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Biomedical subjects

K Chatterjee

Publications and source records attributed to K Chatterjee.

At least 55 records · Page 3Linked to original sources
PubMed1988

Systemic and coronary hemodynamic and neurohumoral effects of levodopa in chronic congestive heart failure.

Systemic and neurohumoral effects of oral levodopa were evaluated in 17 patients with severe chronic heart failure. The maximum mean dopamine level achieved after 1.5 g of oral levodopa was 19.6 +/- 16.4 ng/ml. At peak dopamine level, cardiac index increased by 14% from baseline (1.95 +/- 0.55 to 2.27 +/- 0.45 liters/min/m2, p less than 0.05), stroke volume index increased by 14% (22.4 +/- 6.0 to 25.9 +/- 5.8 ml/min/m2, p less than 0.01). There was a trend toward reduced systemic vascular resistance of 13% (1,773 +/- 769 to 1,535 +/- 432 dynes.s.cm-5, p = 0.08). There was no significant change from baseline in heart rate, mean arterial pressure, right atrial pressure, pulmonary capillary wedge pressure, pulmonary vascular resistance and rate-pressure product. In addition, as the arterial dopamine level increased there was a concomitant decrease in plasma norepinephrine level that was sustained for the period of observation. In a subgroup of 8 patients, there was no change in coronary sinus blood flow, myocardial oxygen consumption, myocardial oxygen extraction, lactate extraction and transmyocardial release of catecholamines after levodopa. These findings suggest that oral levodopa, 1.5 g, can improve left ventricular function without adversely affecting myocardial energetics and catecholamine balance.

Aged↗
PubMed1988

Bedside catheterization of the pulmonary artery: risks compared with benefits.

The decision to use bedside pulmonary artery catheterization for managing patients must involve a careful assessment of the risks compared to the benefits. Complications can be minimized by following specific guidelines for catheter insertion and maintenance. Pulmonary artery catheterization has been shown to be more accurate than clinical assessment alone in critically ill patients for determining the cause of shock (hypovolemic, cardiogenic, or septic) or for assessing the cause of severe pulmonary edema (cardiogenic or noncardiogenic). The diagnosis of cardiac failure in medical or surgical patients with invasive hemodynamic monitoring provides physiologic data that guide pharmacologic treatment that may favorably influence preload and afterload in the failing or ischemic heart. Managing hemodynamics with the aid of pulmonary artery catheterization in patients with the adult respiratory distress syndrome has received considerable attention, but a contribution to better patient outcome has not been established. Similarly, although clinical management of hemodynamic instability in septic shock is facilitated by pulmonary artery catheterization, the mortality remains very high because of the lack of specific therapy to reverse the sepsis syndrome. Adequate volume resuscitation and improved tissue oxygenation are universally accepted goals, but specific hemodynamic endpoints are controversial and direct measurements of tissue oxygenation are not possible. Prospective studies to define the clinical value of pulmonary artery catheterization are needed, but must be designed very carefully in order to identify unequivocally the effect of pulmonary artery catheterization on outcome in critically ill patients.

Catheterization, Swan-Ganz↗
PubMed1988

Dopexamine hydrochloride in chronic congestive heart failure with improved cardiac performance without increased metabolic cost.

Dopexamine hydrochloride is a new intravenous, short-acting agent with agonist activity at beta 2-adrenergic and DA1-dopaminergic receptors. The effects of dopexamine hydrochloride infusion on systemic and coronary hemodynamics, myocardial metabolism and the neuroendocrine system were evaluated in 10 patients with chronic severe congestive heart failure at baseline, at rates of 1, 2, 4 and 6 micrograms/kg/min at 15-minute intervals, and after a 1-hour infusion of the "optimal" dose. Right atrial pressure was reduced by 25% (p less than 0.01), pulmonary capillary wedge pressure by 26% (p less than 0.05), systemic vascular resistance by 44% (p less than 0.001) and pulmonary vascular resistance by 34% (p less than 0.01) after the optimal dose. Heart rate increased by 17% (p less than 0.01), rate-pressure product by 17% (p less than 0.01) and stroke volume index by 31% (p less than 0.001). There was no change in mean arterial pressure, myocardial oxygen consumption, coronary sinus blood flow, myocardial oxygen extraction or norepinephrine balance. None of the patients demonstrated net myocardial lactate production. These findings suggest that dopexamine hydrochloride improves systemic hemodynamics and cardiac performance without adversely affecting myocardial energetics or norepinephrine balance. Thus, dopexamine hydrochloride may be a useful agent for the short-term treatment of congestive heart failure.

