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Biomedical subjects

E Chesler

Publications and source records attributed to E Chesler.

At least 37 records · Page 2Linked to original sources
PubMed1984

Bepridil for chronic stable angina pectoris: results of a prospective multicenter, placebo-controlled, dose-ranging study in 77 patients.

Bepridil, a new calcium-channel blocking agent with an extended plasma elimination half-life of greater than 50 hours, was compared to placebo in 77 patients with confirmed coronary artery disease and chronic stable angina pectoris. The effects of bepridil were compared with those of placebo on angina frequency, nitroglycerin tablet use, the resting ECG and hemodynamics at rest and maximal exercise using a study design comprising 5 sequential 2-week single-blind treatment phases. After 2 weeks of placebo (phase 1), bepridil was given for 3 phases (2, 3 and 4) at total daily dosages of 200, 300 and 400 mg, respectively; the study was completed after a final reintroduction of placebo (phase 5). Within each phase once- and twice-daily regimens of bepridil were randomly compared. Bepridil (300 mg/day) reduced anginal frequency 68%, from 8.5 +/- 1.1 (standard error of the mean) to 2.7 +/- 0.7 attacks/week and nitroglycerin tablet use 76% (p less than 0.001). Bepridil improved exercise duration 26%, from 6.9 +/- 0.4 to 8.7 +/- 0.5 minutes (p less than 0.001) and exercise work 52%, from 2.7 +/- 0.3 to 4.1 +/- 0.4 kpm X 10(-3) (p less than 0.001) on a standardized treadmill protocol. Resting and peak exercise heart rate and blood pressure were unaffected by bepridil. The antianginal effects were similar with either once- or twice-daily treatment schedules. Minor side effects of nausea, epigastric discomfort and tremor were infrequent and there were no major side effects. The results of this large but preliminary, single-blind and short-term study suggest that bepridil is an effective and well tolerated antianginal agent when administered once daily.

Angina Pectoris↗
PubMed1984

Simultaneous measurement of aortic and left ventricular pressures in aortic stenosis using a double lumen pigtail catheter.

This technical note describes a double lumen pigtail catheter that can facilitate measurement of the aortic valve gradient in patients with aortic stenosis. The catheter is passed retrograde into the left ventricle with the aid of a flexible guide wire. In two patients the measured gradient was not significantly different from that obtained using two systemic arterial catheters.

Aorta↗
PubMed1984

"Maximal" drug therapy is not necessarily optimal in chronic angina pectoris.

Beta-adrenergic blocking agents, nitrates and calcium channel antagonists are effective in treating angina pectoris, but much remains unknown about how they act in combination. Consequently, treadmill exercise was used to assess the relative efficacy of nifedipine or isosorbide dinitrate, or both, in 19 patients with stable angina receiving propranolol. Propranolol therapy was continued and either placebo, nifedipine (20 mg), isosorbide dinitrate (20 mg) or both drugs were given randomly 1 1/2 hours before exercise in a double-blind trial. In 16 patients who completed the protocol, heart rate at rest during propranolol therapy was 53.7 +/- 1.9 beats/min (mean +/- standard error of the mean); it increased 4.6 +/- 1.2 beats/min with the addition of nifedipine (p less than 0.01), but was unchanged with isosorbide dinitrate or both combined. Compared with values during treatment with propranolol alone, systolic blood pressure at rest decreased with each vasodilator individually and when combined. Rate-pressure product at maximal exercise was the same with all combinations. Exercise duration was 467 +/- 50 seconds with propranolol, increased to 556 +/- 47 seconds with isosorbide dinitrate (p less than 0.05) and to 636 +/- 50 seconds with nifedipine (p less than 0.001). Exercise duration with all three drugs was 597 +/- 47 seconds (p less than 0.01 compared with propranolol alone). The improvement with nifedipine was greater than with isosorbide dinitrate (p less than 0.05) but exercise duration was not significantly different with the combination of these drugs than when either drug was used alone.(ABSTRACT TRUNCATED AT 250 WORDS)

Aged↗
PubMed1983

Protective effects of aspirin against acute myocardial infarction and death in men with unstable angina. Results of a Veterans Administration Cooperative Study.

