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Biomedical subjects

K Chatterjee

Publications and source records attributed to K Chatterjee.

At least 163 records · Page 9Linked to original sources
PubMed1984

Intravenous and oral prenalterol in congestive heart failure. Effects on systemic and coronary hemodynamics and myocardial catecholamine balance.

Systemic and coronary hemodynamic effects of prenalterol, a beta-1 receptor agonist, were determined in patients with chronic congestive heart failure, initially after intravenous administration (10 patients) and then after oral administration (eight patients). Cardiac index increased by 33 percent and 30 percent after intravenous and oral prenalterol, respectively. The increase in stroke volume index and stroke work index and decrease in pulmonary capillary wedge pressure and systemic vascular resistance were not significant. Myocardial oxygen consumption and coronary sinus blood flow increased in the majority of patients, although these changes were not statistically significant. There were no significant changes in transmyocardial norepinephrine or epinephrine balance. The systemic and coronary hemodynamic effects of both intravenous and oral prenalterol were similar. Major side effects included sudden death (two patients) and hypotension and bradycardia (three patients) during oral prenalterol treatment. It is concluded that improved left ventricular function following both intravenous and oral prenalterol may be associated with increased myocardial oxygen consumption, and serious adverse effects may occur during prenalterol therapy.

Administration, Oral↗
PubMed1984

Intravenous and oral MDL 17043 (a new inotrope-vasodilator agent) in congestive heart failure: hemodynamic and clinical evaluation in 38 patients.

To evaluate the potential benefit of MDL 17043, a new inotrope-vasodilator agent, in the short- and long-term management of severe heart failure, its hemodynamic effects were determined after both intravenous (cumulative average dose 3.7 mg/kg) and oral (average 18.4 mg/kg) administration in 38 patients with severe intractable heart failure. After both intravenous and oral therapy, cardiac index increased from a control value of 2.1 +/- 0.4 to 3.6 +/- 0.9 liters/min per m2, p less than 0.001 (intravenous) and from 2.2 +/- 0.5 to 3.4 +/- 0.6 liters/min per m2, p less than 0.001 (oral). Pulmonary capillary wedge pressure decreased from 26 +/- 6 to 14 +/- 7 mm Hg (p less than 0.001) and from 26 +/- 7 to 18 +/- 8 mm Hg (p less than 0.001) after intravenous and oral routes, respectively. Stroke volume index and stroke work index increased, and right atrial and pulmonary arterial pressures and systemic vascular resistance decreased by similar magnitude after both intravenous and oral MDL 17043 (all p less than 0.001). The hemodynamic effects persisted during 4 hours of observation. Thirty-seven patients were discharged while receiving MDL 17043 therapy and were followed up for a mean of 5.6 months (range 0.5 to 13). Thirty-three of the 37 patients had short-term improvement clinically by at least one New York Heart Association functional class. Undesirable effects, including nausea (35%), anorexia (27%), fluid retention (24%) and thrombocytopenia (less than 1%), necessitated discontinuation of therapy in 11 patients (30%) who were receiving multiple drug therapy.(ABSTRACT TRUNCATED AT 250 WORDS)

Administration, Oral↗
PubMed1984

Hypertrophic obstructive cardiomyopathy. Effects of acute and chronic verapamil treatment on left ventricular systolic and diastolic function.

Changes in left ventricular systolic and diastolic function and outflow gradient were evaluated in patients with obstructive hypertrophic cardiomyopathy after intravenous acute treatment with verapamil (15 patients) and after six months of oral chronic treatment (11 patients). All patients had severe symptoms despite beta blockade, and the condition of all but two improved appreciably after chronic treatment with verapamil. Resting left ventricular outflow tract gradient decreased in six of 15 patients after intravenous verapamil, and in five of 11 patients after long term treatment, but there was no change in provocable gradients nor any correlation between changes in gradient and improvement in symptoms. Left ventricular ejection rate did not change after intravenous or oral treatment. End systolic pressure/end systolic volume index remained unchanged after oral verapamil treatment. Whereas left ventricular total stroke volume index and end diastolic volume index increased without any significant change in left ventricular end diastolic pressure, indicating improved left ventricular diastolic function. In some patients the left ventricular diastolic pressure-volume curve shifted downwards or to the right or both. These findings suggest that improvement in symptoms with verapamil in patients with obstructive hypertrophic cardiomyopathy is unlikely to be related to changes in left ventricular outflow gradient or in systolic function and may be related to improved diastolic function.

Adolescent↗
PubMed1984

Alterations in angina threshold with nifedipine during pacing induced angina.

Changes in coronary haemodynamics and angina threshold were determined during atrial pacing in 11 patients with fixed obstructive coronary artery disease with effort angina before and after the administration of 20 mg of oral nifedipine. Coronary vascular resistance decreased at resting and at "subangina" heart rates but not at "angina" rates. Primary coronary vasodilatation with nifedipine was also suggested by higher coronary sinus oxygen content whether at rest or at subangina or angina heart rates. After nifedipine angina occurred at a lower double product and lower myocardial oxygen consumption. These findings suggest that nifedipine is a coronary vasodilator, but angina can occur at a lower angina threshold in some patients with obstructive coronary artery disease.

