Search PubMed⌕ Search

Biomedical subjects

K Chatterjee

Publications and source records attributed to K Chatterjee.

At least 37 records · Page 2Linked to original sources
PubMed1989

Long-term predictors of sudden and low output death in chronic congestive heart failure secondary to coronary artery disease.

Clinical, hemodynamic and neurohumoral variables in 238 patients with chronic congestive heart failure (CHF) secondary to coronary artery disease were analyzed to determine potential predictors of mortality in a large population and to allow analysis according to mode of death (sudden or low output death). All variables were assessed before initiation of treatment with vasodilators (converting enzyme inhibitors, direct acting vasodilators) or with the nonglycoside, noncatecholamine class of inotropic agents. Survival outcome was determined as alive, sudden death or low output death. When all variables except ejection fraction were analyzed by Cox multiple regression analysis, the most important independent predictor of all deaths was the baseline plasma renin activity (p less than 0.001). When subdivided by cause of cardiovascular death, baseline plasma renin activity was retained as the most important determinant of low output death (p less than 0.001), whereas baseline left ventricular stroke work index (p less than 0.001), pulmonary capillary wedge pressure (p less than 0.002) and absence of sinus rhythm (p less than 0.006) were the most powerful independent predictors of sudden death. Plasma norepinephrine was markedly elevated in the group dying of low output, but only modestly elevated in the group of survivors and the group dying suddenly. However, baseline norepinephrine was not found to be an important independent predictor of mortality in any of the subgroups. Plasma renin activity, but not plasma norepinephrine, is a powerful independent prognostic determinant of mortality in this group of patients with CHF.

Adult↗
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↗
PubMed1979

Reduction in ventricular endocardial and epicardial potentials during acute increments in left ventricular dimensions.

Unipolar potentials were recorded from the endocardium (Endo-Pot) and the epicardium (Epi-Pot) of the left and right ventricles of anesthetized open-chested dogs during acute changes in left ventricular dimension by blood transfusion. A pair of implanted ultrasonic crystals were used to detail changes in left ventricular (LV) anteroposterior diameter. When the diameter increased by an average of 11 per cent, LV Endo-Pot decreased by 28 per cent and LV Epi-Pot decreased by 15 per cent. Right ventricular Endo-Pot and Epi-Pot concurrently decreased by similar magnitude (-36 per cent). The relationship between potentials and LV diameter showed negative linearity over the ranges examined, and was not influenced by changes in hematocrit. No inverse relation between changes in Endo-Pot and Epi-Pot was observed. It is suggested that potentials when recorded directly from the endocardium or epicardium mainly reflect the electrical activity of the tissues in the immediate vicinity of the electrode. It is postulated that an increase in ventricular volume by producing stretching and thinning of ventricular walls, reduces the effective tissue mass represented in the electrode signal, thereby accounting for a reduction in both endo and epicardial potentials. Although the precise mechanisms of changes in ventricular potentials remains unclear, such changes, nevertheless, may indicate, in clinical circumstances, an acute shift in left ventricular volume.

Action Potentials↗
PubMed1979

The influence of left ventricular filling pressure on atrial contribution to cardiac output.

The influence of left ventricular filling pressure on the atrial contribution filling pressure and atrial contribution was seen in studies done at baseline (PCW (r=-.53, p less than .025), as well as in studies done after PCW was modified by volume expansion and/or nitrates (r=-.53, p less than .005). At baseline, atrial contribution averaged 9.3 +/- 1.3 c.c./M.2 in patients with PCW less than 20 mm. Hg, while it was only 2.4 +/- 1.2 c.c./M.2 in patients with PCW greater than or equal to 20 mm. Hg (p less than .005). Atrial contribution was significantly greater in patients who had no history of heart failure when they were volume loaded to a PCW above 20 mm. Hg than in patients with impaired ventricular function whose baseline PCW was above 20 mm. Hg. Thus, atrial contribution tends to be less effective in augmenting cardiac output when filling pressure is already elevated, particularly in patients with impaired left ventricular function.

Adolescent↗
PubMed1979

Paradox of improved exercise but not resting hemodynamics with short-term prazosin in chronic heart failure.

