Biomedical subjects

B Silke

Publications and source records attributed to B Silke.

At least 109 records · Page 6Linked to original sources

PubMed1986

A haemodynamic study of the effects of combined slow-calcium channel blockade (nisoldipine) and beta-blockade (metoprolol) in coronary heart disease.

The interaction of a new slow-calcium blocker (nisoldipine) and the beta-blocker metoprolol was evaluated in 16 patients with stable angina. Haemodynamic parameters were determined in a control rest and exercise period. Patients were then randomised equally to nisoldipine (4-8 micrograms/kg) or metoprolol (10 mg) and the haemodynamics of monotherapy assessed; finally the second drug was administered and the effects of combination determined. At rest nisoldipine reduced systemic blood pressure and vascular resistance (P less than 0.01); heart rate, cardiac and stroke volume indices increased (P less than 0.01) at an unchanged pulmonary artery occluded pressure. Metoprolol alone reduced heart rate (P less than 0.05) and increased the pulmonary artery occluded pressure (P less than 0.05). Combination therapy reduced systemic blood pressure and vascular resistance (P less than 0.01); cardiac index and pulmonary artery occluded pressure increased (P less than 0.01) at an unchanged heart rate. The effect of combination was influenced by the order of administration; an improvement in cardiac performance was particularly evident when nisoldipine was added to metoprolol. The interaction during dynamic exercise was similar to that at rest. Thus these data indicated the haemodynamic safety of concurrent nisoldipine/metoprolol therapy; the addition of nisoldipine to metoprolol appeared to offset in part the cardiodepressant properties of beta-blockade.

Adult↗

PubMed1986

Comparative effects of metoprolol and celiprolol on cardiac hemodynamics and left ventricular volume at rest and during exercise-induced angina.

Celiprolol is a cardioselective beta-adrenoceptor antagonist with attributed cardiostimulant properties. Its hemodynamic profile was compared in a dose-response study with that of metoprolol, which is also cardioselective but lacks cardiostimulatory activity. In 24 patients with angiographically proved coronary artery disease, simultaneous hemodynamic and left ventricular ejection fraction (EF) values were determined at rest in the control (drug-free) state and repeated 3 to 5 minutes after each of four intravenous boluses of celiprolol, 1, 1, 2, and 4 mg, or equivalent beta-blocking doses of metoprolol, 1.25, 1.25, 2.5, and 5.0 mg. The effects of each drug on hemodynamics during exercise-induced angina were determined by exercise testing in the control state and after the maximum cumulative dose of each drug. At rest, metoprolol reduced heart rate, cardiac index, and the left ventricular EF and increased pulmonary artery occluded pressure (PAOP), systemic vascular resistance, and left ventricular end-systolic and end-diastolic volumes. Celiprolol increased cardiac and stroke volume indices and the EF; the PAOP was reduced without change in other measured variables. During exercise, metoprolol significantly increased the PAOP, which was unchanged by celiprolol. At exercise both drugs reduced cardiac index and heart rate, but neither altered the EF. The cardiac function curve demonstrated greater depression at rest after metoprolol than after celiprolol; these differences were attenuated during dynamic exercise. The lesser adverse impact of celiprolol on cardiac function may be attributable to ancillary cardiac stimulatory properties offsetting the cardiac depression after beta-adrenoceptor blockade.

Angina Pectoris↗

PubMed1986

Haemodynamic dose-response effects of intravenous indoramin in acute heart failure complicating myocardial infarction.

The haemodynamic dose-response effects of intravenous indoramin were evaluated in 12 patients with acute heart failure (pulmonary artery occluded pressure of greater than 20 mm Hg) complicating a recent myocardial infarction. Following a 1-h control period with confirmed stable haemodynamics, the effects of three intravenous bolus doses of indoramin (0.125, 0.125, and 0.25 mg/kg at 15-min intervals) were determined in the 10- to 15-min period following each intravenous injection. Plasma drug concentrations rose with the administered dose and were in the previously established therapeutic range. Ten patients tolerated all three doses of the drug; two patients were withdrawn following the second dose owing to clinically evident hypotension (systolic blood pressure of less than 100 mm Hg). Indoramin resulted in progressive falls in systolic, diastolic, and mean systemic arterial pressures (p less than 0.01) without change in cardiac index. There was a dose-related reduction in the heart rate (0.5 mg/kg; -7 beats/min; p less than 0.01). The left ventricular filling pressure showed a significant and quadratic reduction over the dose range (0.5 mg/kg, -5 mm Hg; p less than 0.01). The systemic vascular resistance index was reduced (-333 dynes X s X cm-5 X m2; p less than 0.001) and the stroke volume index increased (+3 ml/m2; p less than 0.05) following the maximum cumulative dosage. These data established the therapeutic safety of indoramin (0.125-0.5 mg/kg) in acute heart failure following myocardial infarction. An improvement in cardiac performance in these patients was compatible with circulatory actions on both cardiac preload and afterload.

