PubMed Health⌕ Search

Biomedical subjects

L Seth

Publications and source records attributed to L Seth.

5 recordsLinked to original sources
PubMed1986

Indoramin in heart failure: possible adverse effects on hemodynamics and exercise capacity.

Indoramin is an alpha 1-adrenergic antagonist vasodilator of potential value in heart failure. We measured hemodynamics and exercise capacity in 12 patients with heart failure, before and after 1 week of indoramin dosing, 75 mg b.i.d. Maximal hemodynamic effects 2 hours after the first dose of indoramin consisted of reduced mean systemic arterial pressure from 96.0 +/- 15.3 to 87.9 +/- 15.3 mm Hg (P less than 0.05) and pulmonary wedge pressure from 23.6 +/- 7.8 to 16.9 +/- 6.6 mm Hg (P less than 0.001). Heart rate, cardiac index, and total systemic resistance did not change acutely after indoramin, but after 1 week mean systemic arterial pressure was still reduced whereas cardiac index fell from 2.69 +/- 0.38 to 2.32 +/- 0.44 L/min/m2 (P less than 0.05) and total systemic resistance rose from 20.4 +/- 2.8 to 21.9 +/- 4.0 U (P less than 0.1). After 1 week maximal exercise oxygen uptake fell from 16.8 +/- 5.6 to 12.5 +/- 3.5 ml/min/kg (P less than 0.02). This limited observation suggests that indoramin is a predominant venodilator acutely in patients with heart failure but that despite this effect it may worsen functional capacity and hemodynamics during continuous dosing in these patients.

Adult↗
PubMed1986

Post-infarction exercise testing in patients under 55 years. Relation between ischaemic abnormalities and the extent of coronary artery disease.

Previous studies have suggested that the early post-infarction exercise test is useful in predicting the extent of coronary artery disease. The results of a heart rate limited exercise test three weeks after infarction and a symptom limited exercise test six weeks after infarction obtained by both standard lead electrocardiograms and 16 lead precordial maps were compared in 100 consecutive survivors of acute myocardial infarction under 55 years of age. Exercise tests were defined as being positive on the basis of angina, ST segment depression greater than or equal to 1 mm in any electrocardiogram lead, or exertional hypotension. Multivessel disease, that is two or three vessel disease, was present in 60 patients, and three vessel disease in 22 patients. The sensitivity, specificity, and predictive value for multivessel disease of the three week test were 38%, 83%, and 76% respectively; and results for the six week test were 55%, 75%, and 77% respectively. Only 32% of patients with three vessel disease were identified at the three week test, and 59% at the six week test. Significantly more patients with multivessel and three vessel disease were identified by the symptom limited six week test. Precordial mapping offered no advantages over the standard 12 lead electrocardiogram in either the identification of patients with multivessel disease or the prediction of the distribution of coronary artery disease. Angina pectoris during the exercise test at six weeks was the single most useful predictor of multivessel disease. Multivessel disease was found in 27 (87%) of the 31 patients with angina with or without ST depression during the test at six weeks compared with 33 (48%) of the 69 patients who did not have angina during the test at six weeks. Exercise testing in the early post-infarction period in patients under 55 years of age is of limited value in predicting the extent of coronary artery disease. It is, therefore, unreasonable to use such exercise tests to select patients for coronary arteriography after myocardial infarction. None the less angina pectoris occurring during a symptom limited exercise test six weeks after infarction is a strong predictor of multivessel disease, and coronary arteriography is recommended in these patients.

Adult↗
PubMed1986

Rapidly developing tolerance to transdermal nitroglycerin in congestive heart failure.

We have reported early attenuation of hemodynamic effects of transdermal nitroglycerin in patients with heart failure. We now report nitroglycerin plasma levels in those same patients. We administered transdermal nitroglycerin, 60 mg/24 h, to eight patients or placebo to seven patients in a double-blind fashion, and monitored pulmonary wedge pressure and nitroglycerin plasma levels for 24 hours. After placebo administration, nitroglycerin plasma levels and pulmonary wedge pressure remained unchanged. During transdermal nitroglycerin administration, the plasma nitroglycerin level rose from 0.04 +/- 0.12 ng/mL at baseline to near peak levels at 2 hours (7.43 +/- 7.21 ng/mL). Between 2 and 24 hours, levels fluctuated at a steady state. Pulmonary wedge pressure fell from 22 +/- 7 mm Hg at control to a nadir of 14 +/- 5 mm Hg at 4 hours (p less than 0.01). Despite persistently high plasma nitroglycerin levels, by 18 hours pulmonary wedge pressure was no longer significantly reduced (20 +/- 9 mm Hg). These results indicate that rapid development of tolerance is the cause of attenuated hemodynamic efficacy of transdermal nitroglycerin.

Administration, Topical↗
PubMed1985

Pulmonary versus systemic hemodynamics in determining exercise capacity of patients with chronic left ventricular failure.

Right, but not left ventricular ejection fraction correlates with exercise capacity in patients with left ventricular failure, suggesting an important role of the pulmonary circulation. Hemodynamics were measured at rest and during bicycle exercise to symptomatic maximum in 41 patients with chronic left ventricular failure. Maximal oxygen consumption averaged only 12.8 +/- 5.2 ml/min/kg. Pulmonary wedge pressure rose from 21.9 +/- 8.2 to 35.9 +/- 9.3 mm Hg during exercise, while pulmonary arterial mean pressure rose from 31.8 +/- 10.9 to 50.4 +/- 12.9 mm Hg (both p less than 0.0001). Resting cardiac index and resting systemic arterial mean pressure did not correlate with maximal oxygen consumption (r = 0.23 and 0.20, respectively), which, however, did correlate with pulmonary wedge pressure (r = -0.54, p less than 0.001), pulmonary arterial mean pressure (r = -0.49, p less than 0.01), and total pulmonary resistance (r = -0.43, p less than 0.01). Maximal oxygen consumption did not correlate with resting systemic vascular resistance (r = -0.20) or resting pulmonary vascular resistance (r = -0.26). During exercise, total pulmonary resistance remained unchanged at 6.5 +/- 3.8 U while systemic vascular resistance fell significantly. The relation between total pulmonary resistance and exercise capacity and the failure of total pulmonary resistance to fall during exercise suggest that afterload on the right ventricle may be an important determinant of exercise capacity in patients with chronic left ventricular failure.

Aged↗