Maintenance of increased coronary blood flow in excess of demand by nisoldipine administered as an intravenous infusion

Systemic and hemodynamic effects of nisoldipine, administered as a 4.5-micrograms/kg intravenous bolus over 3 minutes followed immediately by an infusion of 0.2 microgram/kg/min over 30 minutes, were studied in 13 patients undergoing diagnostic catheterization for suspected coronary artery disease or follow-up catheterization after coronary angioplasty. Responses to the drug tended to be exaggerated in the first 8 minutes of the infusion, but thereafter produced a steady state, with heart rate increased by 14 +/- 3% at 16 minutes and by 15 +/- 3% at 24 minutes (p less than 0.05), mean aortic pressure decreased 12 +/- 2% and 13 +/- 3% at the same times (p less than 0.05) and coronary venous blood flow increased by 31 +/- 5% and 34 +/- 6% (p less than 0.05). Myocardial oxygen consumption and the heart rate-systolic aortic pressure product were unchanged and cardiac output and stroke volume were significantly increased. Study during matched coronary sinus pacing produced similar trends. Nisoldipine is a potent coronary and peripheral vasodilator that maintains an increase in myocardial oxygen supply in excess of demand when given as an intravenous infusion

Coronary and systemic hemodynamic effects of intravenous nisoldipine

Systemic and coronary hemodynamic effects of the new dihydropyridine calcium antagonist nisoldipine were studied over a 30-minute period in 12 patients with angina pectoris. Previously instituted beta-blocker therapy was continued. Nisoldipine was administered in an intravenous bolus of 6 micrograms/kg over 3 minutes. Heart rate increased as mean aortic pressure and systemic vascular resistance decreased in all patients. Cardiac output increased significantly, from 5.8 +/- 0.3 to 7.9 +/- 0.5 liters/min, 10 minutes after nisoldipine infusion. These trends were maintained over the 30-minute observation period. Coronary sinus blood flow increased from 103 +/- 11 to 139 +/- 13 ml/min immediately after nisoldipine, but had returned to the control level by 30 minutes, as had the reduction in coronary vascular resistance. Myocardial oxygen consumption and heart rate-systolic blood pressure product did not change significantly. Nisoldipine is a potent peripheral and coronary vasodilator free of major myocardial depressant effects after acute intravenous administration. The systemic vasodilatory effects appear to outlast the coronary effects over 30 minutes

Nifedipine in the treatment of unstable angina, coronary spasm and myocardial ischemia

The effects of nifedipine, a potent calcium antagonist, were studied in patients with unstable angina, coronary spasm and myocardial ischemia. Data from two separ

Cardiac catheterization under echocardiographic control in a pregnant woman

A 22 year old woman had signs of rheumatic mitral and aortic valve disease early in pregnancy. Cardiac catheterization was performed during her third month of pregnancy under two-dimensional echocardiographic control without the use of ionizing radiation. Severe mitral stenosis with mild aortic stenosis was found. Five cubic centimeters of 5 percent dextrose in water were injected by hand to obtain left ventriculograms and supravalvular aortograms of sufficient quality to diagnose valvular regurgitation. The use of "echo-catheterization" may have significant advantages in selected clinical situations

Coronary vasodilatory action after a single dose of nicorandil

Coronary hemodynamics and vasodilatory effects on major epicardial arteries were investigated after a single dose of nicorandil in 22 patients undergoing cardiac catheterization for suspected coronary artery disease. Nicorandil, 20 mg, was administered sublingually to 11 consecutive patients and 40 mg to 11 others. Systemic blood pressure decreased significantly without affecting the heart rate. Coronary sinus blood flow did not change significantly. As the mean aortic pressure decreased significantly by 13% after 20 mg and 21% after 40 mg of nicorandil, the calculated coronary vascular resistance decreased but did not reach statistical significance. There was a decrease in myocardial oxygen consumption (-14% and -22%, respectively), and this was consistent with a significant decrease in the calculated pressure-rate product of 19% and 24%, respectively. A total of 103 selected coronary segments, including 17 stenotic segments, were analyzed quantitatively using a computer-assisted coronary angiography analysis system. After 20 or 40 mg of nicorandil, a significant increase of the mean diameter was observed in the proximal (+9% and +7%), midportion (+10% and +11%) and distal (+15% and +13%) parts of the left anterior descending coronary artery. Corresponding values for the proximal (+13% and +10%) and distal (+10% and +15%) segments of the circumflex artery were observed. An increase in the obstruction diameter was also observed in all but 3 of the analyzed stenotic segments. The results demonstrate that nicorandil, in the route and doses used, causes a significant vasodilation in the major epicardial coronary segments, including most stenotic segments, and decreases the myocardial oxygen demand with little effect on the resistance vessels

Acute effects of intravenous nisoldipine on left ventricular function and coronary hemodynamics

