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Biomedical subjects

K Chatterjee

Publications and source records attributed to K Chatterjee.

At least 145 records · Page 8Linked to original sources
PubMed1985

Milrinone in congestive heart failure: acute and chronic hemodynamic and clinical evaluation.

Acute and chronic hemodynamic and clinical responses to milrinone, a new oral inotrope-vasodilator agent, were evaluated prospectively in 37 patients with severe congestive heart failure. The majority of patients (n = 31) had not responded to prior vasodilator therapy, with a substantial number (n = 8) requiring intravenous inotropic support at the time of initial study. All patients showed acute hemodynamic improvement with oral milrinone, and an optimal maintenance dose was chosen for each patient during dose-ranging studies (average dose 48 mg/day). Milrinone was discontinued before follow-up hemodynamic study in 12 patients (because of worsening congestive heart failure in 6 patients, sudden death in 3 patients, arrhythmia in 1 patient and refusal by 2 patients). Hemodynamic effects of milrinone both acutely and after chronic therapy (average 37 days) were compared in the remaining 25 patients. Acutely, mean cardiac index increased from 1.9 +/- 0.5 to 2.5 +/- 0.5 liters/min per m2 (p less than 0.001), and mean pulmonary capillary wedge pressure decreased from 28 +/- 9 to 18 +/- 8 mm Hg (p less than 0.001). When oral milrinone was readministered after chronic therapy, mean cardiac index increased from 1.9 +/- 0.5 to 2.5 +/- 1.7 liters/min per m2 (p less than 0.001), and pulmonary capillary wedge pressure decreased from 27 +/- 8 to 20 +/- 8 mm Hg (p less than 0.001) at 1 hour. New York Heart Association functional class improved in 18 of the 25 patients treated over a long-term period (mean 5.5 +/- 2.3 months).(ABSTRACT TRUNCATED AT 250 WORDS)

Actuarial Analysis↗
PubMed1985

Detection and characterization of acute myocardial infarction in man with use of gated magnetic resonance.

To evaluate the capability of magnetic resonance imaging (MRI) in the detection and characterization of alterations in signal intensity and T2 relaxation time in acutely infarcted relative to normal myocardium 16 adult patients and normal volunteers were studied by electrocardiographically gated proton MRI. The seven volunteers were entirely asymptomatic and had no history of cardiovascular abnormality. The nine patients had each suffered an acute myocardial infarction within 5 to 12 days before the MRI studies. The diagnosis in each patient was confirmed by electrocardiographic (ECG) criteria and elevated levels of fractionated creatine kinase (CK) isoenzymes. Electrocardiographically gated MRI was performed with a superconducting system operating at 0.35 tesla. MRI demonstrated infarcted myocardium as a region of high signal intensity relative to that of adjacent normal myocardium; regions of high intensity corresponded anatomically to the site of infarction as defined by the ECG changes. The mean percent difference between normal and infarcted myocardium was substantially greater on 56 msec images (70.2 +/- 21.3%) compared with 28 msec images (27.1 +/- 13.6%). Region of interest analysis revealed that infarcted myocardium had a significantly (p less than .01) prolonged T2 relaxation time (mean T2 = 80.9 msec) relative to that in normal myocardium (mean T2 = 42.3 msec) and relative to the mean T2 of left ventricular myocardium in the volunteers (mean T2 = 42.4 msec). An additional finding for each patient with myocardial infarction was a high intraluminal flow signal on 56 msec images, but this was also observed in normal subjects and is therefore a nonspecific finding.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1985

Bedside hemodynamic monitoring in the cardiac care unit.

Bedside hemodynamic monitoring provides useful information regarding the differential diagnosis of the various pathologic mechanisms of low output syndrome. It also allows recognition of hemodynamic subsets of patients with acute myocardial infarction. Furthermore, hemodynamic monitoring is necessary for prompt evaluation of the response to therapeutic interventions in patients with low output syndrome. In patients with acute myocardial infarction, hemodynamic indices can also be used for evaluation of immediate prognosis. Because bedside hemodynamic monitoring is relatively safe, and with proper precautionary measures the potential complications can be avoided, hemodynamic monitoring should be considered in the management of all critically ill cardiac patients.

Coronary Care Units↗
PubMed1985

Recent advances in the management of chronic heart failure.

A number of newer therapeutic agents are available for the treatment of refractory heart failure. These agents possess either vasodilating, positive inotropic, or combined vasodilating and inotropic properties. In appropriate subsets of patients, these agents have the potential to produce clinical improvement and improvement in cardiac function.

Calcium Channel Blockers↗
PubMed1985

Myocardial infarction shock.