Acute Disease↗

PubMed1986

A randomized double-blind study of atenolol and celiprolol in mild to moderate hypertension.

The antihypertensive effects of equivalent beta-blocking doses of atenolol and celiprolol were compared in 55 patients with mild to moderate hypertension. Patients with diastolic blood pressure between 95 and 114 mm Hg were randomized to celiprolol or atenolol once daily. The dose of each agent was titrated from 50 to 100 mg atenolol or from 200 to 400 mg celiprolol if the supine diastolic blood pressure remained greater than 90 mm Hg after 2 to 4 weeks treatment at 24 h following dosing. Following titration patients were maintained at constant dosage for 12 weeks. The average reductions in blood pressure over the period of double-blind therapy were similar; for atenolol -17/-16 mm Hg and for celiprolol -14/-13 mm Hg. Therapeutic success rate (percentage of patients with diastolic blood pressure less than 90 mm Hg or reduction in diastolic blood pressure greater than 10 mm Hg), based on the mean over the maintenance period, was 71% and 59%, respectively. Adverse events were minor and similar for both therapies. Once daily atenolol and celiprolol appeared similar in efficacy and safety in mild to moderate hypertension.

Adrenergic beta-Antagonists↗

PubMed1986

Celiprolol in the treatment of hypertension: a comparison with propranolol.

A randomized double-blind study compared the antihypertensive efficacy of single daily oral doses of celiprolol 200 or 400 mg to twice daily doses of propranolol 40 or 80 mg in 58 patients with uncomplicated essential hypertension (supine diastolic blood pressure range 95-114 mm Hg). Before treatment there was no significant difference in patient characteristics or in the average systolic or diastolic blood pressures or heart rates between the two groups. Sixty-five percent of the celiprolol group and 56% of the patients randomized to propranolol achieved blood pressure control on the lowest dose of each drug. The mean reductions in the systolic and diastolic pressures at the end of the 4 week titration period were -14/-13 mm Hg for the celiprolol group and -11/-12 mm Hg for the propranolol group. Continued treatment with the same doses of celiprolol and propranolol for a further 8 weeks resulted in blood pressure reductions of -18/14 mm Hg and -8/-9 mm Hg, respectively. In 64% of patients taking celiprolol and in 54% of those taking propranolol the prospective target reduction in supine diastolic blood pressure was achieved, namely a reduction to below 90 mm Hg or a reduction lower after propranolol than after celiprolol; celiprolol reduced the heart rate by an average of 6 bt/min and propranolol by 13 bt/min after 12 weeks treatment (p 0.01). Adverse reactions assessed by patient-volunteered information were similar in character and frequency for both drugs.(ABSTRACT TRUNCATED AT 250 WORDS)

Adrenergic beta-Antagonists↗

PubMed1986

Differential actions of atenolol and celiprolol on cardiac performance in ischemic heart disease.

The therapeutic relevance of differences between beta-adrenoceptor antagonists, related to their ancillary pharmacological properties, is debated. Celiprolol is a novel cardioselective beta-blocking agent with attributed cardio-stimulating properties. Its hemodynamic profile was compared with that of atenolol (cardioselective; no ISA) in a comparative dose-response study of 24 patients with angiographically documented coronary artery disease. Following a stable control period four i.v. boluses of equivalent beta-blocking doses of atenolol (1, 1, 2, and 4 mg) or celiprolol (1, 1, 2, and 4 mg) were administered, and hemodynamics and left ventricular ejection fraction were determined. The comparative actions of the two drugs on the hemodynamics of exercise-induced angina were compared by exercise testing in the control state and following the maximum cumulative dose of each drug. At rest, atenolol reduced heart rate, cardiac index, and left ventricular ejection fraction (EF); systemic vascular resistance index increased without change in systemic arterial or pulmonary artery occluded pressures. Celiprolol increased cardiac index and ejection fraction without change in other variables. During exercise both drugs reduced cardiac index and heart rate; neither altered the exercise EF. The cardiac function curve, relating cardiac index to left ventricular end-diastolic pressure, was significantly depressed by atenolol but was elevated at rest by celiprolol. Thus these studies demonstrated hemodynamic differences between atenolol and celiprolol, presumably related to the ancillary properties of the latter. The relevance of such differences to the therapy of patients with coronary artery disease deserves further examination.

