Roxroy O. West

A hemodynamic study of acute coronary insufficiency precipitated by exercise: With observations on the effects of nitroglycerin

Abstract Twenty-four patients with coronary artery disease and 10 normal subjects were studied at rest and exercise. All patients with coronary artery disease experienced pain of acute coronary insufficiency during exercise, and hemodynamic abnormalities indicative of impaired left ventricular function developed. Eleven of the 14 patients with coronary artery disease who were studied after nitroglycerin administration were able to perform an identical exercise without chest pain and with no associated hemodynamic abnormalities. The exact mechanism of action of nitroglycerin is uncertain, but it is suggested that it may act by decreasing myocardial oxygen needs through a reduction of left ventricular volume.

Reversible Cardiac Failure During Angina Pectoris Hemodynamic Effects of Atrial Pacing in Coronary Artery Disease

Left ventricular end-diastolic pressure and left ventricular stroke work were measured during a 10-min period of atrial pacing in 10 normal subjects and 30 patients with coronary artery disease. The normal subjects and the patients with coronary artery disease who did not experience angina during pacing reacted similarly with a fall in left ventricular end-diastolic pressure from 8 to 2 mm Hg returning to control values on cessation of pacing. The average left ventricular end-diastolic pressure during pacing in the 21 patients who developed angina was similar to control values although this pressure rose to abnormal levels in four patients. On cessation of pacing the left ventricular end-diastolic pressure rose abruptly to an average value of 22 mm Hg. This lack of elevation of filling pressure during pacing and the rise to abnormal levels on termination of pacing can best be explained by relating left ventricular end-diastolic pressure to left ventricular stroke work. Analyzed in this fashion it is evident that the ischemic ventricle is operating on a depressed ventricle function curve. This depression of function is reversible following cessation of pacing and can be prevented by the prior administration of nitroglycerin.

Hemodynamics at rest and during supine and sitting bicycle exercise in patients with coronary artery disease.

To access left ventricular function and compare pulmonary capillary wedge pressure and left ventricular end-diastolic pressure in the supine and sitting positions, 20 men with angina pectoris secondary to coronary artery disease underwent hemodynamic studies at rest and during exercise in the two positions. At rest the values for cardiac index, stroke index, systolic ejection rate index and left ventricular stroke work index were lower in the sitting position; heart rate, left ventricular end-diastolic pressure and pulmonary capillary wedge pressure were similar in the two positions. All patients experienced angina during both exercise periods. At angina during supine exercise, stroke index, systolic ejection rate index and left ventricular stroke work index did not increase significantly from the resting values. In contrast, during sitting exercise, significant increases in these variables were observed. Comparison of data during exercise revealed higher values for heart rate, mean systemic pressure, cardiac index, systolic ejection rate index, left ventricular stroke work index and rate-pressure product and lower values for mean pulmonary capillary wedge pressure (20 +/- 3 versus 27 +/- 3 [mean +/- standard error of the mean] mm Hg, P is less than 0.001), and left ventricular end-diastolic pressure (24+/- 3 versus 31 +/- 3 mm Hg, P is less than 0.02) in the sitting position; stroke index and S-T segment depression were similar during the two exercise periods. Four patients had insignificant increases in left ventricular filling pressure during both exercise periods. Of the 16 patients with abnormal left ventricular filling pressure during supine exercise, only 10 had a similar response during exercise in the sitting position. There was a good correlation between left ventricular end-diastolic pressure and mean pulmonary capillary wedge pressure at rest and during exercise in the two postures.

The Effect of Nitroglycerin on Coronary Blood Flow and the Hemodynamic Response to Exercise in Coronary Artery Disease

Abstract Hemodynamic indexes and coronary blood flow were measured at rest and during exercise before and after nitroglycerin in 15 patients with coronary artery disease. Angina developed in 7 of these patients during the initial exercise period and was associated with an increase in left ventricular end-diastolic pressure to 32.9 mm Hg without an appropriate increase in left ventricular stroke work. During exercise after nitroglycerin only 2 of these patients experienced angina and the hemodynamic response to exercise was normal. In the patients without angina minor alterations in ventricular performance occurred during the initial exercise period, and these were similarly reversed with nitroglycerin. Coronary blood flow measured by the 85 krypton technique was normal at rest and during exercise in both groups of patients before and after the administration of nitroglycerin. Since there was no demonstrable effect on coronary blood flow, we conclude that nitroglycerin acts primarily by reducing left ventricular oxygen requirements and that this reduction is effected primarily through a reduction in left ventricular volume.

Hemodynamic effects of propranolol in coronary heart disease

Abstract The effects of intravenous propranolol have been studied in 10 patients with coronary heart disease and angina pectoris, 12 patients with asymptomatic coronary heart disease and 5 normal subjects. In all three groups there was evidence of depression of myocardial function both at rest and during exercise after beta adrenergic blockade as shown by increased left ventricular end-diastolic pressure with no increase in stroke work. The mean systolic ejection rate was also lower both at rest and during exercise after administration of propranolol. In spite of hemodynamic evidence suggesting a reduction in myocardial oxygen requirements, in only 1 of the 10 patients with angina pectoris was chest pain prevented by this agent.

