Biomedical subjects

K Chatterjee

Publications and source records attributed to K Chatterjee.

At least 73 records · Page 4Linked 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↗

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↗