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Biomedical subjects

K Chatterjee

Publications and source records attributed to K Chatterjee.

At least 109 records · Page 6Linked to original sources
PubMed1983

Vasodilator therapy for acute myocardial infarction and chronic congestive heart failure.

Vasodilator therapy is useful adjunctive therapy in the management of both acute and chronic heart failure. Arteriolar dilators, such as hydralazine, increase cardiac output by decreasing the elevated peripheral vascular resistance that occurs in heart failure. Venodilators, such as nitrates, decrease ventricular filling pressures by redistributing blood so that more is pooled in peripheral veins. Vasodilators that produce both effects (nitro-prusside, prazosin, captopril, for example) are usually helpful in short-term improvement of hemodynamics. Long-term treatment with nonparenteral vasodilators often reduces symptoms and increases exercise tolerance, although there is inconclusive evidence regarding the effects of these agents on mortality. In acute myocardial infarction, intravenous vasodilators frequently improve cardiac performance. Evidence regarding their beneficial effects on infarct size and immediate mortality is encouraging but inconclusive. There is little evidence that they prolong life in patients who survive cardiogenic shock and leave the hospital. Thus, vasodilators can improve hemodynamics and lessen symptoms, but more evidence is needed regarding their long-term effects on survival.

Captopril↗
PubMed1983

Volume loading improves low cardiac output in experimental right ventricular infarction.

To evaluate the effect of volume loading in the low output state associated with right ventricular infarction, isolated right ventricular infarction was produced in seven dogs with the pericardium intact. Volume loading and pericardiotomy were then sequentially performed. After the production of right ventricular infarction, right ventricular systolic pressure decreased by 25%, aortic pressure by 36% and cardiac output by 32%. Right ventricular ejection fraction decreased by 57%, but left ventricular ejection fraction did not change significantly. Left ventricular transmural pressure and diastolic size decreased, and right ventricular diastolic size increased. Intrapericardial pressure increased and equalization of diastolic pressures was noted. Volume loading resulted in increased right ventricular systolic pressure and stroke work, increased aortic pressure and cardiac output and increased transmural pressure and diastolic size in both ventricles. Pericardiotomy resulted in further increases in right and left ventricular filling, stroke work and cardiac output, as well as resolution of equalized diastolic pressures. These results indicate that cardiac output in experimental right ventricular infarction increases with volume loading, which enhances left ventricular preload by augmenting right ventricular output. Elevated intrapericardial pressure affects filling of both ventricles and may play a role in the pathophysiology of low cardiac output in right ventricular infarction.

Animals↗
PubMed1983

Variability in coronary hemodynamics in response to ergonovine in patients with normal coronary arteries and atypical chest pain.

Because an increase in coronary vascular resistance in response to ergonovine maleate has been suggested as a possible diagnostic aid for variant angina, changes were evaluated in coronary hemodynamics and serial myocardial thallium-201 perfusion scans in 15 patients without angina and with normal coronary arteries in response to ergonovine (0.05, 0.10 and 0.20 mg intravenously). For the group, heart rate-blood pressure product increased significantly (p less than 0.001) without any change in coronary sinus flow, coronary vascular resistance, myocardial oxygen extraction, arterial-coronary sinus oxygen difference and lactate extraction. In 7 of 15 patients, however, coronary vascular resistance increased (mean 39%, range 11 to 75%, probability [p] less than 0.001), and coronary sinus flow decreased (14%, p less than 0.001), despite an increase in heart rate-blood pressure product (36%, p less than 0.02). No electrocardiographic, metabolic or thallium-201 scan abnormalities occurred. Therefore, significant increases in coronary vascular resistance in response to ergonovine may occur in patients with normal coronary arteries and atypical chest pain.

Adolescent↗
PubMed1983

Enalapril: a new angiotensin-converting enzyme inhibitor in chronic heart failure: acute and chronic hemodynamic evaluations.