Shock syndrome results from severe depression of cardiac function due to loss of a large mass of functioning myocardium. The resulting hemodynamic abnormalities need to be monitored for appropriate therapy.

Combined Modality Therapy↗
PubMed1984

Value of noninvasive assessment of patients with atypical chest pain and suspected coronary spasm using ergonovine infusion and thallium-201 scintigraphy.

Twenty-six patients with known benign coronary anatomic characteristics and atypical chest pain syndromes were evaluated for the possibility of coronary spasm. Incremental intravenous ergonovine maleate infusions were administered, and thallium-201 scintigraphy was performed at the peak dosage and during recovery in the coronary care unit. With ergonovine therapy, 4 patients (16%) had chest pain associated with electrocardiographic (ECG) or scintigraphic changes. Nine patients (35%) had chest pain without associated ECG or scintigraphic changes, and 13 patients did not have chest pain in response to ergonovine administration, although 2 (8%) had ergonovine-induced scintigraphic defects. All 4 patients with ergonovine-induced chest pain and associated ECG or scintigraphic abnormalities had resolution or reduction of chest pain after medical treatment. However, 7 of the 9 patients with ergonovine-induced chest pain in the absence of ECG or scintigraphic abnormalities continued to have symptoms despite medical treatment a mean of 18 months later. In this limited study of a select group, bedside ergonovine provocation appeared safe. Many patients had chest pain, but few showed ECG or scintigraphic evidence of ischemia. Perfusion scintigraphy appears to have potential complementary value for the identification of an ischemic cardiac cause of atypical chest pain and provides a rationale for appropriate therapy.

Adolescent↗
PubMed1984

Comparison of myocardial catecholamine balance in chronic congestive heart failure and in angina pectoris without failure.

To evaluate myocardial catecholamine balance in heart failure, systemic hemodynamics, coronary sinus blood flow, and arterial and coronary sinus venous norepinephrine (NE) and epinephrine (E) concentrations were determined in 30 patients with chronic left ventricular failure (CHF), and in 25 patients with angina pectoris (AP) but without heart failure. In the group with CHF, stroke work index was lower (CHF 20 +/- 9, AP 53 +/- 13 g-m/m2, p less than 0.001) and pulmonary capillary wedge pressure higher (CHF 28 +/- 8, AP 11 +/- 4 mm Hg, p less than 0.001), indicating depressed left ventricular function. Coronary sinus blood flow was similar in 2 groups (CHF 97 +/- 70, AP 73 +/- 32 ml/min, difference not significant). In the group with CHF, arterial (634 +/- 582 pg/ml) and coronary sinus venous (1,038 +/- 1,014 pg/ml) NE concentrations were significantly higher than in the group with AP (arterial 185 +/- 135, coronary sinus 231 +/- 167 pg/ml, p less than 0.001). The net myocardial NE release in patients with CHF was approximately 20 times higher than that in patients with AP (CHF 38,548 +/- 48,622, AP 2,245 +/- 10,242 pg/min, p less than 0.001). Arterial E and myocardial E uptake was similar in both groups. Although mechanisms for increased myocardial net NE release remains unknown, it probably represents enhanced cardiac sympathetic tone in response to heart failure.

Adult↗
PubMed1984

Mechanisms of improved left ventricular function following intravenous MDL 17,043 in patients with severe chronic heart failure.

To evaluate the mechanisms for improved left ventricular function with MDL 17,043 in patients with severe chronic heart failure, 24 patients were evaluated by simultaneous determination of hemodynamics by right heart catheterization and ejection fraction by computerized nuclear probe before and following intravenous administration of MDL 17,043 (mean cumulative dose 3.6 mg/kg). Following MDL 17,043, there was an increase in cardiac index (+62%), stroke volume index (+42%), and stroke work index (+68%), together with a decrease in pulmonary capillary wedge pressure (-46%), indicating improved left ventricular pump function. There was a marked reduction in systemic vascular resistance (-40%) and a modest reduction in arterial pressure, indicating decreased left ventricular outflow resistance. The ratio of peak systolic blood pressure to calculated left ventricular end-systolic volume tended to increase, but the change was not statistically significant. Despite a marked increment in stroke volume index, left ventricular ejection time corrected for heart rate was shortened, suggesting enhanced contractility. In the group as a whole, the calculated left ventricular end-diastolic volume remained unchanged, but it increased in 14 patients. Since pulmonary capillary wedge pressure fell in each patient, this suggests improved overall left ventricular distensibility. Thus, decreased left ventricular outflow resistance, and possibly increased contractile function, and improved left ventricular diastolic compliance may all contribute to improved left ventricular pump function with MDL 17,043 in patients with severe heart failure.

Aged↗
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↗