The hemodynamic effects of nisoldipine were investigated in 16 patients with suspected coronary artery disease who underwent routine cardiac catheterization. Nisoldipine was given intravenously in a dose of 6 micrograms/kg over 3 minutes and measurements made before and after drug administration during spontaneous and matched atrial paced heart rate. During sinus rhythm, nisoldipine produced a significant increase in heart rate (19%, p less than 10(-5]. Left ventricular systolic pressure decreased 28% (p less than 10(-6) and left ventricular end-diastolic pressure did not change significantly (5%, difference not significant). Coronary sinus and great cardiac vein blood flow increased by 21% (p less than 0.02) and 25% (p less than 0.005), respectively, after nisoldipine administration. Simultaneously, mean aortic pressure decreased 33% (p less than 10(-6]; consequently, the global and regional coronary vascular resistances decreased by 50% (p less than 10(-4]. The decreases in global (-8%) and regional (-4%) myocardial oxygen consumption did not reach statistical significance. A 6% (not significant) increase in end-diastolic volume and an 11% (p less than 0.002) decrease in end-systolic volume resulted in an increase of 21% in stroke volume (p less than 10(-4] with a consistent increase in ejection fraction (+16%, p less than 10(-5]. Total systemic vascular resistance was reduced by 30% (p less than 0.0002). During spontaneous heart rate and matched atrial pacing, the time constant of isovolumic relaxation as assessed by a biexponential model, was significantly shortened.(ABSTRACT TRUNCATED AT 250 WORDS

Acute effects of intravenous nisoldipine on left ventricular function and coronary hemodynamics

The hemodynamic effects of nisoldipine were investigated in 16 patients with suspected coronary artery disease who underwent routine cardiac catheterization. Nisoldipine was given intravenously in a dose of 6 micrograms/kg over 3 minutes and measurements made before and after drug administration during spontaneous and matched atrial paced heart rate. During sinus rhythm, nisoldipine produced a significant increase in heart rate (19%, p less than 10(-5]. Left ventricular systolic pressure decreased 28% (p less than 10(-6) and left ventricular end-diastolic pressure did not change significantly (5%, difference not significant). Coronary sinus and great cardiac vein blood flow increased by 21% (p less than 0.02) and 25% (p less than 0.005), respectively, after nisoldipine administration. Simultaneously, mean aortic pressure decreased 33% (p less than 10(-6]; consequently, the global and regional coronary vascular resistances decreased by 50% (p less than 10(-4]. The decreases in global (-8%) and regional (-4%) myocardial oxygen consumption did not reach statistical significance. A 6% (not significant) increase in end-diastolic volume and an 11% (p less than 0.002) decrease in end-systolic volume resulted in an increase of 21% in stroke volume (p less than 10(-4] with a consistent increase in ejection fraction (+16%, p less than 10(-5]. Total systemic vascular resistance was reduced by 30% (p less than 0.0002). During spontaneous heart rate and matched atrial pacing, the time constant of isovolumic relaxation as assessed by a biexponential model, was significantly shortened.(ABSTRACT TRUNCATED AT 250 WORDS

Effects of successful percutaneous transluminal coronary angioplasty on global and regional left ventricular function in unstable angina pectoris

Sixty-eight patients (58 men, 10 women, mean age 56.3 years, range 31 to 72) with unstable angina pectoris, either initially stabilized with or refractory to optimal pharmacologic treatment, were studied to determine whether regional dysfunction due to stunning of the myocardium caused by attacks of chest pain at rest could be improved with percutaneous transluminal coronary angioplasty (PTCA). Patients were included in the study if they had successful 1-vessel PTCA, no angiographic restenosis, no reocclusion or late myocardial infarction and 2 serial left ventriculograms of sufficient quality to allow automated contour analysis before and after PTCA. Global ejection fraction increased significantly (from 56% to 60%, p less than 0.05) only after successful dilatation of a stenosis of the left anterior descending coronary artery. Analysis of regional wall displacement showed significant improvement of regional wall motion in the areas supplied by the dilated vessel of either the left anterior descending, the left circumflex or the right coronary artery. Thus, regional myocardial dysfunction due to stunning of the myocardium in patients with unstable angina improves after successful PTCA

Assessment of percutaneous transluminal coronary angioplasty by quantitative coronary angiography: diameter versus densitometric area measurements

Cineangiograms of 138 patients who underwent percutaneous transluminal coronary angioplasty (PTCA) were analyzed with a computer-based coronary angiography analysis system. The results before and after dilatation are presented. In a first study group (120 patients), the severity of the obstructive lesions derived from the automatically detected contours was evaluated in absolute terms and in percent-diameter reduction. In a second group of patients, 18 coronary lesions were selected for their extreme severity and symmetric aspect before angioplasty as assessed from multiple views. In the second group, the densitometric percent-area stenosis was used to assess the changes in cross-sectional area after PTCA and was compared with the circular percent-area stenosis computed from the diameter measurements. Before PTCA, a good agreement exists between the densitometric percent-area stenosis and the circular percent-area stenosis. After PTCA, important discrepancies between these 2 types of measurements are observed. It is suggested that these discrepancies in results after PTCA can be accounted for by asymmetric morphologic changes in luminal cross section, which cannot be assessed accurately from diameter measurements in a single-plane view

Early detection of restenosis after successful percutaneous transluminal coronary angioplasty by exercise-redistribution Thallium scintigraphy

The value of exercise testing and thallium scintigraphy in predicting recurrence of angina pectoris and restenosis after a primary successful transluminal coronary angioplasty (PTCA) was prospectively evaluated. In 89 patients, a symptom-limited exercise electrocardiogram (ECG) and