Adult↗
PubMed1988

Vasodilator therapy in chronic congestive heart failure.

Benefits from vasodilator therapy in patients with chronic heart failure are partly related to the severity of functional derangements. Agents with an arteriolar-dilating effect are more likely to be effective in patients with higher left ventricular outflow resistance. Vasodilators with primary venodilating properties are more likely to be effective in the presence of an increased ventricular preload. The mechanisms by which preload and left ventricular outflow resistance increase in patients with cardiac insufficiency are not well understood and may not be similar in all patients. Vasodilators also have the capacity to ameliorate myocardial metabolic functional abnormalities by influencing myocardial energetics, but the effects of different agents on coronary hemodynamics may not be uniform. Effects on renal hemodynamics may also vary, as may neurohumoral changes after therapy. Angiotensin-converting enzyme inhibitors have been shown to exert beneficial effects on both coronary and renal hemodynamics in patients with chronic heart failure, while producing favorable neurohumoral changes. These agents provide some advantages over direct-acting vasodilators in that myocardial oxygen consumption is decreased, myocardial metabolic function is improved, and norepinephrine and aldosterone levels are reduced. Further controlled studies are needed to assess the efficacy of angiotensin-converting enzyme inhibitors in relation to other vasodilators for the long-term management of these patients.

Cardiomyopathy, Dilated↗
PubMed1988

The clinical and pathophysiologic implications of pain, ST abnormalities, and scintigraphic changes induced during dipyridamole infusion: their relationships to the peripheral hemodynamic response.

In order to determine their significance during dipyridamole perfusion scintigraphy, symptomatic, ECG, and scintigraphic findings were related to each other, to the hemodynamic response, and to angiographic findings in 73 consecutive patients having coronary angiography within 3 months of scintigraphy. The group having induced "cardiac" pain differed from the group without induced pain only in their higher incidence of induced ischemic ST changes, the "marked" hemodynamic response, and their lower incidence of an "absent" hemodynamic response (all p less than 0.01). Induced ST depression was found only in patients with coronary disease. In this population, dipyridamole-induced pain was a moderately specific marker and induced ST abnormalities a more highly specific marker for coronary disease. However, both were insensitive for coronary disease diagnosis. If induced pain or ST abnormalities in the presence of significant coronary disease were accepted as indicators of ischemia, then scintigraphic abnormalities appeared to be produced by dipyridamole in roughly equal incidence by ischemic and nonischemic mechanisms. Induced ischemia related frequently to an exaggerated hypotensive response with no change in double product, suggesting its cause to be an induced increase in myocardial oxygen demand. Dipyridamole-induced image defects were noted even in the absence of a peripheral hemodynamic response. This indicates that the peripheral response does not always correlate with its central coronary effect and an absent peripheral hemodynamic response does not necessarily invalidate scintigraphic results.

Angina Pectoris↗
PubMed1988

Abnormal coronary hemodynamics and myocardial energetics in patients with chronic heart failure caused by ischemic heart disease and dilated cardiomyopathy.

