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A small residual stenosis and a low residual translesional pressure gradient after percutaneous transluminal coronary angioplasty (PTCA) are thought to be associated with lower rates of restenosis. However, these two posprocedure parameters have not been studied simultaneously in relation to late angiographic outcome. Restudy angiograms after successful single-vessel and single-lesion PTCA were performed in 1261 patients, who were divided into three groups according to final residual stenosis: group 1, 0% to 19%, group 2, 20% to 34%, and group 3, 35% to 49%. This study population also was divided into two groups by final residual pressure gradient: < or = 17 and > or = 18 mm Hg. Luminal patency at restudy and restenosis rates by these definitions were studied. By the definition of > or = 50% stenosis at restudy, group 1 had the lowest restenosis rate, and group 3 had the highest. By the definition of an increase of > or = 30% stenosis compared with the immediate post-PTCA result, group 1 had the highest restenosis rate, and group 3 had the lowest. Although it had the greatest loss of luminal diameter over the follow-up period, group 1 maintained the greatest luminal patency at restudy. A residual pressure gradient < or = 17 mm Hg was associated with lower restenosis rate regardless of the definition used. Despite greater loss of luminal diameter over the follow-up period, optimal postprocedure angiographic results may result in better long-term luminal patency. Transluminal pressure gradient is more predictive of late angiographic results regardless of the definition used. Further studies, with hemodynamic measurements, may reveal potential clinical implications.

To evaluate the effect of contrast agents on percutaneous transluminal coronary angioplasty (PTCA) complications, 913 patients undergoing 1,058 separate PTCA procedures were prospectively randomized to receive either nonionic iopamidol (Isovue-370) [n = 507 PTCA procedures] or ionic contrast media, meglumine sodium diatrizoate (Renografin-76) [n = 551 PTCA procedures]. Angioplasty operators, technicians, nurses and patients were blinded to the agent used. All patients were pretreated with 0.6 mg of atropine sulfate intravenously before any contrast injections. Hypotension (mean arterial pressure less than 65 mm Hg associated with contrast injections) occurred during 8.5% of PTCA procedures in which the patients were receiving iopamidol and during 9.5% of the procedures in which the patients were given diatrizoate (difference not significant). Bradycardia (heart rate of less than 40 beats/min associated with contrast injections) developed during 5.7% of procedures when patients were given iopamidol and during 5.1% of procedures when patients were given diatrizoate (difference not significant). The need for additional atropine or temporary pacing during the procedure was similar for patients given iopamidol and diatrizoate. The overall incidence of ventricular tachycardia or fibrillation, or both, during the procedure occurred less frequently when iopamidol was used compared with diatrizoate (1 vs 2.5%, p = 0.045). These serious ventricular arrhythmias were attributable to contrast injections in 0.6% of the PTCA procedures when iopamidol was given and in 2.0% of the cases in which diatrizoate was the contrast agent (p = 0.09). Only 1 patient had an allergic reaction to the contrast agent, and this was in a patient who received iopamidol.(ABSTRACT TRUNCATED AT 250 WORDS)

Hemodynamic and metabolic changes were measured at rest and during exercise in 23 patients with chronic heart failure and in 6 control subjects. Exercise was limited by leg fatigue in both groups and capacity was 40% lower in the patients with failure. At rest, comparing patients with control subjects, heart rate and right atrial and pulmonary wedge pressure were higher; cardiac output, stroke volume and work indexes and ejection fraction were lower; mean arterial and right atrial pressure and systemic resistance were similar. During all phases of exercise in patients with heart failure, pulmonary wedge pressure and systemic vascular resistance were higher and pulmonary vascular resistance remained markedly elevated compared with values in control subjects. Cardiac output was lower in the patients with failure, but appeared to have the same physiologic distribution in both groups during exercise. Although arterial-femoral venous oxygen content difference was higher in patients with heart failure, this increase did not compensate for the reduced blood flow. Even though the maximal oxygen consumption was significantly reduced, femoral venous lactate and pH values were higher than values in control subjects, but femoral venous pH was similar in both groups at their respective levels of maximal exercise. Ejection fraction was lower in those with heart failure at rest and did not increase with exercise. Ventilation in relation to oxygen consumption was higher in patients with failure than in control subjects.(ABSTRACT TRUNCATED AT 250 WORDS)

To assess the relationship between left ventricular (LV) response to exercise and myocardial ischaemia, 40 patients with coronary artery disease (CAD) and 17 control subjects underwent radionuclide ventriculography at rest and during semiupright exercise. In 14 of the 40 patients with CAD, radionuclide exercise studies were repeated 20 min after 20 mg of sublingual nifedipine. Patients with CAD had increases in both LV end-diastolic and end-systolic volumes and no change in ejection fraction during exercise. End-systolic volume increased and ejection fraction decreased significantly more in patients with multivessel disease, exercise-induced angina and/or ischaemic ST segment depression. Nifedipine reduced angina and ST-segment depression during exercise, attenuated exercise-induced increase in end-diastolic and end-systolic volumes and improved ejection fraction. This study suggests that in patients with CAD, the response of LV volumes and ejection fraction to exercise is related to the degree of exercise-induced myocardial ischaemia and nifedipine improves exercise LV performance.