The Effect of Ischemia and Alterations of Heart Rate on Myocardial Potassium Balance in Man

Myocardial electrolyte balance and lactate metabolism were studied in 30 patients before, during, and after a period of atrial pacing utilizing a continuous automated sampling technic with simultaneous electrocardiographic and hemodynamic observations. Eight patients with coronary artery disease who had no symptoms during pacing and four normal subjects demonstrated myocardial potassium loss but no abnormalities in lactate metabolism, the electrocardiogram, and hemodynamics during pacing. Myocardial potassium loss was correlated with increments in heart rate and was followed by potassium uptake during the post-pacing period. Eighteen subjects developed angina during pacing associated with hemodynamic and electrocardiographic abnormalities. This ischemic group showed significantly greater myocardial potassium loss during pacing than the non-ischemic group, and this was closely associated with myocardial lactate production at a ratio of 1 mEq of potassium being lost for each 2 millimoles of lactate produced. Increased acidity of coronary sinus blood also accompanied potassium loss during ischemia. No significant changes were seen in sodium balance in either group during the study.

Hemodynamic Effects of Aminophylline in Cor Pulmonale

Nine patients with cor pulmonale due to chronic obstructive pulmonary disease were studied by means of right and left heart catheterization. Hemodynamic and respiratory observations were made during a control period and during the infusion of 1 g of aminophylline.Aminophylline produced a significant reduction in mean pulmonary artery pressure from 39.4 to 25.4 mm Hg, in right ventricular end-diastolic pressure from 8.6 to 2.1 mm Hg, in left ventricular end-diastolic pressure from 7.9 to 3.0 mm Hg, and in brachial artery mean pressure from 95.3 to 85.6 mm Hg. The heart rate and oxygen consumption increased, but there was no change in cardiac index. The alveolar ventilation increased significantly from 2.1 to 2.9 L/min/m2 (BTPS).Evidence is presented to suggest that the decrease in pulmonary artery pressure was due to pulmonary arteriolar dilatation.

Effect of nitroglycerin ointment on the clinical and hemodynamic response to exercise

The effects of nitroglycerin ointment (15 mg nitroglycerin) on hemodynamics at rest and during exercise were studied in 12 patients with coronary artery disease and exertional angina (angina group) and in 8 patients with normal coronary arteriograms or with nonsignificant arteriographic abnormalities who did not have exertional chest pain (nonangina group). In both groups at rest nitroglycerin ointment induced within 15 minutes a significant decrease in left ventricular end-diastolic pressure that was sustained for at least 60 minutes; systemic arterial pressure also decreased within 15 minutes and continued to decrease during the 60 minutes of observation. By 30 to 60 minutes there were significant decreases in cardiac index, stroke index, left ventricular stroke work index and tension-time index. During exercise performed 60 minutes after receiving nitroglycerin ointment, 10 of the 12 patients in the angina group had no pain, whereas 2 had delayed and less severe symptoms. Hemodynamic observations during this exercise period revealed significant decreases in left ventricular end-diastolic pressure, systemic pressure and tension-time index from values in the initial exercise period; heart rate remained unchanged. These data document the protective effect of nitroglycerin ointment for a period of at least 60 minutes and also suggest that the beneficial effects are related to a reduction in myocardial oxygen requirements.

Hemodynamic Effects of Aminophylline in Chronic Obstructive Pulmonary Disease

Ten patients with chronic obstructive pulmonary disease without complicating cor pulmonale were studied by right and left heart catheterization. Hemodynamic and respiratory observations were made during a control period and during the infusion of 1 g of aminophylline. Aminophylline produced a significant reduction in mean pulmonary artery pressure from 19.7 mm Hg to 14.8 mm Hg, right ventricular end-diastolic pressure from 3.4 mm Hg to 1.4 mm Hg, left ventricular end-diastolic pressure from 6.5 mm Hg to 2.9 mm Hg, and the brachial artery mean pressure from 96.7 mm Hg to 86.2 mm Hg. The heart rate, oxygen consumption, and cardiac index increased. There was a significant fall in both peripheral and pulmonary vascular resistance. Evidence is presented to suggest that the decrease in pulmonary artery and systemic pressures was due to pulmonary and peripheral arteriolar dilatation.

Assessment of Ventricular Function in Coronary Artery Disease by Means of Atrial Pacing and Exercise

Abstract Left ventricular hemodynamics were studied in 20 patients with coronary artery disease and 7 normal subjects during atrial pacing and exercise. Angina developed in 13 patients during pacing and exercise, but was absent in 7 during both periods. Ventricular function curves during each stress, using left ventricular end-diastolic pressure and left ventricular stroke work, clearly distinguished the 3 groups. During pacing in the normal subjects and those without angina there was a downward movement on the normal ventricular function curve, and in the group with angina there was a shift to a depressed curve. During exercise in the normal group there was a shift to an augmented ventricular function curve, in the group without angina, an upward movement on the original curve, and in the group with angina, a shift to a depressed curve. Exercise and pacing are useful in evaluating hemodynamic function in patients with coronary artery disease. When ischemic symptoms are induced by either exercise or pacing they are associated with depression of left ventricular performance. When angina is not proyoked, only exercise demonstrates abnormal ventricular function since the response to pacing is indistinguishable from that of the normal group.