Adrenergic beta-Antagonists↗

PubMed1986

A rest and exercise haemodynamic evaluation of a new cardio-selective beta-adrenoceptor blocker celiprolol alone and in combination with nitroglycerine in ischaemic heart disease.

The symptomatic benefits of combining beta-adrenoceptor blockers and nitrates in angina pectoris are well recognised. Their actions on cardiac haemodynamics and volumes when combined have been poorly characterized. Accordingly this study investigated a new cardioselective beta-adrenoceptor blocking agent celiprolol and buccal nitroglycerine in 24 patients with angiographically documented coronary artery disease. Following a control period, with confirmed stable haemodynamics, three groups (n = 8/group) of prospectively matched patients, were studied following intravenous celiprolol (8 mg), buccal nitrate (10 mg) or their combination. Haemodynamics and left ventricular ejection fraction (nuclear probe) were determined following each intervention. The actions of each regimen on the haemodynamics of exercise-induced angina were compared by exercise testing in the control state and following each regimen. At rest, celiprolol did not alter haemodynamic parameters. Nitrate therapy reduced left ventricular filling pressure (pulmonary artery occluded pressure--PAOP) and volumes; the ejection fraction and heart rate increased. Combination therapy resulted in a highly significant reduction in left ventricular preload and afterload (PAOP and mean arterial blood pressure) at an increased left ventricular ejection fraction and reduced cardiac volumes; there was a trend to reduce cardiac double product (HR X SBP). During exercise celiprolol reduced systolic blood pressure, heart rate and cardiac index; systemic vascular resistance index increased. Nitrate therapy reduced blood pressure and PAOP, and increased ejection fraction. Combination therapy reduced all components of the triple product (heart rate, systolic blood pressure and PAOP) without affecting the other haemodynamic or radionuclide parameters. These data suggest improvements in cardiac function from the combination of celiprolol and nitrate therapy which were not achieved by either agent when used as monotherapy; they afford an interesting insight into the manner in which such widely utilised therapeutic modalities interact in coronary artery disease.

Adrenergic beta-Antagonists↗

PubMed1986

Comparative haemodynamic effects of intravenous lignocaine, disopyramide and flecainide in uncomplicated acute myocardial infarction.

A prospective study evaluated the comparative haemodynamic effects of three Class I antiarrhythmics (lignocaine Class 1B, disopyramide Class 1A and flecainide Class 1C) in 30 patients with uncomplicated acute myocardial infarction. Three groups, each of 10 patients, were allocated to lignocaine (Group I) 1.5 mg kg-1 i.v. loading dose over 10 min followed by infusion at 3 mg kg-1 h-1, disopyramide (Group II) or flecainide (Group III), both administered as a 1.0 mg kg-1 i.v. loading bolus over 10 min followed by a 1.6 mg kg-1 h-1 infusion for 120 min. The plasma levels of each drug were in the described therapeutic range. Lignocaine decreased cardiac index (-0.3 l min-1 m-2 (9%); P less than 0.05) and stroke volume index (-5 ml m-2 (11%); P less than 0.01). Systemic blood pressure, heart rate and systemic vascular resistance index were unchanged. There was a small increase (+3 mm Hg (30%); P less than 0.01) in pulmonary artery occluded pressure (PAOP). Both disopyramide and flecainide increased systemic blood pressure; the maximum increases for mean blood pressure were +10 mm Hg (11%) and +4 mm Hg (4%) respectively. Both drugs reduced cardiac index (-0.5 l min-1 m-2 (16%): -0.4 l min-1 m-2 (11%)) and stroke volume index (-11 ml m-2 (25%): -5 ml m-2 (11%)). There were increases in heart rate (+13: +5 beats min-1) pulmonary artery occluded pressure (+2: +3 mm Hg) and systemic vascular resistance index (+696: +275 dyn s cm-5 m2).(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗

PubMed1986

A haemodynamic dose finding study with a new slow-calcium channel blocker (amlodipine) in coronary artery disease.