We conducted a multicenter, double-blind, placebo-controlled randomized trial of aspirin treatment (324 mg in buffered solution daily) for 12 weeks in 1266 men with unstable angina (625 taking aspirin and 641 placebo). The principal end points were death and acute myocardial infarction diagnosed by the presence of creatine kinase MB or pathologic Q-wave changes on electrocardiograms. The incidence of death or acute myocardial infarction was 51 per cent lower in the aspirin group than in the placebo group: 31 patients (5.0 per cent) as compared with 65 (10.1 per cent); P = 0.0005. Nonfatal acute myocardial infarction was 51 per cent lower in the aspirin group: 21 patients (3.4 per cent) as compared with 44 (6.9 per cent); P = 0.005. The reduction in mortality in the aspirin group was also 51 per cent--10 patients (1.6 per cent) as compared with 21 (3.3 per cent)--although it was not statistically significant; P = 0.054. There was no difference in gastrointestinal symptoms or evidence of blood loss between the treatment and control groups. Our data show that aspirin has a protective effect against acute myocardial infarction in men with unstable angina, and they suggest a similar effect on mortality.

Adrenergic beta-Antagonists↗
PubMed1983

Comparative effects of nifedipine, verapamil, and diltiazem on experimental pulmonary hypertension.

The role of calcium-channel blocking agents in the treatment of pulmonary hypertension is not well defined. Consequently, the effects of diltiazem, nifedipine, and verapamil were compared in 3 groups of anesthetized dogs (n = 6 for each group). In each group, normoxic hemodynamic variables were recorded before and after increasing doses of diltiazem, nifedipine, and verapamil (5 X 10(-8) M/kg, low; 10(-7) M/kg, medium; and 10(-6) M/kg, high dose; given intravenously over 2 minutes). In addition, the effect of these doses on the pulmonary pressor responses to hypoxia (fractional inspired oxygen concentration [FIO2] 12%) and prostaglandin F2 alpha (PGF2 alpha) (5 micrograms/kg/min, intravenously for 4 minutes) was measured. During normoxia, high-dose nifedipine and verapamil decreased mean aortic pressure and systemic vascular resistance while increasing cardiac output in all dogs in both groups (p less than 0.01). Pulmonary vascular resistance, however, remained unchanged. High-dose diltiazem did not significantly alter cardiac output or pulmonary vascular resistance. During acute hypoxic pulmonary hypertension, verapamil decreased cardiac output by 30% (p less than 0.01) without appreciably altering pulmonary arterial pressure; thus pulmonary vascular resistance increased slightly (4.9 +/- 0.6 to 6.4 +/- 1.0 mm Hg/liter/min, difference not significant [NS]). Nifedipine decreased hypoxic pulmonary vascular resistance to normoxic values (p less than 0.01). Cardiac output increased 71% while pulmonary arterial pressure remained unchanged. Diltiazem administration produced no change in hypoxic pulmonary hemodynamic variables. The responses to diltiazem, nifedipine, and verapamil during acute pulmonary vasoconstriction induced by PGF2 alpha were similar to those induced by hypoxia. After verapamil, pulmonary vascular resistance tended to increase (7.3 +/- 1.3 to 8.1 +/- 1.4 mm Hg/liter/min, NS). Nifedipine, however, completely blocked pulmonary vasoconstriction by decreasing pulmonary vascular resistance to pre-PGF2 alpha levels (p less than 0.01). This was accompanied by a 157% increase in cardiac output and only a small increase in pulmonary arterial pressure (7 mm Hg). Again, diltiazem produced no change in pulmonary hemodynamic variables. In these acute studies, nifedipine appeared to be a more effective pulmonary vasodilator than verapamil or diltiazem.

Animals↗
PubMed1983

Zymosan activation of plasma reduces hypoxic pulmonary vasoconstriction.

