PubMed Health⌕ Search

Biomedical subjects

K Chatterjee

Publications and source records attributed to K Chatterjee.

At least 145 records · Page 8Linked to original sources
PubMed1986

Pharmacokinetics of the bipyridines amrinone and milrinone.

The pharmacokinetics of milrinone were studied in sequential ascending doses in New York Heart Association Class III and IV patients receiving oral and intravenous medication. The parameters determined after parenteral administration were estimated by fitting the plasma concentration data to an open two-compartment body model. After oral medication, regression-independent parameters were determined. After either oral or parenteral administration of milrinone, plasma levels were dose dependent and the drug had an apparent first-order terminal elimination half-life of approximately 2 hr. The apparent volume of distribution was approximately 400 to 500 ml/kg, and total body clearance was approximately 130 ml/kg/hr. These values obtained in patients receiving milrinone were compared with those obtained for milrinone in volunteers, as well as those noted with the other inotropic bipyridine, amrinone. Milrinone's elimination from the blood stream patients was slower that that in normal healthy subjects and faster than amrinone's elimination in patients with congestive heart failure. Milrinone's pharmacokinetic parameters in these patients were unchanged after approximately 30 days of continuous oral medication.

Administration, Oral↗
PubMed1985

RO13-6438, a new inotrope-vasodilator: systemic and coronary hemodynamic effects in congestive heart failure.

Systemic and coronary hemodynamics and transmyocardial norepinephrine release were determined before and after oral administration of RO13-6438, a new inotrope-vasodilator agent, in 12 patients with severe chronic heart failure unresponsive to conventional and vasodilator therapy. Improvement in left ventricular (LV) function was evident from a marked increase in cardiac index (from 2.09 +/- 0.45 to 3.30 +/- 0.73 liters/min/m2, p less than 0.01), stroke volume index (from 23 +/- 7 to 36 +/- 11 ml/m2, p less than 0.01), and stroke work index (from 23 +/- 11 to 36 +/- 14 g-m/m2, p less than 0.01), and concomitant fall in pulmonary capillary wedge pressure (from 26 +/- 7 to 16 +/- 8 mm Hg, p less than 0.01). Myocardial oxygen consumption did not change significantly (from 15.3 +/- 6.8 to 14.9 +/- 6.8 ml/min), but the ratio of minute work/myocardial oxygen consumption, an index of LV efficiency, increased significantly (p less than 0.05). Although average coronary sinus flow did not change, coronary sinus oxygen increased (from 3.2 +/- 0.8 to 4.2 +/- 1.5 vol%, p less than 0.05), and arterial-coronary sinus oxygen difference decreased (from 11.8 +/- 2.1 to 10.4 +/- 1.9 vol%, p less than 0.05), suggesting a primary vasodilating effect of RO13-6438 on the coronary vascular bed. Net transmyocardial norepinephrine release did not change despite the marked hemodynamic improvement. These findings suggest that RO13-6438 has the potential to cause marked improvement in LV function and LV efficiency in patients with severe, refractory congestive heart failure.

Adult↗
PubMed1985

Magnetic resonance imaging in hypertrophic cardiomyopathy.

Gated magnetic resonance imaging (MRI) was performed using a 0.35-Tesla cryogenic system in 14 patients with hypertrophic cardiomyopathy (HC) in order to define the site and extent of abnormal wall thickness. These studies were compared with 2-dimensional (2-D) echocardiograms. Gated magnetic resonance imaging studies in 12 normal volunteers were used for comparison. In normal subjects and in patients with HC, the sharp demarcation of the myocardial wall permitted measurement of wall thickness. The thickness of the septal and posterolateral walls in normal subjects was 10.2 +/- 0.4 mm (+/- standard deviation) and 10.8 +/- 0.5 mm, respectively, whereas septal thickness in all but 1 patient with HC was 15.0 mm or greater. In patients with HC, septal and posterolateral wall thickness were 2.2 +/- 0.8 cm and 1.3 +/- 0.17 cm, respectively, by MRI. The 2-D echocardiographic measurements for septal and posterolateral walls were 2.4 +/- 0.6 cm and 1.4 +/- 0.7 cm, respectively. The severity and distribution of abnormal wall thickness were comparable on 2-D echo and MRI. Gated MRI is an effective and completely noninvasive technique for demonstrating the presence, site and extent of abnormal wall thickness in HC. The large field of view, ability to image directly in multiple planes, and discrete blood-endocardial interfaces are advantages for cardiovascular imaging.