The haemodynamic dose-response effects of a new long-acting slow-calcium channel blocking agent, amlodipine were evaluated in 20 patients with angiographically confirmed coronary heart disease. At rest, following a control saline period, four i.v. doses of the drug (cumulative dosage 1.25, 2.5, 5 and 10 mg) were administered to ten patients and haemodynamics determined in the ten to 15 minutes following injection. Effects on circulatory parameters were only evident following the maximum cumulative dosage. Accordingly in a further ten patients, the regimen was doubled (cumulative i.v. dosage 2.5, 5, 10 and 20 mg). In each study the haemodynamic effects during constant load supine bicycle exercise were evaluated by comparison of values during the control exercise period and following the final cumulative dosage. On the higher regimen, amlodipine significantly reduced resting systolic, diastolic and mean (p less than 0.01) systemic arterial pressure and systemic vascular resistance index (p less than 0.01). Heart rate (p less than 0.01), stroke volume index (p less than 0.01) and cardiac index (p less than 0.01) increased; pulmonary artery occluded pressure was unchanged. During constant load bicycle exercise, the mean arterial pressure was significantly reduced (p less than 0.01), and the heart rate and cardiac index increased (p less than 0.01). Thus the immediate impact of amlodipine in stable coronary artery disease was to reduce left ventricular afterload and augment cardiac pumping performance. The minimum effective i.v. dosage appeared to be 10 mg. Amlodipine appears sufficiently promising to warrant longer-term studies in ischaemic heart disease.

Adult↗

PubMed1985

Intravenous amrinone in left ventricular failure complicated by acute myocardial infarction.

Hemodynamic dose-response effects of intravenous amrinone were studied in 22 male patients aged 38 to 62 years with left ventricular failure occurring within 18 hours of acute myocardial infarction. After hemodynamic confirmation of a raised left-sided cardiac filling pressure--pulmonary artery occluded pressure greater than 20 mm Hg--patients were randomized to either low-dose infusion of amrinone (200 micrograms/kg/hr for 30 minutes, 400 micrograms/kg/hr for 30 minutes and then 800 micrograms/kg/hr for 30 minutes) or high-dose infusion of the drug (800, 1,600 and 3,200 micrograms/kg/hr sequentially, each for 30 minutes). Hemodynamic measurements were obtained at 1 hour before amrinone and at the end of each infusion step. Low-dose infusion of amrinone resulted in a progressive increase in cardiac output (p less than 0.05) and stroke volume (p less than 0.05) and progressive reductions in pulmonary artery occluded pressure (p less than 0.01) and systemic vascular resistance (p less than 0.05). Systemic blood pressure and heart rate were unchanged. High-dose infusion resulted in a similar increase in cardiac output (p less than 0.05) but no change in stroke volume owing to associated tachycardia (p less than 0.01). There was a significantly greater decrease in pulmonary artery occluded pressure compared with the low-dose infusion (p less than 0.05), and systemic arterial diastolic and mean pressures were also decreased (p less than 0.05). The decrease in systemic vascular resistance was of a similar order to that induced by the low-dose infusion.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗

PubMed1985

The effects on left ventricular performance of verapamil and metoprolol singly and together in exercise-induced angina pectoris.

Concurrent therapy with the calcium channel blocker, verapamil, and the beta-blocking group of compounds is usually felt to be clinically contraindicated due to the former's potent dromotropic and negative inotropic actions. The basis of this assumption was examined in a rest and exercise hemodynamic study of the effects of verapamil and the cardioselective beta-blocking drug, metoprolol, in 22 patients with stable angina pectoris and angiographically confirmed coronary artery disease. In a randomized study, 11 patients were assessed following intravenous verapamil (16 mg) alone, 11 following intravenous metoprolol (10 mg) alone, and all 22 were assessed on combination therapy. The plasma levels achieved at the time of each hemodynamic assessment were in the therapeutic range. At rest, verapamil alone significantly lowered systemic arterial pressure and vascular resistance; metoprolol alone lowered heart rate and increased systemic vascular resistance without change in systemic arterial pressure. Combination therapy reduced systemic arterial pressure and heart rate without change in cardiac output and systemic vascular resistance. During upright bicycle exercise, the changes were directionally similar. Depression of cardiac function (i.e., reduced cardiac output at increased pulmonary artery occluded pressure) occurred following metoprolol but not following verapamil; the addition of verapamil did not accentuate the depression of function induced by metoprolol. These results suggested that in patients with stable coronary artery disease, without manifest conduction system abnormality, the cardiac depressant actions of verapamil were countered by its vasodilator properties.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗

PubMed1985

Circulatory effects of intravenous and oral acebutolol in acute myocardial infarction.