Hemodynamic effects of the new oral angiotensin-converting enzyme inhibitor, enalapril, were evaluated acutely in 15 patients with chronic heart failure and in 7 patients after 4 weeks of maintenance therapy. Initial hemodynamic effects were characterized by a significant increase in cardiac index (from 2.1 +/- 0.7 to 2.6 +/- 0.7 liters/min per m2) and a decrease in pulmonary capillary wedge pressure (from 30 +/- 6 to 24 +/- 7 mm Hg), right atrial pressure (from 14 +/- 5 to 11 +/- 4 mm Hg), mean arterial pressure (from 96 +/- 16 to 80 +/- 17 mm Hg) and systemic vascular resistance (from 1,820 +/- 480 to 1,200 +/- 410 dynes . s . cm-5) without any significant change in heart rate, pulmonary artery pressure and pulmonary vascular resistance. During maintenance therapy, the dose of diuretic drugs had to be increased because of systemic venous hypertension. Repeat hemodynamic study showed that after chronic therapy, cardiac index (2.1 +/- 0.7 vs. 3.0 +/- 0.08 liters/min per m2) and stroke volume index (24 +/- 10 vs. 36 +/- 7 ml/m2) remained elevated and pulmonary capillary wedge pressure was lower than control (30 +/- 6 vs. 16 +/- 6 mm Hg), indicating sustained improvement in left ventricular performance. Plasma renin activity increased and plasma norepinephrine levels decreased after enalapril therapy and these humoral changes persisted during maintenance therapy. All patients receiving chronic therapy had symptomatic improvement. Significant hypotension, which occurred in five patients at the initiation of therapy, appears to be the major side effect.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1983

Mechanism of relief of pacing induced angina with oral verapamil: reduced oxygen demand.

To evaluate the influence of oral verapamil (80 and 120 mg) on angina threshold, coronary blood flow, myocardial oxygen consumption and left ventricular function, we subjected 13 patients with effort angina and fixed obstructive coronary artery disease to atrial pacing at progressively higher heart rates. After 120 mg of verapamil, the time to onset of angina and the heart rate at the onset of ST-segment depression increased by 18% (p less than 0.005) and 10% (p less than 0.001), respectively, without any change in the angina threshold (rate-pressure product at the onset of angina). The rate-pressure product, coronary blood flow and myocardial oxygen consumption were lower at rest and at pre-angina heart rates but not when the angina threshold was reached. Thus, the beneficial effect of verapamil was primarily due to decreased myocardial oxygen demand rather than to increased coronary blood flow. The decreased demand resulted from a lower arterial pressure at each pacing rate. In these patients without heart failure, left ventricular pump function did not deteriorate. This beneficial response was less with 80 mg of oral verapamil. These findings suggest that oral verapamil has a potential role in the management of patients with effort angina due to fixed obstructive coronary artery disease.

Administration, Oral↗
PubMed1983

Influence of atrial systole on the Frank-Starling relation and the end-diastolic pressure-diameter relation of the left ventricle.

The influence of atrial systole on the left ventricular function curve (stroke volume vs end-diastolic pressure or end-diastolic diameter) and on the left ventricular end-diastolic pressure diameter relation was studied in nine anesthetized, open-chest dogs whose atrioventricular (AV) node had been completely blocked. Measurements were made during volume loading with the pericardium closed and opened and during alternate AV sequential pacing (to permit atrial contribution to ventricular filling) and AV simultaneous pacing (to prevent atrial contribution). When the pericardium was closed, withdrawal of the atrial contribution shifted the stroke-volume end-diastolic pressure relation downward, but did not shift the stroke volume-end-diastolic diameter relation, i.e., it reduced stroke volume for a given end-diastolic pressure according to a reduction in end-diastolic volume. The downward shift of the stroke volume-end-diastolic pressure relation was caused by an upward shift of the end-diastolic pressure-diameter relation, which, for a given end-diastolic pressure, resulted in a smaller end-diastolic diameter and, thus, in a smaller stroke volume. The reason for the upward shift in the end-diastolic pressure-diameter relation was that the atrium remained full and thus increased pericardial pressure by increasing pericardial volume. Opening the pericardium shifted the end-diastolic pressure-diameter relation downward and to the right, shifted the stroke volume-end-diastolic diameter relation upward and abolished the effect of withdrawal of the atrial contribution on these curves. We conclude that in the presence of an intact pericardium, atrial systole shifts the stroke volume-end-diastolic pressure relation because it shifts the end-diastolic pressure-diameter relation and it improves left ventricular performance by increasing preload.