Adult↗
PubMed1985

Acute dose range study of milrinone in congestive heart failure.

To determine the magnitude and time course of the optimal acute hemodynamic response to oral milrinone, an ascending dose range study was performed in 34 patients with severe chronic congestive heart failure (2.5 to 10 mg, n = 21; 7.5 to 15 mg, n = 13). With the 7.5- and 10-mg doses in both groups, cardiac index increased 26%, pulmonary capillary wedge pressure decreased 25% and systemic vascular resistance decreased 20%, with peak effect at 90 minutes. The hemodynamic improvement with 10 mg was sufficient to normalize cardiac index in 29% of patients. There was a clear dose-response relation, with the largest increases of cardiac index seen with the 15-mg dose (1.67 +/- 0.10 to 2.31 +/- 0.11; p less than 0.005). This dose-response relation was confirmed by the correlation of drug levels and change in cardiac index. However, some patients had significant hypotension and tachycardia with the 15-mg dose. Thus, although 10 mg appears to be optimal for most patients, the dose of milrinone should be individualized for all patients.

Administration, Oral↗
PubMed1985

A cooperative multicenter study of captopril in congestive heart failure: hemodynamic effects and long-term response.

The acute hemodynamic effects, long-term clinical efficacy, and safety of the oral angiotensin-converting enzyme inhibitor, captopril, were assessed in a multicenter cooperative study of 124 patients with heart failure resistant to digitalis and diuretics. The cardiac status of most patients was deteriorating prior to the study. Favorable acute hemodynamic effects consistently occurred with captopril. Maximal mean percentage increases in cardiac index, stroke index, and stroke work index were, respectively, 35%, 44%, and 34%. Systemic and pulmonary vascular resistances were each decreased by approximately 40%, as were the filling pressures of the right and left heart. Infusion of nitroprusside in some of the same patients to an end point of a pulmonary capillary wedge pressure of 12 to 18 mm Hg (equivalent to that after captopril) revealed no significant difference in the effect of either drug on the other hemodynamic parameters. Recatheterization after 8 weeks of captopril therapy revealed sustained hemodynamic changes. Significant and sustained improvements in clinical status were observed in most patients as measured by changes in New York Heart Association (NYHA) functional classification and exercise tolerance times. Seventy-nine percent of patients for whom there were adequate NYHA class data improved. Twenty percent remained unchanged and 1% deteriorated. Those patients who had both pretreatment and post-treatment exercise stress testing exhibited a highly significant mean increase in exercise tolerance times of 34% (317 +/- 32 seconds pretreatment to 425 +/- 34 seconds, final measurement). There was no evidence of tachyphylaxis over an 18-month period.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1985

Myocardial catecholamine balance during angina: effects of calcium entry blockers, verapamil and nifedipine.