The hemodynamic dose-response effects of intravenous (25 and 50 mg) and oral (200 and 400 mg) acebutolol were compared in a randomized between-group study in men within 17 hours of an acute uncomplicated myocardial infarction. Six subjects were evaluated in each of the four groups. After a 1-hour control period, hemodynamic variables and plasma drug concentrations were determined at 15 (intravenous therapy only), 30, 60, 90, 120, and 240 minutes after dosing. At the doses studied, hemodynamic dose-response effects were not evident after either intravenous or oral acebutolol. In all groups acebutolol reduced systolic and mean systemic arterial pressure, heart rate, cardiac output, and stroke volume. Pulmonary artery occluded pressure and systemic vascular resistance were transiently increased. Maximum changes developed between 15 and 30 minutes after intravenous dosing and between 1 and 2 hours after oral dosing. However, there were substantial reductions in cardiac output (-0.7 L/min/m2; P less than 0.05) by 30 minutes after oral dosing. Effects lasted for 2 hours after intravenous dosing and for 4 hours after oral dosing. Our data confirm the hemodynamic safety of acebutolol after acute myocardial infarction. The relevance of the time-dependent hemodynamic differences between intravenous and oral initiation of beta-blockade to the overall goal of reducing myocardial oxygen requirements after acute coronary artery occlusion merits closer examination.

Acebutolol↗

PubMed1985

Hemodynamic dose-response effects of flecainide in acute myocardial infarction with and without left ventricular decompensation.

We evaluated the hemodynamic effects of the class I antiarrhythmic flecainide in 20 patients within 18 hours of an acute myocardial infarction. Equal numbers of patients with normal (group 1) or decompensated (group 2) ventricular function were studied. Both groups received flecainide, 1 mg/kg, as an intravenous bolus over 10 minutes, followed by infusion (1.6 mg/kg/hr) over the next 120 minutes. Plasma concentrations increased linearly with the cumulative flecainide dosage in both groups. There was no difference between the groups in the plasma levels reached, which were within the recognized antiarrhythmic range for flecainide (200 to 1000 ng/ml) throughout the infusion. The hemodynamic effects of flecainide for each group were decreases in systolic blood pressure (maximum 3% fall in group 1 and 8% fall in group 2), cardiac index (9% fall in group 1 and 18% fall in group 2), stroke volume index (13% fall in group 1 and 23% fall in group 2), stroke work index (14% fall in group 1 and 27% fall in group 2), with an increased heart rate (8% rise in group 1 and 5% rise in group 2), pulmonary artery occluded pressure (27% rise in group 1 and 21% rise in group 2), and systemic vascular resistance (11% rise in group 1 and 18% rise in group 2). Diastolic and mean arterial blood pressures did not change. Our data demonstrate that flecainide induced significant cardiodepression in both groups of patients. These effects were not significantly greater in patients with adequately controlled heart failure. These data suggest that the mild negative inotropic properties of flecainide in patients with recent myocardial infarction are comparable to those described for other class I antiarrhythmics.

Adult↗

PubMed1985

Haemodynamic analysis of the effects of nicardipine and metoprolol alone and in combination in coronary artery disease.

The circulatory consequences of concurrent slow-calcium channel (nicardipine) and cardioselective beta blockade (metoprolol) were evaluated in 20 patients with angiographically proven coronary artery disease. The rest and exercise haemodynamic impact of intravenous nicardipine (10 mg) or metoprolol (10 mg) alone was determined by randomly allocating 10 patients to each drug; finally all patients were assessed on combination therapy. The plasma levels of nicardipine (17 +/- 3 to 53 +/- 6 ng ml-1) and metoprolol (36 +/- 5 to 97 +/- 16 ng ml-1) achieved at the time of each study were in the established therapeutic range. At rest nicardipine reduced systemic mean arterial pressure and systemic vascular resistance index; cardiac and stroke volume indices increased without change in pulmonary artery occluded pressure. Metoprolol alone reduced systemic blood pressure, heart rate and cardiac index, and increased systemic vascular resistance index. Combination therapy reduced systemic arterial blood pressure and heart rate with relatively modest effects on cardiac index, systemic vascular resistance index and pulmonary artery occluded pressure. During dynamic exercise nicardipine reduced systemic mean and diastolic arterial pressure and stroke work index without change in other haemodynamic variables. Metoprolol reduced exercise systemic arterial pressures, heart rate and cardiac index, and increased systemic vascular resistance index and pulmonary artery occluded pressure. Combination therapy produced changes similar to those at rest; at peak nicardipine pharmacodynamic activity, the cardiac depressant actions of metoprolol were largely offset by the induced reduction in left ventricular afterload.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗

PubMed1985

Coronary insufficiency and beta-blockade.

