatment the standard exercise was accomplished at a similar cardiac index but at a substantially lower heart rate (7%), arterial pressure (10%), systemic vascular resistance (17%), and left ventricular filling pressure (19%), and a higher stroke volume (13%). During both placebo and felodipine administration there were substantial reductions in cardiac filling pressure during upright tilting. Upright tilting during the placebo phase did not increase the heart rate. It also caused a greater fall in systemic vascular resistance while the arterial pulse pressure but not the mean pressure was maintained and the cardiac index and stroke volume increased. The reduced cardiac filling pressures during the felodipine upright tilt were accompanied by reductions in arterial pulse pressure and stroke volume and the patients were able to maintain the mean arterial pressure by an increase in both the heart rate and systemic vascular resistance. Thus three weeks treatment with felodipine improved haemodynamic function at rest and during standard exercise and normalised the baroreflex mediated haemodynamic response in patients with congestive heart failure. The haemodynamic efficacy of the drug in such patients may be associated with a baroreceptor mediated effect as well as direct vasodilatation.

Adult↗
PubMed1987

Cardiovascular and neurohumoral postural responses and baroreceptor abnormalities during a course of adjunctive vasodilator therapy with felodipine for congestive heart failure.

Studies in patients with congestive heart failure (CHF) have demonstrated an abnormal beta-adrenergic reflex vasodilation during orthostatic tilt. Baroreflex modulation of vascular resistance in patients with CHF was investigated during therapy with a vasoselective calcium antagonist, felodipine. Eight patients on conventional therapy for severe CHF were studied after a 3 week course of additional felodipine or placebo treatment under randomized, double-blind, and crossover conditions. Forearm subcutaneous vascular resistance (FSVR) was estimated with use of the local 133Xe washout. Aortic pulsatile stretch, expressed as the systolic distension in percent of diastolic diameter, was calculated from echocardiographic measurements of aortic root diameters. At 3 weeks, felodipine reduced the arterial pressure, systemic vascular resistance, and FSVR, preserved cardiac filling pressures and heart rate, and increased cardiac output, stroke volume, and aortic pulsatile stretch. Upright tilt (45 degrees) was used to study baroreflex-mediated cardiovascular responses. The unloading of cardiopulmonary baroreceptors during upright tilt was substantial and about equal during both treatment courses, but the pulse pressure was maintained during the placebo and decreased during the felodipine period. During tilt, the patients on placebo failed to increase heart rate and their FSVR, systemic vascular resistance, and arterial mean pressure were decreased, whereas during tilt after felodipine, heart rate and systemic vascular resistance increased to maintain arterial mean pressure and FSVR also tended to increase. Both the stroke volume and aortic pulsatile stretch increased during tilt in patients on placebo but they decreased in those on felodipine. The tilt caused increments in circulating norepinephrine and epinephrine levels during both treatment regimens. Regulation of FSVR during the sympathetic stimulation of orthostatic stress was further elucidated. Proximal neural blockade caused an increase in FSVR during tilt in patients on placebo and a decrease in FSVR during tilt in those on felodipine. Local beta-adrenoceptor blockade caused similar increments in FSVR during tilt in patients on both treatments. Combined proximal and local blockade still increased FSVR during tilt in those on placebo, but caused no change in FSVR during tilt in those on felodipine. This study demonstrates that felodipine normalizes baroreflex control of vascular resistance in patients with CHF.(ABSTRACT TRUNCATED AT 250 WORDS)

Aged↗
PubMed1986

Sympathetic reflex control of subcutaneous blood flow in patients with congestive heart failure.