Animals↗
PubMed1983

Vasodilator therapy in chronic congestive heart failure.

Vasodilator agents are relatively new additions to the armamentarium for the management of patients with congestive heart failure. Myocardial failure, irrespective of the aetiology, tends to create a vicious cycle characterised by reduced cardiac output and elevated systemic vascular resistance, which further decrease cardiac output by increasing left ventricular ejection impedance. The rationale for the use of vasodilators is to interrupt the vicious cycle by decreasing the left ventricular ejection impedance by peripheral vasodilatation. Although most vasodilator agents produce qualitatively similar haemodynamic responses, quantitatively their haemodynamic effects differ considerably. Knowledge of the haemodynamic effects of the various vasodilators helps in the selection of a particular drug for the management of such patients. This article reviews the mechanisms of action, haemodynamic effects, pharmacokinetics, clinical usage and adverse effects of non-parenteral vasodilator agents currently available for the management of patients with chronic heart failure.

Captopril↗
PubMed1983

Electroacupuncture and its effect on rat hepatic functions.

The effect of single, acute (7 pulses/sec., 0.75 volt) and chronic (4 pulses/sec., 0.75 volt) electroacupuncture (EA) treatment on alternate days for a period of 21 days on hepatic functions of rats were studied at cellular and subcellular levels. The points used for EA were Shenshu, Dachangshu and Zusanli. After chronic treatment, (a) protein, RNA, phospholipid, and cholesterol contents of whole liver and liver microsomal fraction increased significantly, (b) liver microsomal G-6-Pase activity increased significantly, (c) microsomal lipid peroxidation value decreased, (d) lipase activity increased. After acute treatment, (e) phospholipid, and cholesterol contents of the whole liver and liver microsomal fraction increased significantly, (f) liver microsomal G-6-Pase activity increased significantly, (g) liver microsomal lipid peroxidation value decreased, (h) GPT and lipase activity of liver increased. The parameters unchanged in acute treatment were as follows: (i) protein, RNA content, (j) GOT activity of the liver, (k) SGOT and SGPT activity, (1) hepatic triglyceride. The parameters unchanged in chronic treatment were as follows: (m) GOT and GPT activity of the liver, (n) SGOT and SGPT activity, (o) hepatic triglyceride. No apparent harmful effect of EA on rat hepatic functions is obvious from present study.

Acupuncture Therapy↗
PubMed1983

Hydralazine in heart failure.

Hydralazine is a smooth muscle relaxant and a potent arteriolar dilator. The major hemodynamic effect of hydralazine in patients with heart failure are increased cardiac output and stroke volume, and decreased vascular resistance without any significant change in pulmonary and systemic venous pressure. Hydralazine also produces beneficial hemodynamic effects in patients with mitral and aortic regurgitation and in some patients with large ventricular septal effect with reduced systemic output. However, the role of long-term hydralazine therapy in these patients remains uncertain. In many patients with chronic heart failure with low cardiac output, hydralazine produces sustained beneficial hemodynamic and clinical effects. The long-term prognosis of patients with chronic heart failure, however, remains unchanged, although certain subsets of patients appear to have better prognoses than others during long-term hydralazine therapy.

Animals↗
PubMed1983

Analysis for Fusarium toxins in various samples implicated in biological warfare in Southeast Asia.