The acute effects of nifedipine (20 mg sublingually) on hemodynamics and cardiac function were studied at rest and during supine bicycle exercise in 20 patients with aortic regurgitation. At rest, heart rate increased by 13%, systemic vascular resistance decreased by 34% and regurgitant index decreased by 17%. The change in systemic vascular resistance was related to its initial rest level (r = 0.82, p less than 0.001) and to the changes in forward cardiac output (r = 0.58, p less than 0.01) and regurgitant index (r = 0.60, p less than 0.01). Left ventricular end-diastolic and end-systolic volumes, stroke volume and ejection fraction were unchanged, whereas right ventricular ejection fraction increased. During exercise, nifedipine administration further increased heart rate by 8% and decreased systemic vascular resistance by 19%. Both forward stroke volume and forward cardiac output increased, but total left ventricular stroke volume was unchanged, resulting in a significant decrease in regurgitant index. Although left ventricular end-diastolic volume was slightly decreased, end-systolic volume did not increase; thus, ejection fraction was higher than that during control exercise (p less than 0.01). Right ventricular ejection fraction increased further. In aortic regurgitation, the acute administration of nifedipine improved cardiac performance and reduced regurgitation at rest and during exercise as a result of afterload reduction and increased heart rate. Whether these beneficial effects will occur during long-term therapy requires further investigation.

Oxygen utilization, arterial and venous blood gas levels, hemodynamic values and exercise tolerance were compared before and after administration of propranolol and verapamil in 10 patients with stable angina pectoris. During exercise, propranolol decreased cardiac output (CO) by 22%; O2 extraction was increased and O2 consumption (VO2) did not change. With verapamil treatment, CO modestly increased (7%), O2 extraction decreased and VO2 did not change. In contrast to O2 utilization, the drugs produced opposite changes in mixed venous and arterial blood gas levels. Propranolol decreased mixed venous pH, increased CO2 tension and decreased the pH of arterial blood. Verapamil increased venous pH and decreased CO2 tension; pH of arterial blood did not change. The drugs yielded similar levels of antianginal efficacy, but patients exercised longer during verapamil therapy and were less fatigued. The hemodynamic and metabolic differences suggest that muscle perfusion during exercise influences the onset of fatigue and may help determine the choice of therapy.

The effects on hemodynamics and left ventricular function of propranolol and pindolol, beta-blockers without and with intrinsic sympathomimetic activity (ISA), respectively, were compared in six men with stable exertional angina at rest and during symptom-limited bicycle exercise. The study was controlled and double blinded, and the order of drug administration was randomized. The dosage of each drug (propranolol 0.15 mg/kg i.v., pindolol 0.02 mg/kg i.v.) was chosen to reduce exercise tachycardia by approximately 18%. Exercise capacity and duration were similar after each drug, and both drugs similarly reduced ST depression during exercise. At rest, propranolol significantly reduced heart rate, systolic arterial pressure, rate-pressure product, stroke volume index, cardiac index, and left ventricular ejection fraction, and increased systemic vascular resistance. In contrast, pindolol significantly reduced only the rate-pressure product and cardiac index, and to a lesser extent than propranolol. During exercise on the other hand, both drugs reduced the heart rate, arterial pressure, rate-pressure product, and cardiac index to a similar degree. Neither drug altered pulmonary artery wedge pressure, systemic vascular resistance, stroke volume index, left ventricular ejection fraction, or left ventricular end-diastolic and end-systolic volume indices. At equipotent beta-blocking dosages, ISA in pindolol reduced the effects of beta-blockade on resting hemodynamics and left ventricular function compared to propranolol, but during exercise the influence of ISA was reduced; and both pindolol and propranolol exert similar effects on hemodynamics and left ventricular function.

The absorption of nifedipine (10 mg) and haemodynamic response were studied in 10 patients with myocardial infarction before (Phase A) and after (Phase B) a standardized breakfast. In Phase A, the peak nifedipine concentration (Cmax) and maximum haemodynamic changes were found 1 h after drug administration. In Phase B, the Cmax was lower than that in phase A (43 +/- 6 vs 136 +/- 23 ng/ml, p less than 0.001), and both Cmax and maximum haemodynamic changes were delayed to the fourth hour after administration. Nifedipine plasma concentration correlated significantly with the percent changes in systolic and diastolic blood pressure and heart rate. This study suggests that not only dose but also the time intervals between nifedipine administration and food intake are important in determining the haemodynamic effects.