Central and local regulation of forearm subcutaneous vascular resistance (FSVR) during postural changes were studied in congestive heart failure (CHF). Blood flow was measured by the local 133Xe-washout technique. Nine patients with severe CHF (baseline angiographic ejection fraction, 23 +/- 2%, mean +/- SEM; cardiac index, 2.2 +/- 0.2 litres min-1 m-2; increased left ventricular pressures and dimensions) were compared with seven control subjects who had normal cardiac performance. Baseline FSVR and plasma concentrations of noradrenaline and adrenaline were substantially higher in patients with CHF than control subjects. However, the patients, like control subjects, increased FSVR by 46 +/- 3% in response to increase in local venous transmural pressure and disclosed a normal response to decrease in forearm perfusion pressure. Both responses to changes in vascular transmural pressure were preserved after either proximal nervous blockade or local beta-receptor blockade. Central sympathetic stimulation was induced with use of 45 degrees upright tilt. Control subjects developed vasoconstriction (FSVR increased by 59 +/- 5%), which was completely abolished after proximal nerve blockade. Patients with CHF developed vasodilatation (FSVR decreased by 24 +/- 8%), which was not only abolished but reversed after proximal nerve blockade (FSVR increased by 22 +/- 7%), probably owing to the increased humoral vasoconstrictor activity. The paradoxical vasodilator response to central sympathetic stimulation in these patients was reversed after local beta-receptor blockade (FSVR increased by 19 +/- 9%). The local vasoconstrictor reflex responsiveness and intrinsic vascular reactivity were not affected by the augmented baseline sympathetic vasoconstrictor activity in patients with CHF.(ABSTRACT TRUNCATED AT 250 WORDS)

Blood Flow Velocity↗
PubMed1986

Sympathetic reflex control of skeletal muscle blood flow in patients with congestive heart failure: evidence for beta-adrenergic circulatory control.

Mechanisms controlling forearm muscle vascular resistance (FMVR) during postural changes were investigated in seven patients with severe congestive heart failure (CHF) and in seven control subjects with unimpaired left ventricular function. Relative brachioradial muscle blood flow was determined by the local 133Xe-washout technique. Unloading of baroreceptors with use of 45 degree upright tilt was comparably obtained in the patients with CHF and control subjects. Control subjects had substantially increased FMVR and heart rate to maintain arterial pressure whereas patients with CHF had decreased FMVR by 51 +/- 11% (mean +/- SEM, p less than .02) and had no increase in heart rate despite a fall in arterial pressure during upright tilt. The autoregulatory and local vasoconstrictor reflex responsiveness during postural changes in forearm vascular pressures were intact in both groups. Further investigations were carried out in the patients with CHF. The left axillary nerve plexus was blocked by local anesthesia in the seven patients. No alterations in forearm vascular pressures were observed. This blockade preserved the local regulation of FMVR but reversed the vasodilator response to upright tilt as FMVR increased by 30 +/- 7% (p less than .02). Blockade of central neural impulses to this limb combined with brachial arterial infusions of phentolamine completely abolished the humoral vasoconstriction in the tilted position. Infusions of propranolol to the contralateral brachial artery that did not affect baseline values of heart rate, arterial pressure, or the local reflex regulation of FMVR reversed the abnormal vasodilator response to upright tilt as FMVR increased by 42 +/- 12% (p less than .02). Despite augmented baseline values, forearm venous but not arterial plasma levels of epinephrine increased in the tilted position, as did arterial rather than venous plasma concentrations of norepinephrine in these patients. The results suggest a beta-adrenergic reflex mechanism elicited by spinal or supraspinal neural impulses and probably modulating a cotransmitter release in the patients with CHF.

Adult↗
PubMed1986

Development of apical hypertrophic cardiomyopathy.

A 40-year old male patient with a mild, rather diffuse hypertrophic cardiomyopathy (HCM) developed a marked apical hypertrophy of the left ventricle during nine years of observation. The apical HCM showed a characteristic "ace of spades" diastolic configuration on the left ventriculogram. There was no change in the patient's symptoms or haemodynamics. The ECG showed constantly inverted T-waves whereas the precordial QRS amplitude and the corrected QT-interval increased during the observation period. Previous studies have proposed that abortive forms of the apical HCM exist that might become complete later. The present case demonstrates that such a morphological change can take place and that the clinical and haemodynamic picture can be unaffected by the progression of the left ventricular hypertrophy.

Adult↗
PubMed1985

The prognostic value of maximal exercise testing soon after first myocardial infarction.

The prognostic value of ST-segment depression during maximal exercise test performed in the third to fourth week after acute myocardial infarction (AMI), was studied in 126 consecutive patients with no evidence of previous myocardial infarction, unstable angina pectoris or severe heart failure. All patients on average increased their pressure-rate product by 2.6 and no complications occurred. Within the first year of follow-up, major cardiac events occurred in 9 patients (20%), and were fatal in 6 (13%), of the 46 patients who developed ST-segment depression during exercise. Only 3 major cardiac events (4%) occurred in the 80 patients without exercise induced ST-segment depression. Depression of the ST-segment on maximal exercise was a significant predictor of subsequent cardiac events in these survivors of first AMI.

Adult↗