Aged↗
PubMed1984

New concepts in ischemic heart disease.

Over the past several years a number of new concepts have greatly increased our knowledge about the pathophysiology and therapy of ischemic heart disease. These concepts include (1) reperfusion following acute myocardial infarction, (2) balloon angioplasty of coronary lesions, (3) secondary prevention of coronary events, (4) the role of coronary tone in producing ischemia, and (5) prevention of atherosclerosis. The use of calcium entry blockers has emphasized the potential importance of spasm or increased tone in the genesis of myocardial ischemia. In standard exercise-induced angina, however, the primary mechanism whereby calcium entry blockers relieve angina appears to be related to a reduction in myocardial oxygen demand rather than to an increase in coronary flow. The calcium entry blockers have also been shown experimentally to retard the development of atherosclerosis in animals fed high-lipid diets. This emphasizes the potential role of calcium in the atherosclerotic process and the potential role of calcium blockers in preventing this sequence.

Arteriosclerosis↗
PubMed1983

Hemodynamic effects of intravenous amiodarone in patients with depressed left ventricular function and recurrent ventricular tachycardia.

The systemic hemodynamic effects of intravenously administered amiodarone were evaluated in patients with depressed left ventricular function and recurrent sustained ventricular tachycardia. Heart rate decreased linearly up to 1 hour after amiodarone infusion (5 mg/kg). Cardiac index varied in a cubic fashion, diminishing at 10 minutes and returning to baseline by 60 minutes (p less than 0.05). Stroke work index also showed a similar decrease at 10 minutes, which was transient (p less than 0.005). These changes occurred without any significant change in systemic vascular resistance and with slight or no increase in pulmonary capillary wedge pressure, indicating a negative inotropic effect of amiodarone. The depression of left ventricular function in these patients, however, was mild and transient, and intravenously administered amiodarone was tolerated by the vast majority of patients. In two patients with overt heart failure and severely depressed left ventricular ejection fraction and marked hemodynamic abnormalities, profound hypotension occurred during amiodarone therapy; in such patients, therefore, hemodynamic monitoring is preferable. Limited data are available on the hemodynamic effects of orally administered amiodarone, but the determination of left ventricular ejection fraction by radionuclide ventriculography before and during long-term amiodarone administration has shown no reduction of function even in patients with severely reduced myocardial performance.

Administration, Oral↗
PubMed1983

Trimazosin in chronic congestive heart failure: improved left ventricular function at rest and during exercise.

The hemodynamic effects of the oral vasodilator trimazosin were evaluated in patients with chronic congestive heart failure (CHF), initially over a 72-hour period (13 patients), and after 3 months of maintenance therapy (seven patients). During the initial evaluation, cardiac index and stroke work index increased an average of 24% and 37% respectively, and pulmonary capillary wedge pressure decreased by 26%. These beneficial hemodynamic effects were maintained during supine bicycle exercise. After 3 months of maintenance therapy, cardiac index (+30%) and stroke work index (+38%) remained elevated, and pulmonary capillary wedge pressure was lower (-38%). Improved hemodynamics during exercise were also seen after maintenance therapy. Withdrawal of trimazosin was associated with deterioration in hemodynamics and left ventricular function. Thus trimazosin has the potential to cause sustained improvement in left ventricular function, both at rest and during exercise, in patients with chronic CHF.

Adrenergic alpha-Antagonists↗
PubMed1983

Late prognostic value of scintigraphic parameters of acute myocardial infarction size in complicated myocardial infarction without heart failure.

Perfusion scintigraphy with thallium-201, infarct scintigraphy with technetium-99m pyrophosphate (TcPYP), and equilibrium blood pool scintigraphy were performed during the initial hospitalization for acute myocardial infarction (MI) in 25 patients without evidence of heart failure who presented with advanced electrocardiographic rhythm and conduction disturbances requiring treatment. Scintigraphic findings during short-term hospitalization were related to the late clinical follow-up performed an average of 14 months later, where patients were grouped as asymptomatic, 8 patients; symptomatic, 9 patients; and deceased, 8 patients. Quantitation of perfusion abnormalities, TcPYP image abnormalities, and left ventricular ejection fraction (EF) revealed that the deceased group had significantly larger TcPYP abnormalities (36 +/- 20 cm2), absolute perfusion abnormalities (32 +/- 16 cm2), and perfusion abnormalities expressed as a percentage of the projected left ventricular area (42 +/- 8%) than the asymptomatic group (13 +/- 8 cm2, 14 +/- 6 cm2, and 20 +/- 9%; p less than 0.05, p greater than 0.05, and p less than 0.01, respectively). The percent perfusion abnormality was significantly larger in the deceased group (42 +/- 8%, p less than 0.01) than in either the symptomatic group (35 +/- 13%, p less than 0.01) or the asymptomatic group (20 +/- 9%), and this parameter in the symptomatic group also differed from that in the asymptomatic group (p less than 0.01). The study indicates that patients with rhythm and conduction disturbances and without congestive heart failure during acute MI may follow an uncomplicated or a complicated late clinical course. Early scintigraphic measurements of MI and perfusion correlate well with this outcome; however, EF could not differentiate among prognostic subgroups.

Adult↗
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↗