Beta-blocking drugs were specifically introduced for the treatment of exercise-induced angina pectoris. Their therapeutic utility in this specific presentation of coronary insufficiency is undoubted. However, since they were introduced, evolution of the pathological, haemodynamic, and electrophysiological understanding of the disease syndrome has undergone considerable reappraisal, in no small measure owing to the physiological tool that these drugs have furnished. Their influence on the various aspects of the syndrome of exercise-induced ischaemic myocardial pain is widely known. The physiological conflict posed by unopposed blockade of one sympathetic outflow pathway remains the source of many of their clinical disadvantages. Many important questions directly related to their therapeutic use remain unanswered. The potential benefits and hazards of their long-term administration in patients with advanced coronary heart disease remains to be established.

Adrenergic beta-Antagonists↗

PubMed1985

Effects of buccal nitrate on left ventricular haemodynamics and volume at rest and during exercise-induced angina.

A novel approach has been employed to characterize the effects of a cardioactive drug on left ventricular haemodynamics and volume by simultaneously determining cardiac stroke volume (thermodilution) and left ventricular ejection fraction (nuclear probe). The effects of glyceryl trinitrate were evaluated in 12 patients with angiographically proven coronary artery disease at rest and 3, 7, 15 and 30 min following 10 mg buccal nitroglycerin (Suscard) administration. The impact of the drug on left ventricular haemodynamics and volume during exercise-induced angina was determined by repeating exercise 30 min following drug administration, at the workload that reliably induced angina during control exercise. At rest buccal nitroglycerin reduced systemic arterial pressure, cardiac and stroke volume indices, and increased heart rate. The left ventricular ejection fraction (E.F.) increased; its filling pressure together with end-diastolic and end-systolic volumes were significantly reduced. Compared with control supine-bicycle exercise, the drug reduced mean systemic arterial pressure and left ventricular filling pressure without change in cardiac and stroke volume indices. There was a smaller increase in left ventricular volume during exercise, and the fall in E.F. was attenuated. These data demonstrated differential actions of glyceryl trinitrate on left ventricular function related to the physiological state in obstructive coronary artery disease. These techniques appear to hold promise in the evaluation of the effects of other therapies on left ventricular volume in coronary artery disease.

Adult↗

PubMed1985

Haemodynamic dose-response effects of intravenous nisoldipine in coronary artery disease.

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.

Adult↗

PubMed1985

Anti-hypertensive dose-response effects of nicardipine in stable essential hypertension.

The dose-response effects of oral nicardipine on the systemic blood pressure were examined in 54 patients with uncomplicated essential hypertension (DBP greater than or equal to 100 mm Hg). The study was designed in four sequential stages. A 2 week single-blind placebo run-in period was followed by dose titration with nicardipine at 2 week intervals. Patients achieving the target DBP less than or equal to 95 mm Hg were then crossed over to placebo for 2 weeks, following which the previous dose of nicardipine was readministered for 6 weeks. Forty-eight patients completed the dose-titration phase. The target DBP 95 mm Hg was achieved in 33; in eight after 10 mg three times daily, in 21 after 20 mg three times daily, in three after 30 mg three times daily and in one after 40 mg three times daily. In the 48 patients, systolic blood pressure was reduced from 188 +/- 25 to 158 +/- 21 mm Hg (P less than 0.001) and diastolic blood pressure from 111 +/- 9 to 93 +/- 13 mm Hg (P less than 0.001); heart rate increased from 81 +/- 7 to 87 +/- 13 beats min-1 (P less than 0.01). Thirty-one of the 33 patients completed the crossover to placebo, which was accompanied by a significant increase towards pretreatment blood pressure levels. Reinstitution of nicardipine at the previous dose resulted in a reduction of SBP and DBP to levels not significantly different from those at the end of the dose-titration stage.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