To evaluate the effects of calcium entry blocking agents on cardiac sympathetic tone during angina pectoris, arterial and coronary sinus (CS) norepinephrine (NE) and epinephrine (E) concentrations and CS blood flow were determined at rest and during pacing-induced angina, both before and after verapamil in nine patients and after nifedipine in nine patients, all of whom had fixed obstructive coronary artery disease. Resting arterial NE and E concentrations and myocardial NE release and E uptake remained unchanged during angina before verapamil and nifedipine, suggesting unaltered systemic and cardiac sympathetic tone and myocardial E handling. Following verapamil and nifedipine, arterial NE and E concentrations remained unchanged. After verapamil, net myocardial NE release increased from 16,072 +/- 18,881 to 35,520 +/- 30,595 at preverapamil angina rate (p less than 0.01) and to 39,643 +/- 29,728 pg/min at postverapamil angina rate (p less than 0.01). NE release after nifedipine increased from -4207 +/- 8898 to 10,988 +/- 30,711 (p less than 0.05) at prenifedipine angina rate and to 19,942 +/- 26,644 pg/min (p less than 0.05) at postnifedipine angina rate. NE release was independent of changes in CS flow after verapamil or nifedipine. E uptake after verapamil and nifedipine remained unchanged. Although the precise mechanism is not known, myocardial alpha-adrenergic receptor blockage with verapamil and nifedipine remains a possible explanation for increased myocardial NE release.

Aged↗
PubMed1985

Endogenous catecholamine levels in chronic heart failure. Relation to the severity of hemodynamic abnormalities.

Plasma free epinephrine, norepinephrine, and dopamine concentrations were determined in 48, 63, and 45 patients, respectively, with overt congestive heart failure, and compared with those in 26 patients with stable angina but without heart failure. Systemic hemodynamic values were determined to assess the severity of heart failure. Arterial epinephrine levels were not different between patients with heart failure (73 +/- 92 pg/ml) and patients without heart failure (55 +/- 73 pg/ml). In patients with congestive heart failure, norepinephrine (665 +/- 510 pg/ml, mean +/- SD) and dopamine (407 +/- 405 pg/ml) levels were significantly higher than in patients with stable angina without heart failure (norepinephrine 184 +/- 136 pg/ml, p less than 0.001, and dopamine 197 +/- 259 pg/ml, p less than 0.02). However, in patients with congestive heart failure, the plasma norepinephrine levels did not correlate with cardiac index (r = 0.21, p = NS), pulmonary capillary wedge pressure (r = 0.11, p = NS), mean arterial pressure (r = 0.11, p = NS), or systemic vascular resistance (r = 0.18, p = NS). Similarly, there was no correlation between dopamine levels and the hemodynamic abnormalities in patients with congestive heart failure. These findings suggest that although endogenous norepinephrine and dopamine levels are frequently elevated in patients with heart failure, reflecting enhanced sympathetic activity, catecholamine levels do not reflect the severity of heart failure.

Adult↗
PubMed1985

Alterations in left ventricular function, coronary hemodynamics and myocardial catecholamine balance with MDL 17043, a new inotropic vasodilator agent, in patients with severe heart failure.

To evaluate changes in myocardial energetics and systemic and cardiac sympathetic activity associated with improved left ventricular function after MDL 17043, a new inotropic vasodilator agent, systemic and coronary hemodynamics and myocardial catecholamine balance were determined in 17 patients with severe heart failure. After the administration of MDL 17043, cardiac index increased by 67% and pulmonary capillary wedge pressure decreased (25 +/- 5 to 14 +/- 7 mm Hg, p less than 0.01), indicating improved left ventricular function. Coronary sinus blood flow (75 +/- 29 to 111 +/- 51 ml/min, p less than 0.01) and myocardial oxygen consumption (9.9 +/- 3.3 to 11.8 +/- 5.4 ml/min, p less than 0.05) increased despite decreased myocardial oxygen extraction (11.7 +/- 2 to 10.1 +/- 3.3 vol%, p less than 0.05) and a higher coronary sinus oxygen content. Although transmyocardial lactate extraction remained unchanged, increased myocardial oxygen consumption has potential deleterious effects on myocardial metabolic function. Arterial norepinephrine concentrations and transmyocardial norepinephrine release also remained unchanged. These findings suggest that MDL 17043 improves left ventricular pump function, but produces no detectable change in systemic and cardiac sympathetic activity. Improved left ventricular function is associated with increased myocardial oxygen consumption despite primary coronary vasodilation.

Adult↗
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↗