Samples of leaves, water, cereal grains, soil, and yellow powder as well as blood, urine, and body tissues from chemical warfare victims were analyzed for Fusarium toxins by using gas chromatography and mass spectrometry. The leaves, water, and yellow powder samples contained various combinations of T-2 toxin, diacetoxyscirpenol, deoxynivalenol, nivalenol, and zearalenone in concentrations ranging from trace (1.0 ppb) amounts to 143 ppm. These trichothecenes do not occur naturally on the substrates described and were correlated with the so-called "yellow rain" chemical attacks against Hmong people in Southeast Asia. Analysis of leaves, soil, water, and cereals collected in areas adjacent to but apart from the area where chemical attacks had been staged did not contain any Fusarium toxins. Moreover, T-2 and HT-2 toxins were found in human blood, urine, and body tissues (heart, esophagus, kidney, lung, and large intestine) of alleged victims. In addition, diacetoxyscirpenol was found in the kidney of one person who had died.

Adult↗
PubMed1982

Captopril in congestive heart failure: improved left ventricular function with decreased metabolic cost.

The oral angiotensin-converting enzyme inhibitor captopril (CPT) produces beneficial hemodynamic and clinical responses in patients with chronic congestive heart failure (CHF). Cardiac output and stroke volume increase, along with a decrease in pulmonary capillary wedge pressure, indicating improved left ventricular function. During maintenance CPT therapy, the beneficial hemodynamic and clinical effects appear to be sustained. Improved left ventricular pump function with CPT is associated with decreased metabolic cost, as myocardial oxygen consumption consistently decreases in proportion to the decrease in myocardial oxygen demand. Myocardial ischemia occurs infrequently, as is evident from the abnormal myocardial lactate metabolism. Hypotension appears to be the major adverse effect, particularly after the first dose. However, with dose titration and the use of a smaller initial dose, a marked precipitous fall in blood pressure can be avoided in the majority of patients. Thus, CPT may prove to be a useful agent in the vasodilator therapy of chronic CHF.

Angiotensin-Converting Enzyme Inhibitors↗
PubMed1982

Minoxidil therapy in chronic congestive heart failure: acute plus long-term hemodynamic and clinical study.

The hemodynamic response to minoxidil, an orally active, potent vasodilator, was evaluated in 11 patients with severe chronic congestive heart failure (CHF). The hemodynamic response was determined following single doses of 10, 15, 20, 25, and 30 mg of minoxidil. The hemodynamic response was characterized by marked increases in cardiac index (+63%) and stroke volume index (+52%) and by decrease in systemic vascular resistance (-38%). There was also a slight decrease in pulmonary capillary wedge pressure from an average of 24 +/- 8 to 21 +/- 7 mm Hg. Although the average mean arterial pressure remained unchanged, one patient developed significant hypotension. Chronic minoxidil therapy (eight patients) was associated with fluid retention and weight gain. In four patients in whom fluid retention could be minimized with larger doses of diuretics, a sustained clinical and hemodynamic improvement was observed. These findings suggest that minoxidil has the potential to improve cardiac function and may be useful in chronic vasodilator therapy of CHF, provided fluid retention can be controlled.

Adult↗
PubMed1982

Vasodilators in heart failure secondary to coronary artery disease.

Although vasodilators produce acute beneficial hemodynamic effects in patients with chronic congestive heart failure, their effects on the long-term management of such patients are unclear. In 56 patients followed up for an average of 13 months, there was a 37% mortality at 1 year. Because of the potential adverse effects of vasodilators in patients with coronary artery disease, we evaluated the effects of prazosin, hydralazine, and isosorbide dinitrate on hemodynamics, coronary sinus flow, and myocardial oxygen consumption (MVO2). Isosorbide dinitrate reduced ventricular filling pressure with no change in heart rate or mean arterial pressure; coronary sinus flow and MVO2 fell significantly. With prazosin there was a reduction in ventricular filling pressures and rate-pressure product but no change in coronary sinus flow or MVO2. With hydralazine there were parallel changes in the rate-pressure product and MVO2. Results emphasize the differing effects of vasodilators on oxygen supply and demand, which may influence the long-term course of patients with coronary artery disease.

