Metabolic assessment of exercise in chronic heart failure patients treated with short-term vasodilators.
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Biomedical subjects
Publications and source records attributed to K Chatterjee.
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The influence of acute myocardial ischemia and changes in ventricular dimensions on endocardial and epicardial electrograms were evaluated in 17 anesthetized open-chest dogs before and after left ventricular volume expansion and before and after coronary artery ligation. In eight dogs, regional myocardial blood flow was determined by the labeled microsphere technique. Endocardial QRS (endo-QRS) amplitude in ischemic and nonischemic zones, and epicardial QRS (epi-QRS) in nonischemic zones maintained a negative linear relation with left ventricular end-diastolic dimension before and after coronary artery ligation, although acute ischemia decreased endo-QRS independently. Epi-QRS amplitude in the ischemic zone decreased after coronary artery ligation but changed inconsistently during volume expansion. Ischemia-induced epicardial ST-segment elevation decreased during volume expansion and was associated with improved epicardial blood flow. Changes in epi-QRS in ischemic zones, however, were not related to epicardial blood flow during volume expansion. These findings indicate the potential problems of using changes in QRS amplitude for determining the extent of myocardial ischemic injury.
Twenty-three coronary bypass graft patients were evaluated by a contrast-enhanced computed tomography (CT) technique to determine graft patency. Four to six 4.8-second sequenced scans with a 1-second interscan interval were obtained in each patient during the hand injection of 25-30 ml of contrast medium in a peripheral vein. Patency of grafts was determined by a characteristic contrast enhancement. The CT technique correlated with angiographic assessment of graft patency in 59 of 62 grafts (95%). We conclude that this relatively noninvasive technique shows promise as a method for determining coronary bypass graft patency.
The hemodynamic effects of an oral angiotensin-converting enzyme inhibitor, captopril, were evaluated in 10 symptomatic patients with chronic congestive heart failure. In all patients there was a significant increase in cardiac output (average 28%), stroke volume (49%), and stroke work index (26%), along with a decrease in pulmonary capillary wedge pressure (48%), indicating improved left ventricular function. Modest decreases in heart rate and arterial pressure were also observed. In seven patients maintained on captopril therapy, repeat hemodynamic studies at 2 months revealed sustained effects. These beneficial hemodynamic effects were accompanied by clinical improvement and improved exercise tolerance during maintenance therapy. These findings suggest that captopril may be a useful therapeutic adjunct for the long-term management of patients with chronic congestive heart failure.
Hemodynamic effects of oral hydralazine (200 to 400 mg/d) were evaluated in 11 patients with chronic heart failure after short-term (24 hours) and long-term (average, 8.3 months) therapy. In seven of 11 patients, hemodynamic changes were evaluated after withdrawal of hydralazine. During early study, cardiac index, stroke volume index, and stroke work index increased by an average of 56%, 59%, and 68%, respectively, and systemic vascular resistance decreased by 39%. During late study, cardiac index (+65%), stroke volume index (+88%), and stroke work index (+98%) remained higher and systemic vascular resistance (-41%) lower than control values. Withdrawal of hydralazine caused a decrease in cardiac index, stroke volume index, and stroke work index and an increase in systemic vascular resistance. Heart rate and arterial, pulmonary capillary wedge, and right atrial pressures did not change significantly. These findings suggest that oral hydralazine produces sustained beneficial hemodynamic effects in patients with chronic heart failure.
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Changes in oxyhemoglobin dissociation compensate partially for decreased O2 transport caused by high altitude, anemia, and cardiac disease. This investigation determined whether similar changes occurred in patients undergoing myocardial revascularization and the possible significance of such changes. In 15 patients scheduled for coronary vein bypass surgery the following were inserted: a #7 French catheter into the coronary sinus or great cardiac vein, a pulmonary arterial catheter (Swan-Ganz), and a radial arterial catheter. Patients were anesthetized with either halothane-N2O 50% or morphine (2 mg/kg IV) with N2O 50%. Hemodynamic status was measured and blood samples were taken from the catheters in the preoperative period and after endotracheal intubation, sternotomy, bypass, and chest closure. Blood samples were analyzed for pH, blood gas tensions, and O2 saturation. Values for P50 for mixed venous and coronary sinus blood were calculated from O2 tension and saturation. Patients were divided into two groups on the basis of peroperative mixed venous P50 values: group I had normal P50 levels of 26.1 +/- 2.0 torr (mean +/- SD); group II had elevated values for mixed venous blood P50 of 32.5 +/- 1.6 (mean +/- SD). Unlike group I, group II had depressed ventricular function and higher P50 values for coronary sinus blood than for mixed venous blood. Induction of anesthesia increased P50 values in group I but not in group II and removed the significant differences between group I and group II mixed venous P50 values. In group II patients, cardiopulmonary bypass lowered the elevated P50 of coronary sinus blood so that it equaled P50 for mixed venous blood. It is concluded that induction of anesthesia may elevate P50 in patients who have normal preoperative P50 values. The already elevated P50 values of patients with ventricular dysfunction did not change. Cardiopulmonary bypass decreased coronary sinus P50 in group II patients, and this change might be deleterious if the original elevation represents a compensatory response to a reduction in O2 transport.
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.
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.
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.
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.
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.
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.
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In patients with pump failure complicating acute infarction, vasodilating drugs, by reducing impedance to left ventricular outflow and venous return to the heart, improve cardiac performance without affecting myocardial contractility. Sodium nitroprusside currently is the vasodilator of choice in most patients with both elevated left ventricular filling pressures and reduced cardiac output. Patients with accompanying mechanical defects, such as acute mitral regurgitation or ventricular septal rupture, are particularly amenable to vasodilator therapy. Some patients may require combined therapy, with inotropic catecholamines or mechanical assistance devices together with vasodilators, in order to avoid undesirable hypotension. Side effects and toxicity are rare when patients are carefully selected and monitored. It is uncertain whether vasodilators reduce ischemia or salvage jeopardized myocardium, but they appear to improve the initial prognosis of some patients with severe pump failure. The long-term prognosis of these patients remains poor, however, and therefore a more aggressive approach to their chronic management seems warranted.
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The comparative haemodynamic effects of oral prazosin hydrochloride and hydralazine were evaluated in 11 patients with chronic congestive heart failure. The maximum total dose of prazosin received by an individual varied up to 25 mg. Ten patients received a maximum of 75 mg and one received 50 mg of hydralazine at six-hour intervals. There was no significant change in heart rate with either drug. Decrease in mean arterial and left ventricular filling pressures were modest and similar with both agents. With prazosin, the average cardiac index increased 20 per cent and systemic vascular resistance decreased 20 per cent. By contrast, hydralazine increased cardiac index by 58 per cent and decreased systemic vascular resistance by 40 per cent. The increase in stroke work and stroke volume indices was significantly greater with hydralazine than with prazosin. These findings suggest that in some patients with severe chronic congestive heart failure, improvement in left ventricular performance may be greater with hydralazine than with prazosin.