In 14 patients during exercise, intravenous nitroglycerin improved anginal threshold and increased workload compared with control subjects. At similar workloads, the decreased left ventricular volumes suggested decreased myocardial oxygen consumption due to peripheral unloading. At maximal exercise with nitroglycerin (50 +/- 17 to 79 +/- 15 watts), rate-pressure product and end-diastolic volumes were higher with less ischemia, suggesting myocardial supply was improved by nitroglycerin.

Eleven patients with severe left ventricular impairment (mean ejection fraction 24%) and moderate impairment of exercise tolerance underwent a double-blind, placebo-controlled, cross-over trial of the orally administered beta-agonist prenalterol. Exercise hemodynamics and tolerance were measured during bicycle and treadmill exercise after 2 weeks of therapy with placebo or prenalterol. Cardiac index, ejection fraction, and stroke work index were not improved and exercise duration and peak oxygen consumption were not significantly different during the two treatments. During prenalterol treatment heart rate during exercise was consistently reduced. These results show that prolonged therapy with prenalterol does not improve hemodynamics or exercise tolerance and is associated with a diminished heart rate response to exercise.

In 10 men with stable exertional angina, the changes in exercise capacity, hemodynamics, and left ventricular (LV) function were measured after 20 mg sublingual nifedipine (N) and again after adding 100 mg oral metoprolol (M). Nifedipine alone did not significantly improve exercise workloads (+18%) and duration (+21%), but the addition of metoprolol increased both parameters by a further 37 and 32%, respectively (both p less than 0.005 vs. N). After nifedipine the onset of angina was slightly delayed (5.14 +/- 2.41 min placebo (P), 6.00 +/- 2.31 min N, p less than 0.1) and occurred at higher workloads (36 +/- 17 W P, 43 +/- 8 W N, p less than 0.1). After the addition of metoprolol, the onset of angina was delayed substantially more (9.57 +/- 2.22 min, p less than 0.001 vs. P and N) and occurred at much higher workloads (62 +/- 20 W, p less than 0.001 vs. P and N). At rest (R) and during exercise (E), nifedipine decreased systemic vascular resistance (-36% R, -27% E, both p less than 0.001) and mean arterial pressure (-18% R, -21% E, both p less than 0.001), and increased heart rate (+15% R, +11% E, both p less than 0.001), Pulmonary artery wedge pressure on exercise increased less (22 +/- 7 mmHg P, 13 +/- 5 mmHg N, p less than 0.001). After adding metoprolol, the major change was a reduced heart rate (-25% vs. N at R and E, both p less than 0.001), and arterial pressure was unaltered. Pulmonary artery wedge pressure on exercise increased to 18 +/- 5 mmHg (p less than 0.05 vs. N). Exercise LV ejection fraction and volume did not change significantly after adding metoprolol despite marked improvement in angina. In this acute exercise study in patients with stable exertional angina, metoprolol added to nifedipine markedly improved exercise capacity by preventing the increase in heart rate seen with nifedipine. In our patients with relatively normal LV function at rest, the combination was safe and produced no deleterious effects on LV function.

To investigate the antianginal action of nitroglycerin and nifedipine, systemic and right heart pressures, cardiac output, oxygen consumption, and radionuclide left ventricular ejection fraction and volume were measured in 14 men with stable effort angina and a positive exercise electrocardiogram. Exercise tests were performed on a semiupright bicycle ergometer on no therapy and after intravenous nitroglycerin and sublingual nifedipine, which lowered mean arterial pressure by 20 mm Hg. Exercise tolerance improved from 50 +/- 4 to 61 +/- 5 W on nifedipine and to 79 +/- 4 W on nitroglycerin (p less than 0.01, nitroglycerin vs. nifedipine). At submaximal workloads, both drugs decreased arterial pressure and ventricular volumes, but heart rate was higher on nifedipine. At peak exercise on nitroglycerin (79 W), oxygen consumption, cardiac index, heart rate, and rate-pressure product were significantly increased over peak control and nifedipine values, while systolic pressure and end-diastolic volume were unchanged. Nitroglycerin reduced pulmonary wedge pressure more and systemic diastolic pressure less than nifedipine, so the coronary perfusion gradient was reduced by nifedipine and maintained by nitroglycerin. Also, there was less angina and ST-segment depression after nitroglycerin compared to control or nifedipine, and the left ventricular diastolic pressure-volume relationship was improved only by nitroglycerin. This suggests that the action of nitroglycerin in reducing ischemia is not only due to reduced myocardial oxygen demand, but that myocardial oxygen delivery may also be increased.