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 147,016 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

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.
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PMID:Maintenance of increased coronary blood flow in excess of demand by nisoldipine administered as an intravenous infusion. 378 8

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)
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PMID:Acute effects of intravenous nisoldipine on left ventricular function and coronary hemodynamics. 401 20

The circulatory consequences of slow-calcium channel blockade with a new dihydropyridine nisoldipine were evaluated at rest and during exercise-induced angina in 16 patients with angiographically proven coronary artery disease. In 10 patients resting cardiac stroke output (thermodilution) and pulmonary artery occluded pressure were determined following four intravenous nisoldipine injections (cumulative dosage of 1, 2, 4 and 8 micrograms kg-1). The exercise effects of nisoldipine were evaluated by comparing the effects of the 8 micrograms kg-1 cumulative dosage with a control exercise period at the same workload. At rest nisoldipine reduced systemic vascular resistance and mean arterial pressure, and increased heart rate, cardiac and stroke volume indices. During 4 min supine-bicycle exercise nisoldipine reduced systemic mean arterial pressure and vascular resistance; this resulted in augmented cardiac and stroke volume indices at an unchanged pulmonary artery occluded pressure. In six additional patients rest and exercise ejection fractions were measured using a nonimaging nuclear probe. Nisoldipine (4 micrograms kg-1) resulted in a small trend to increase left ventricular rest and exercise ejection fraction. These data demonstrated improved rest and exercise cardiac performance following nisoldipine in patients with severe coronary artery disease.
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PMID:Haemodynamic dose-response effects of intravenous nisoldipine in coronary artery disease. 409 98

The hemodynamic effects of oral nisoldiopine in 12 hypertensive patients aged 35-55 years were determined using the impedance cardiography method. Hemodynamic measurements were performed at hourly intervals before and following ingestion of the medication. Nisoldipine significantly decreased systolic and diastolic blood pressure, with a slight increase in heart rate. Stroke volume did not change significantly following the medication. Total peripheral resistance decreased gradually reaching its lowest values 2 h after ingestion of nisoldipine. We conclude that nisoldipine is a potent oral antihypertensive agent that induces peripheral vasodilatation without decrease in cardiac output.
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PMID:Acute hemodynamic effects of nisoldipine in young hypertensive patients. 775 24

The DEFIANT-I study (Doppler Flow and Echocardiography in Functional cardiac Insufficiency: Assessment of Nisoldipine Therapy) was a multicenter, multinational double-blind randomized study of the effects of the new calcium channel blocking drug nisoldipine on left ventricular (LV) size and function after acute myocardial infarction. Randomization to placebo or to long-acting nisoldipine core coat (20 mg once daily) was performed in 135 eligible patients with mild to moderate systolic LV dysfunction (LV ejection fraction < or = 50%) 20 days (range 7-35) after infarction, with serial clinical, echocardiographic, and Doppler cardiographic measurements during a 4 week follow-up period. At the end of the follow-up period, exercise capacity was determined by bicycle ergometry. Nisoldipine improved indices of diastolic LV function. Early diastolic transmitral blood flow velocity increased, with an increase in peak E wave of 0.06 m/sec (95% confidence intervals [CI], 0.01, 0.11) and an increase in time velocity integral of 1.2 cm (95% CI, 0.16, 2.27). Isovolumic relaxation time was reduced by 14.7 msec (95% CI, -22.5, -6.9), a change not explained by the very small (and not significant) changes in systemic arterial pressure, heart rate, or cardiac output. There was no change in systolic and diastolic LV volume, nor in LV ejection fraction. Exercise capacity was greater by 12 watts (95% CI, 0.8, 23.3) in patients receiving nisoldipine, while the incidence of > or = 1 mm ST-segment depression (relative occurrence 0.54, 95% CI, 0.30-0.97) and the incidence of angina pectoris (relative occurrence 0.67, 95% CI, 0.42-1.08) during exercise testing tended to be lower in this group. Although the relations were not exact, peak exercise workload 7 weeks after infarction correlated with resting measurements of diastolic LV function. Exercise workload was inversely related to peak late diastolic transmitral blood flow velocity (A wave, slope, -86.6; 95% CI, -120.9, -52.2) and directly to the E/A ratio (slope, 20.5, 95% CI, 6.0, 35.1). The relations between exercise workload and peak late diastolic flow velocity remained significant after correction for age, sex, resting heart rate, and usage of beta-blocking drugs or nisoldipine. Exercise capacity was not related to measurements of systolic LV function (LV end-diastolic and end-systolic volume, LV ejection fraction, stroke volume, cardiac index). In summary, the calcium channel blocker nisoldipine improved measurements of diastolic LV function in patients recovering from acute myocardial infarction. Exercise capacity was higher in patients receiving the drug, and there was less exercise induced ischemia.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:The DEFIANT study of left ventricular function and exercise performance after acute myocardial infarction. Doppler Flow and Echocardiology in Functional Cardiac Insufficiency: Assessment of Nisoldipine Therapy Study Group. 794 83

1. The acute haemodynamic effects of intravenous nisoldipine (1, 2, 4 microg kg(-1)) and nifedipine (2.5, 5, 10 microg kg(-1)) were compared in a randomised, within-patient crossover study. Fifteen male patients with stable angina pectoris treated with atenolol were studied after undergoing routine cardiac catheterisation. 2. Nisoldipine caused a dose-related fall in systemic vascular resistance (maximum 22%) associated with an increase in heart rate and cardiac index (18%) and a fall in mean arterial pressure (7%). 3. By contrast, nifedipine was associated with a significant increase in heart rate but systemic vascular resistance, cardiac index and mean arterial pressure remained unaltered. 4. At doses with equivalent effects on heart rate (2 microg kg(-1) nisoldipine; 10 microg kg(-1) nifedipine) acute dosing with nisoldipine caused a significantly greater fall in systemic vascular resistance and increase in cardiac index, whilst nifedipine caused a greater reduction in stroke volume index and left ventricular stroke work index. 5. The results suggest that, when combined with atenolol, acute dosing with nisoldipine may have a more complementary haemodynamic profile than nifedipine. The implications of this finding for chronic oral dosing in patients with impaired left ventricular function should be evaluated.
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PMID:A comparison of the acute haemodynamic effects of nisoldipine and nifedipine during treatment with atenolol in patients with coronary artery disease. 1295 9


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