Coronary sinus blood flow, transmyocardial oxygen extraction, myocardial oxygen consumption, and transmyocardial lactate extraction were determined, along with systemic hemodynamics, in 34 patients with chronic stable angina without heart failure (group 1), in 66 patients with heart failure associated with coronary artery disease (group 2), and in 28 patients with heart failure caused by dilated cardiomyopathy without coronary artery disease (group 3). Compared with group 1 patients, in patients with heart failure in groups 2 and 3, resting coronary sinus blood flow was 30% and 24% higher, respectively (p less than 0.05), myocardial oxygen consumption was 25% higher (p less than 0.01), and coronary sinus oxygen content was 33% lower (p less than 0.01). The rate-pressure product was not different between the three groups. In eight patients with heart failure (five in group 2 and three in group 3), myocardial lactate production was observed without angina. Thus in patients with chronic heart failure resulting from either chronic coronary artery disease or dilated cardiomyopathy, resting coronary blood flow and myocardial oxygen consumption tend to increase probably because of an increase in myocardial oxygen requirements. Silent myocardial ischemia may also occur in both the presence and absence of coronary artery disease in patients with chronic heart failure. The abnormal coronary hemodynamics and myocardial metabolic function may play a role in causing progressive deterioration in cardiac function in dilated cardiomyopathy.

Adult↗
PubMed1988

Silent myocardial ischemia: an update.

Silent myocardial ischemia is diagnosed by several different techniques and has been documented in all the anginal syndromes. In addition to other factors, its presence may be related to increased pain threshold and increased pain tolerance. Although some patients with painless ischemia may have less extensive coronary artery disease, cumulative evidence indicates that silent myocardial ischemia does not necessarily signify a lesser degree of cardiac ischemia or a less severe coronary abnormality. As judged by ambulatory monitoring studies, it shows circadian variation; occurs more frequently than symptomatic ischemia; and appears to depend, in large part, on activation of the sympathetic nervous system. Frequent silent ischemic events during ambulatory monitoring are worrisome because they reflect the disease "activity" of single or multiple coronary atherosclerotic lesions. Thus, there may be a direct association between the severity of ischemia seen during Holter monitoring, the extent of underlying coronary artery disease or disease activity, and prognosis. When diagnosed by exercise testing, silent myocardial ischemia may be associated with significant coronary involvement. In this regard, patients with three vessel coronary disease, impaired left ventricular function, and silent ischemia during stress testing should benefit from coronary revascularization. Compared with symptomatic patients, other evidence suggests that patients with exercise-induced asymptomatic ischemia have at least the same or perhaps even a worse outlook; this may be related to the lack of symptoms that would prompt evaluation and therapy. Awareness of the possibility of silent myocardial ischemia and use of commonly available tests, both to establish its presence and severity and to guide treatment, are emerging as new clinical goals. Further data, however, are necessary to determine how vigorously this should be pursued in different patient subgroups. In association with unstable angina or post-myocardial infarction, the added risk of silent myocardial ischemia warrants a more aggressive approach.

Coronary Disease↗
PubMed1987

Role of nitrates in silent myocardial ischemia.

Assessment of systemic and coronary hemodynamics, myocardial metabolic and mechanical function and scintigraphic and electrocardiographic studies has provided ample evidence for the existence of asymptomatic silent myocardial ischemia in both acute and chronic coronary artery syndromes. There is growing evidence to suggest that a primary decrease in coronary blood flow, resulting from increased coronary arterial resistance, is the principal cause for spontaneous symptomatic and asymptomatic myocardial ischemia in these patients. The precise mechanism for increased coronary arterial resistance has not been clarified, and it is likely to be different in different angina syndromes but similar for both symptomatic and asymptomatic myocardial ischemia. Since nitroglycerin and nitrates can decrease coronary arterial tone and coronary artery resistance, as well as myocardial oxygen requirements, these agents have the potential to relieve episodes of silent myocardial ischemia in patients with coronary artery syndromes.

Angina Pectoris↗
PubMed1987

Potential mechanisms of improved left ventricular function with enoximone in severe congestive heart failure.

Enoximone, a phosphodiesterase inhibitor, is a potent inotropic vasodilator agent that causes a marked improvement in systemic hemodynamics in patients with severe chronic congestive heart failure. Cardiac index, stroke volume index and stroke work index increase, and there is a significant decrease in pulmonary capillary wedge pressure. Left ventricular dP/dt increases, despite a decrease in arterial pressure and systemic vascular resistance and without any significant change in heart rate, indicating a positive inotropic effect. A marked decrease in systemic vascular resistance indicates that decreased left ventricular outflow resistance resulting from peripheral vasodilation also contributes to improvement in left ventricular function. In some patients, left ventricular end-diastolic volume increases despite a marked decrease in pulmonary capillary wedge pressure, suggesting an improvement in apparent left ventricular compliance, which may also be contributory to improved left ventricular function.