Cardiac Output↗
PubMed1982

The significance of nitroglycerin-induced changes in ventricular function after acute myocardial infarction.

The potential of nitroglycerin for improving global and regional ventricular function after acute myocardial infarction and predicting serial change in ventricular function at the time of hospital discharge was investigated. Equilibrium multiple gated blood pool scintigrams were performed at rest before and after sublingual administration of nitroglycerin in 18 patients an average of 36 hours after infarction and again at discharge. Global right and left ventricular function and regional left ventricular function of infarct and noninfarct zones were determined scintigraphically. In the early study nitroglycerin increased both mean (+/- standard deviation) left ventricular ejection fraction (0.51 +/- 0.15 to 0.55 +/- 0.15 ; p less than 0.02) and mean right ventricular ejection fraction (0.42 +/- 0.14 to 0.47 +/- 0.13; p less than 0.05). Left ventricular ejection fraction significantly increased in 5 of the 18 patients. It increased late in five of the six patient who exhibited an increase early after nitroglycerin but in only 2 of the 12 patients who did not exhibit an early increase (p less than 0.06). Regional ejection fraction in the infarct zone increased late in 7 of the 12 patients who exhibited an early increase after nitroglycerin and in none of the 6 who did not exhibit an early increase (p less than 0.05). Both right and left ventricular global ejection fraction and regional ejection fraction showed little late responsiveness to nitroglycerin. Early after infarction, sublingual nitroglycerin improved left, right and regional ejection fraction at the infarct site in some patients. These nitroglycerin-induced changes predicted those patients whose global ventricular function and regional left ventricular function at the infarct site improved late.

Administration, Oral↗
PubMed1982

Haemodynamic and myocardial metabolic effects of captopril in chronic heart failure.

In 15 patients with chronic left ventricular failure caused by ischaemic heart disease, cardiac output and right heart pressures were measured before and after the oral angiotensin-converting enzyme inhibitor, captopril, which was administered in increasing doses. In 12 of 15 patients, coronary blood flow, and in 11 patients myocardial oxygen extraction and consumption and lactate extraction were also determined before and after captopril therapy. Cardiac index and stroke volume index increased by an average of 25% and 27%, respectively. Pulmonary capillary wedge pressure also decreased in all patients (average 27%), suggesting improved left ventricular function. The rate-pressure product, coronary blood flow, and myocardial oxygen consumption decreased significantly; in one of 11 patients there was myocardial lactate production, despite decreased myocardial oxygen demand and consumption. These findings suggest that in patients with chronic heart failure, improved left ventricular function with captopril is generally associated with decreased metabolic cost and that deterioration of metabolic function occurs infrequently.

Aged↗
PubMed1982

The role of right ventricular systolic dysfunction and elevated intrapericardial pressure in the genesis of low output in experimental right ventricular infarction.

To elucidate the pathophysiology of severe right ventricular infarction (RVI), isolated RVI was produced in 15 dogs with the pericardium intact or open. After RVI in dogs with the pericardium intact, RV systolic pressure decreased by 27%, aortic pressure by 29% and cardiac output by 34%. RV transmural pressure, RV end-diastolic size and intrapericardial pressure increased, left ventricular transmural pressure and end-diastolic size decreased and the diastolic pressures equalized. Pericardiotomy after RVI resulted in increased ventricular transmural pressures and diastolic size, improved cardiac output and resolution of equalized diastolic pressures. RVI in dogs with the pericardium open resulted in similar changes, but of lesser magnitude and without equalization of diastolic pressures. These results indicate that reduced left ventricular preload due to impaired RV systolic function contributes to low cardiac output in RVI. Elevated intra-pericardial pressure further reduced left ventricular preload and produces equal diastolic pressures.

Animals↗