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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
PubMed1989

Congestive heart failure--advances in treatment. Hemodynamic studies--their uses and limitations.

Hemodynamic studies are useful in the diagnosis of the pathophysiologic mechanisms of pump failure and low output state in patients with acute heart failure. Hemodynamic monitoring is extremely useful for the appropriate manipulation of the vasoactive drugs to optimize hemodynamic and clinical improvement of patients with acute heart failure and to stabilize patients with severe refractory or unstable chronic heart failure. Determinations of the hemodynamic indexes of left ventricular function during hemodynamic studies also provide information regarding prognosis of patients with acute or chronic heart failure. In patients with stable chronic heart failure, correlations between the changes in hemodynamics after initiation of vasodilator therapy and subsequent changes in the clinical status and exercise tolerance are poor; thus, the value of hemodynamic studies for vasodilator therapy in patients with stable chronic heart failure is limited.

Acute Disease↗
PubMed1989

Phosphodiesterase inhibitors: alterations in systemic and coronary hemodynamics.

This paper reviews the effect on myocardial contractility, left ventricular afterload and left ventricular distensibility induced by the following phosphodiesterase inhibitors: Enoximone, piroximone, RO 13-6438, amrinone and milrinone. For all these compounds, direct positive inotropic effects have been shown in experimental studies. For amrinone and milrinone, a direct stimulating effect on myocardial contractility has been demonstrated by an increase in dP/dtmax when intracoronary applications of the compounds were performed. A direct stimulating effect on the myocardium was also demonstrated for enoximone and piroximone by analyzing the systolic pressure versus end-systolic volume ratio. For all of the phosphodiesterase inhibitors, a marked decrease of systemic vascular resistance has been observed indicating direct peripheral vasodilation. Although it has been demonstrated that phosphodiesterase inhibition increases left ventricular distensibility, the nature of this effect is not clear. For most of the phosphodiesterase inhibitors an increase in myocardial oxygen requirements was demonstrated due to overall contractility increase. However, these phosphodiesterase inhibitors induce increased coronary blood flow in excess so that a direct effect of these compounds on the coronary vasculature has been postulated. The clinical significance of such changes, however, remains unclear.

Coronary Circulation↗
PubMed1989

Long-term clinical results after vasodilator evaluation in patients with primary (unexplained) and secondary precapillary pulmonary hypertension: acute hemodynamic comparisons and long-term survival.

Acute hemodynamic and long-term clinical effects of 6 different vasodilators (oxygen, isoproterenol, isosorbide, phentolamine, diazoxide, and hydralazine) were evaluated in 16 consecutive patients with precapillary pulmonary hypertension. Acute symptomatic and quantitative hemodynamic responses to different vasodilators in different patients were nonuniform and unpredictable. For the whole patient group, cardiac outputs increased slightly after all drugs except oxygen. Mean pulmonary pressure decreased after oxygen and increased after isoproterenol. In general, the hemodynamic effects of vasodilators in primary and secondary precapillary pulmonary hypertension were similar. In 10 patients, an acute increase in cardiac output (4.4 to 5.4 l/min, P less than 0.005) was associated with a small but significant decrease in the mean pulmonary artery pressures (59 to 53 mm Hg, P less than 0.05) after one of the oral vasodilators, and continued treatment with this drug transiently decreased symptoms in 6 of these 10 patients. However, only 1 patient could be continued on treatment beyond 5 months. Long-term survival was related to initial New York Heart Association Functional Class (P less than 0.02) and the initial cardiac output (r2 = 0.84, P less than 0.002). Patient stratification according to these variables may be useful in future clinical trials treating patients with precapillary pulmonary hypertension.

Adult↗
PubMed1989

Metabolic and hemodynamic consequences of sodium bicarbonate administration in patients with heart disease.