Cardiotonic Agents↗
PubMed1987

Calcium antagonist agents in hypertrophic cardiomyopathy.

Calcium antagonists have emerged as important adjuncts to pharmacotherapy of hypertrophic cardiomyopathy. Calcium antagonists cause significant symptomatic improvement in both obstructive and nonobstructive forms and even in patients refractory to beta-blocker therapy. Exercise hemodynamics and exercise tolerance improve in the majority of patients during long-term therapy with calcium antagonists. Reduction in left ventricular (LV) outflow pressure gradient is not consistent after short- or long-term therapy. The provokable gradient tends to remain unchanged. The changes in LV outflow gradient do not appear to be contributory to symptomatic improvement. LV ejection fraction, mean normalized systolic ejection rate and end-systolic pressure volume ratio remain unchanged, suggesting that calcium antagonists agents do not alter LV systolic function. LV diastolic function and its relaxation properties, however, improve in many patients, which might be contributory to symptomatic improvement and improved exercise tolerance.

Calcium Channel Blockers↗
PubMed1987

Measurement of left ventricular stroke volume using continuous wave Doppler echocardiography of the ascending aorta and M-mode echocardiography of the aortic valve.

A number of reports have described different Doppler echocardiographic methods to calculate left ventricular stroke volume and cardiac output, but the clinical application of the noninvasive measurements of cardiac function remains in the early stages of development. This slow dissemination may be partly explained by the varying success of these ultrasound methods in determining accurate left ventricular stroke volume. The purpose of this study was to improve the simplicity and accuracy of Doppler stroke volume determination so that it could be more easily applied to patient management. Stroke volume was measured using the product of the integral of aortic velocity obtained by continuous wave Doppler technique and the M-mode tracing of the aortic valve, validating the data against cardiac output obtained by thermodilution technique in 41 patients (r = 0.95, SEE = 7 cc). Intra- and interobserver variability was between 9 and 11%. The results of different sampling sites and the temporal relation between Doppler and thermodilution measurements were also studied. Analysis of 21 patients who had M-mode and two-dimensional echocardiographic studies of the aortic root revealed that the method using M-mode measurement of aortic valve area was most accurate in determining left ventricular stroke volume (r = 0.94, SEE = 10 cc), stroke volume being overestimated when area measurements of the ascending aorta were used. In conclusion, maximal ascending aortic velocity determined by continuous wave Doppler echocardiography with M-mode measurement of aortic valve area can be used to calculate left ventricular stroke volume and cardiac output. The simplicity and practicality of this method should enhance the clinical application of Doppler echocardiography as a noninvasive monitoring technique.

Adult↗
PubMed1987

Hemodynamic and clinical evaluation of piroximone, a new inotrope-vasodilator agent, in severe congestive heart failure.

To assess the potential utility of piroximone (MDL-19,205), an investigational inotrope-vasodilator agent, in severe heart failure, 15 patients with severe left ventricular failure refractory to conventional agents were enrolled in an acute hemodynamic study. After incremental intravenous dosing (mean total dose 1.8 +/- 0.4 mg/kg body weight), cardiac index increased (1.7 +/- 0.3 to 2.6 +/- 0.6 liters/min per m2; p less than 0.001) and left ventricular filling pressure decreased (25 +/- 7 to 19 +/- 7 mm Hg; p less than 0.001). Also decreasing significantly were right atrial pressure (13 +/- 6 to 7 +/- 5 mm Hg; p less than 0.005) and systemic vascular resistance (1,633 +/- 394 to 1,183 +/- 278 dynes.s.cm-5; p less than 0.001). Heart rate and mean arterial pressure did not change, whereas stroke work index increased significantly (13.3 +/- 4.3 to 21.6 +/- 7.3 g.m/m2; p less than 0.005). The increase in stroke work index with a concomitant decrease in left ventricular filling pressure indicates an improvement in systolic performance after treatment with piroximone. Similar responses were obtained after incremental doses of piroximone in oral solution. After oral doses of piroximone tablets, cardiac index also increased significantly (2.1 +/- 0.6 to 2.4 +/- 0.5 liters/min per m2; p less than 0.05), although this magnitude of increase was comparatively low. In a subgroup of 10 patients who underwent equilibrium gated radionuclide blood pool scintigraphy before and after intravenous piroximone, end-diastolic volume index tended to increase (106 +/- 42 to 132 +/- 60 ml/m2; p = 0.07), whereas left ventricular filling pressure decreased significantly (26 +/- 8 to 19 +/- 9 mm Hg; p less than 0.01).