Small doses of endotoxin (15 micrograms/kg IV) inhibit the pulmonary vascular pressor response to alveolar hypoxia in the anesthetized dog. One of the actions of endotoxin is to initiate the alternate pathway of complement activation. Incubation of human plasma with zymosan (ZAP) will activate this pathway. We wished to see if ZAP would mimic the effect of endotoxin. Prior to ZAP, hypoxia (F1O2 12%) in 5 anesthetized dogs increased pulmonary vascular resistance (PVR: mm Hg/L/min) from 3.7 +/- 0.8 to 7.1 +/- 1.5. After 50 ml ZAP IV the PVR change with hypoxia was only from 3.6 +/- 0.6 to 3.9 +/- 0.8. Plasma heated to destroy complement prior to ZAP incubation in one experiment did not reduce the pressor response. In a further 5 dogs pretreated with meclofenamate (2 mg/kg IV) the PVR increased from 3.7 +/- 0.4 to 7.5 +/- 0.4 with hypoxia prior to IV ZAP and from 4.4 +/- 0.5 to 6.5 +/- 0.6 after ZAP. The effect of ZAP indicates that endotoxin may work through the activation of complement. The protection of the hypoxic pressor response by meclofenamate suggests that the ZAP inhibition (like endotoxin inhibition) may involve dilator prostaglandin-like substances.

Animals↗
PubMed1983

The myxomatous mitral valve and sudden death.

The clincopathologic features of 14 cases of sudden death attributable to dysrhythmias associated with the myxomatous mitral valve are described. The patients were 14-59 years old (mean 27 +/- 11 years). Eleven were female and three male. Of the seven ECGs available, none showed prolongation of the QT interval, but two showed repolarization abnormalities. The material was classified according to the degree of prolapse in the pathologic specimen. When obvious prolapse was found, the expected auscultatory findings had been documented. In three cases there was minimal prolapse, casting some doubt on the hypothesis that traction on the papillary muscles or diastolic dumping of the leaflets may be implicated in the pathogenesis of the dysrhythmias. In one of the cases with minimal prolapse there was a strong family history of sudden death. Endocardial friction lesions were present in 11 cases, including two of the three with minimal prolapse. In five cases there was a thrombotic lesion in the angle between the posterior leaflet and the left atrial wall containing fibrin and platelets. These abnormalities may be important in the pathogenesis of the ventricular dysrhythmias.

Adolescent↗
PubMed1983

Diamide inhibits pulmonary vasoconstriction induced by hypoxia or prostaglandin F2 alpha.

Diamide oxidizes glutathione and other cellular sulfhydryl groups. It decreases calcium ATPase activity and alters mitochondrial calcium flux, probably as a result of the sulfhydryl oxidation. We examined the effect of diamide (5 mg/kg, iv) on pulmonary vascular reactivity in 12 anesthetized dogs. Diamide reversed the pulmonary vasoconstriction caused by hypoxia in seven dogs (control delta PVR + 2.5 +/- 0.6 mm Hg/liter/min; postdiamide delta PVR - 0.1 +/- 0.4 mm Hg/liter/min; P less than 0.01). The pulmonary pressor response to prostaglandin F2 alpha (5 micrograms/kg/min, iv) was also reduced (control delta PVR + 3.8 +/- 0.5 mm Hg/liter/min; postdiamide delta PVR + 1.1 +/- 0.7 mm Hg/liter/min; P less than 0.01). However, in a further five dogs, diamide had only a small effect on the pulmonary vasoconstriction caused by angiotensin II, while the pressor response to hypoxia was again inhibited. The mechanism by which diamide reverses pulmonary vasoconstriction is not certain but the effect is rapid, consistent, and reversible. Because the intravenous infusion of diamide does not produce systemic hypotension, during its period of action on the pulmonary vasculature, unlike the drugs currently available for the clinical treatment of pulmonary hypertension, further studies of its mechanism of action are indicated.

Angiotensin II↗
PubMed1982

Analysis of the complications of cardiac catheterization over nine years.

The mortality and morbidity associated with cardiac catheterization at the Minneapolis VA Medical Center has been analysed over a period of nine years (1971-1979) in order to identify correctable problem, obtain accurate data for patient information, and allow comparison with other institutions. In common with reports from other catheter laboratories, the mortality has fallen from 0.74% (952 patients) between 1971 and 1975 to 0.24% (819) patients between 1976 and 1979. There has been a similar decline in the combined incidence of myocardial infarction and cerebral embolism from 1.05% to 0.24% over the same period. Our patients with ischemic heart disease included many at high risk of complications in that three vessel disease was present in 53% and the ejection fraction was less than 50% in 24% of cases. In order to ensure that the best standards of cardiac catheterization are maintained, we agree with a recent suggestion that there should be a national surveillance program monitoring fatality and complication rates in all catheterization laboratories.