PURPOSE: The use of sodium bicarbonate (NaHCO3) in cardiopulmonary arrest has been questioned, but the effects of NaHCO3 in patients with heart disease are not known. We therefore prospectively evaluated the effects of NaHCO3 in patients with congestive heart failure. PATIENTS AND METHODS: Ten patients received NaHCO3 and control infusions of equimolar sodium chloride (NaCl). Measurements were made of blood gases, 2,3-diphosphoglyceric acid (2,3-DPG), glucose, lactate, cardiac hemodynamics, and oxygen consumption. RESULTS: The arterial oxygen tension (pO2) fell an average of 10 mm Hg after NaHCO3 administration in patients with congestive heart failure, whereas it rose with NaCl (p less than 0.005). Myocardial oxygen consumption decreased by 17% (p less than 0.002) without an accompanying change in oxygen demand. Systemic oxygen consumption fell by 21%. Red blood cell 2,3-DPG levels were elevated at baseline, but did not change with NaHCO3 administration. The oxygen pressure at 50% hemoglobin saturation (P50) was correspondingly elevated at baseline in these patients and decreased significantly with NaHCO3 (Bohr effect) (p less than 0.003). The arterial and mixed venous carbon dioxide tensions increased with NaHCO3 but decreased with NaCl administration (p less than 0.05). Blood glucose concentrations fell by 1.7 mmol/L with NaHCO3 (p less than 0.003) and blood lactate concentrations increased uniformly (p less than 0.001). Three patients developed net myocardial lactate generation during NaHCO3 administration; two of these three developed symptoms of angina. Coronary blood flow did not change with NaHCO3 but increased with NaCl (p less than 0.04). Two patients developed transient pump failure. CONCLUSION: These data demonstrate that NaHCO3 impairs arterial oxygenation and reduces systemic and myocardial oxygen consumption. The decrease in oxygen utilization is associated with anaerobic metabolism, enhanced glycolysis, and elevation of the blood lactate level, and may lead to transient myocardial ischemia in some patients. Thus, the use of NaHCO3 in such patients warrants re-evaluation.

Aged↗
PubMed1989

Central and peripheral adrenergic receptor agonists in heart failure.

The subtypes of alpha- and beta- and dopaminergic receptors have been identified along with specific agonists and antagonists. The effects of alpha-receptor agonists on haemodynamics results from the interaction of relative changes in vascular tone and increase in myocardial contractility. Predominantly, beta 1 agonists improve cardiac performance by increasing contractility which is usually accompanied by increased myocardial oxygen consumption. Dopaminergic receptor agonists improve left ventricular function primarily by reduction in systemic vascular resistance usually without a change in myocardial oxygen consumption. beta 2-receptor agonists improve cardiac function both by increasing contractility and by peripheral vasodilation usually without an increase in metabolic cost. The effects of various adrenoreceptor agonists such as dobutamine, dopamine, prenalterol, levodopa and dopexamine on systemic and coronary haemodynamics and on myocardial energetics in heart failure are reviewed.

Adrenergic alpha-Agonists↗
PubMed1989

Potential use of third-generation beta-blockers in heart failure.

Elevated systemic vascular resistance in heart failure causes further depression of cardiac function. Decreased systemic vascular resistance, on the other hand, is associated with an improvement in cardiac performance. Thus, peripheral vasodilators, irrespective of their mechanism of action, have the potential to improve cardiac function in heart failure. Increased peripheral vascular tone appears to result from a number of interrelated neuroendocrine dysfunctions--an activated renin-angiotensin-aldosterone system, inappropriate release of arginine vasopressin, and enhanced systemic and cardiac sympathetic activity (indicated by increased levels of circulating norepinephrine and markedly increased cardiac norepinephrine release). Augmented sympathetic activity may not only increase systemic vascular resistance but can also induce myocardial cellular dysfunction. Furthermore, downregulation of cardiac beta-adrenoceptors may contribute to inadequate cardiac performance. Reduction of sympathetic tone and upregulation of the beta-adrenoceptors is the rationale for beta-blocker therapy in heart failure and, indeed, cardioselective beta-blockers improve cardiac function in some patients with dilated cardiomyopathy. Third-generation beta-blockers, such as celiprolol, possess both cardioselective and peripheral vasodilatory properties and are therefore potentially beneficial in heart failure.

Adrenergic beta-Antagonists↗
PubMed1989

Digitalis and non-ACE inhibitor vasodilators in heart failure.

Digitalis therapy is usually ineffective in heart failure complicating myocardial infarction but may be of benefit in some selected patients with chronic heart failure. However, digitalis therapy in the long-term should be considered in conjunction with vasodilators or ACE inhibitors. This article reviews the practical and clinical aspects of vasodilator and digitalis therapy.

Angiotensin-Converting Enzyme Inhibitors↗
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↗