Aged↗
PubMed1987

Enalaprilat, a new parenteral angiotensin-converting enzyme inhibitor: rapid changes in systemic and coronary hemodynamics and humoral profile in chronic heart failure.

Systemic and coronary hemodynamic, metabolic and humoral effects of a new intravenous angiotensin-converting enzyme inhibitor, enalaprilat, were evaluated in 14 patients with chronic heart failure. Onset of hemodynamic action occurred within 15 minutes and persisted for 6 hours. At the time of peak effect, there was a significant reduction in mean arterial pressure (-21%) and pulmonary capillary wedge pressure (-33%). Systemic vascular resistance decreased by 32% and stroke volume index increased by 20%. These systemic hemodynamic changes indicate improved left ventricular function. There was a substantial sustained reduction in rate-pressure product initially without a change in coronary sinus blood flow or myocardial oxygen consumption. There was also reduced myocardial oxygen extraction and augmented coronary sinus oxygen saturation at 30 minutes and 1 hour. In three patients, abnormal myocardial lactate extraction, present before enalaprilat, changed to uptake after enalaprilat, indicating amelioration of myocardial ischemia that was not clinically manifest. Systemic catecholamine levels and myocardial catecholamine balance did not change. Plasma renin activity increased and plasma aldosterone decreased. These findings suggest that enalaprilat produces inhibition of the angiotensin-converting enzyme and consequent beneficial systemic hemodynamic changes in heart failure. In some patients with heart failure, silent myocardial ischemia at rest can occur and can be alleviated with enalaprilat. Decreased myocardial oxygen extraction, increased coronary sinus oxygen saturation and lack of expected decrease in coronary sinus blood flow despite reduced rate-pressure product suggest transient coronary vasodilation by enalaprilat.

Aged↗
PubMed1987

Survival in severe left ventricular failure treated with the new nonglycosidic, nonsympathomimetic oral inotropic agents.

Survival in severe left ventricular failure is poor but has not been widely assessed since the introduction of several new nonglycosidic, nonsympathomimetic oral inotropic agents for long-term therapy. We examined retrospectively the survival of 82 patients with severe left heart failure during long-term treatment with oral milrinone (17 patients), posicor (12 patients), enoximone (47 patients), and piroximone (6 patients). Sixty-five patients were in New York Heart Association (NYHA) functional class 4, 15 patients were in class 3, and two patients were in class 2. There were 57 patients with ischemic and 25 patients were in class 2. There were 57 patients with ischemic and 25 patients with nonischemic etiology of left heart failure. Most patients were referred for inotropic therapy after failing to respond to conventional agents, including vasodilators. However, in almost all patients, marked hemodynamic and clinical improvement occurred initially. Overall survival was 36 percent at six months, the majority of deaths occurring during the first three months. Survival in relation to etiology of heart failure showed a trend toward increased mortality in patients associated with ischemic heart disease vs non-ischemic dilated cardiomyopathy. Sudden death mortality was also higher in the ischemic group (28 percent at six months vs 5 percent at six months; p less than 0.05). There was a trend toward reduced sudden death mortality in patients on antiarrhythmic agents during inotropic therapy (p = 0.06). We conclude that overall survival in symptomatic patients with severe left ventricular failure remains very low during long-term therapy with several new oral inotropic agents. Sudden death appears higher in patients with an ischemic etiology during therapy with these agents.

Administration, Oral↗