Cardiac Catheterization↗
PubMed1982

Congenital aneurysms adjacent to the anuli of the aortic and/or mitral valves.

The unusual occurrence of non-infected submitral and aortic aneurysms developing sequentially in an adult prompted us to review the pathogenesis of congenital aneurysms adjacent to the aortic and mitral valves. The findings support the suggestion that subvalvular aneurysms, like aortic sinus aneurysms, are a result of a congenital defect at the valve anulus. Submitral aneurysms occur only subjacent to the posterior leaflet. Whereas aortic sinus aneurysms may arise from any of the three sinuses, subaortic aneurysms occur only under the intermediate portion of the left aortic sinus. In the absence of rupture, the clinical presentation of these aneurysms results from valvular insufficiency or compression of the left coronary artery or of the conduction system.

Aortic Aneurysm↗
PubMed1981

Diagnosis of aortic stenosis in older age groups using external carotid pulse recording and phonocardiography.

Measurements made from carotid pulse tracings and phonocardiograms are helpful in the prediction of severe aortic stenosis in young patients. In the elderly, however, analysis of the carotid pulse tracing and, in particular, its maximum rate of rise has proved unreliable because the range of normal values for this age group has not been established. Consequently, we studied 44 young normal and 44 older normal subjects, 15 older patients with systolic hypertension, and 36 older patients with significant aortic stenosis. Measurements obtained from the carotid pulse included the left ventricular ejection time, upstroke time, half-rise time, and the maximum rate of rise. The peak of the systolic murmur in aortic stenosis was measured phonocardiographically from the Q wave of the simultaneously recorded electrocardiogram (QP interval). The results confirm that the maximum rate of rise of the carotid pulse of normal older subjects is much more rapid than that of young subjects. Among elderly patients with aortic stenosis, the maximum rate of rise falls within the range of the normal young. Measurement of the half-rise time is imprecise, and there is considerable overlap with the normal. This is also true of left ventricular ejection time. The upstroke time is unreliable because of wave distortion produced by the arteriosclerotic vascular bed. The two most valuable and easily recorded measurements are the maximum rate of rise and the QP interval. A maximum rate of rise of more than 1000 mmHg/s and a QP interval of less than 220 ms argue strongly against the diagnosis of severe aortic stenosis. These measurements provide a simple, non-invasive means of avoiding left heart catheterisation in older subjects suspected of having severe aortic stenosis.

Age Factors↗
PubMed1981

Perioperative risk of complete heart block in patients with bifascicular block and prolonged PR interval.

Because there is a paucity of information on the perioperative risk of developing complete heart block among patients with bifascicular block (either right bundle branch block and left anterior hemiblock or left bundle branch block) and a long PR interval on the surface electrocardiogram, we undertook an analysis of 76 such patients. Twenty-three patients had right bundle branch block and left axis deviation with a long PR interval and 53 had left bundle branch block with along PR interval. Thirty patients had 37 general anaesthetics, 23 had 32 spinal anaesthetics, and 50 had 64 local anaesthetics or endoscopic procedures. No patient developed complete heart block. Four patients developed sinus bradycardia during general anaesthetics, responsive to atropine or isoproterenol. Similarly, none of the 23 such patients in the literature reviewed had developed complete heart block. Because placement to temporary pacemakers is not without risk, we conclude that prophylactic pacing is not necessary in asymptomatic patients with bifascicular block even in the presence of a long PR interval. Since we did not study patients with recent syncope or myocardial infarction, caution should be exercised in applying these results to such patients.

Aged↗
PubMed1981

A report of Uhl's disease in identical adult twins: evaluation of right ventricular dysfunction with echocardiography and nuclear angiography.

The first example of Uhl's disease affecting identical adult twins is reported, offering support for the contention that a congenital developmental defect or hereditable tendency is the responsible cause. In one case, echocardiography and nuclear angiography proved to be valuable in making the diagnosis. Uhl's disease in the adult should be suspected among cases of isolated right ventricular enlargement and failure complicated by ventricular dysrhythmias. The diagnosis may be made using a combination of noninvasive tests, obviating the need for cardiac catheterization.

Adipose Tissue↗