In patients with chronic heart failure exercise allows the simultaneous observation of the cardiovascular pathophysiology and the symptoms of these patients. We administered short-term, oral prazosin to 10 patients with severe chronic heart failure. Prazosin increased cardiac output and stroke volume significantly during exercise (both P less than 0.05) but not at rest (both P greater than 0.10). Prazosin decreased the arteriovenous oxygen difference and left ventricular filling pressure significantly during exercise (both P less than 0.05) but not at rest (both P greater than 0.10). There was no significant correlation between prazosin-induced changes at rest and during exercise in cardiac output (r = 0.12), stroke volume (r = 0.02), arteriovenous oxygen difference (r = 0.33) or left ventricular filling pressure (r = 0.43). Prazosin predominantly affects hemodynamics during exercise because its pharmacologic activity as an alpha-adrenergic blocking agent is most prominent during exercise. The full evaluation of prazosin-induced changes in the hemodynamics of patients of patients with chronic heart failure requires evaluation during exercise.

Aged↗
PubMed1979

Detection of left ventricular functional reserve by supine exercise hemodynamics in patients with severe, chronic heart failure.

Hemodynamic changes during exercise were evaluated in 20 patients with severe, chronic congestive heart failure. Two groups were identified by their stroke work response to maximal exercise. Group I (eight patients) showed an increase in stroke work index. This occurred because the stroke volume increased and the difference between mean systolic pressure and left ventricular filling pressure increased. Group II (12 patients) showed a decrease in stroke work index. This occurred because stroke volume decreased while the difference between mean systolic pressure and left ventricular filling pressure did not change. Despite hemodynamic differences, the groups could not be distinguished by the usual clinical criteria for heart failure including etiology, New York Heart Association functional class, heart size on chest X-ray film or duration of heart failure. Clinical criteria are relatively insensitive in predicting the exercise hemodynamics of any given patient with chronic severe heart failure. Determining the exercise hemodynamics may be helpful as a means of assessing left ventricular functional reserve in heart failure. Prognostic implications, drug therapy and prescription of activities may require adjustment based on this spectrum of hemodynamic response to exercise in patients with chronic heart failure.

Adult↗
PubMed1979

Influence of short-term oral hydralazine therapy on exercise hemodynamics in patients with severe chronic heart failure.

Changes in left ventricular performance were evaluated in 14 patients with functional New York Heart Association class III or IV chronic heart failure before and after the addition of oral hydralazine to conventional therapy. With conventional therapy, cardiac output increased from 3.4 +/- 0.8 (mean +/- 1 standard deviation) at rest to 4.7 +/- 1.4 liters/min during exercise. This increase in cardiac output on exercise during conventional therapy was mainly due to an increase in heart rate. After the addition of hydralazine, cardiac output at rest increased to 5.0 +/- 1.4 liters/min. The increase in cardiac output was essentially due to an increase in stroke volume. This enhanced stroke volume after hydralazine therapy was maintained during exercise. Hydralazine therapy did not change either the left ventricular filling pressure at rest or the magnitude of increase in left ventricular filling pressure during exercise. Nevertheless, increased cardiac output and stroke volume with similar changes in left ventricular filling pressure during exercise indicated improved left ventricular performance after hydralazine therapy. After short-term hydralazine therapy, symptom-limited peak exercise work load, duration of exercise and maximal oxygen consumption during exercise did not increase. Clinical follow-up at 2 months after long-term therapy revealed subjective improvement in exercise tolerance in 13 of the 14 patients.

Administration, Oral↗
PubMed1979

Lack of correlation between echocardiographic pulmonary valve morphology and simultaneous pulmonary arterial pressure.

Pulmonary valve echograms recorded simultaneously with right heart pressures were correlated with mean and end-diastolic pulmonary arterial pressures and the peak magnitude of the right atrial a wave in an attempt to predict noninvasively levels and changes in pulmonary arterial pressure. Satisfactory pulmonary valve echograms were obtained in 16 of 23 patients studied. No significant correlation was found between hemodynamic measurements and the echographic pulmonary valve a wave amplitude, diastolic E-F slope or the systolic opening B-C slope. Changes in hemodynamic measurements observed in serial observations were not associated with predictable changes in configuration of the pulmonary valve echogram. The combination of mid systolic pulmonary valve notching and an absent a wave was observed in more advanced degrees of pulmonary hypertension and was specific, but not sensitive, for that condition.

Adult↗