1 The haemodynamic and radionuclide effects of a new long-acting slow-calcium channel blocking agent, amlodipine, were evaluated in 32 patients with coronary artery disease. 2 Haemodynamic measurements in 24 patients were made at rest and 10 to 15 min after 20 mg i.v. amlodipine. Amlodipine significantly reduced systemic arterial blood pressure and vascular resistance index with an increased heart rate and augmented cardiac index. Cardiac stroke volume index rose and stroke work fell without change in pulmonary artery occluded pressure (PAOP). 3 The exercise effects were determined by comparison of measurements during 4 min of supine bicycle exercise at a fixed workload before and after drug treatment. During dynamic exercise, amlodipine reduced systemic arterial pressure and vascular resistance index. Exercise cardiac index, stroke volume index and heart rate were higher. The left ventricular filling pressure was significantly reduced. 4 Radionuclide parameters were studied in 16 patients at rest and on exercise; ejection fraction was unaltered following amlodipine. 5 Pre-therapy haemodynamic values correlated with response following amlodipine for resting mean blood pressure, systemic vascular resistance and exercise PAOP. 6 Thus, the immediate impact of amlodipine in stable coronary artery disease was to reduce left ventricular afterload and thereby improve cardiac pumping performance.
1 We have utilised a non-imaging echo-Doppler cardiac output device, using the principle of attenuated compensation volume flow (ACVF), to assess the cardiovascular effects of amlodipine and atenolol over 3 months in 24 patients with essential hypertension. 2 Both amlodipine and atenolol, at 4 and 12 weeks, similarly reduced mean arterial pressure (12 weeks amlodipine -12.6 mmHg, atenolol -14.9 mmHg; P < 0.01 for each vs baseline). 3 The heart rate fell on atenolol, both at 4 weeks (amlodipine -3 vs atenolol -12 beats min-'; P < 0.05) and 12 weeks (-1 vs -11 beats min-'; P < 0.05), without change on amlodipine. 4 Stroke volume initially rose on atenolol without change on amlodipine (4 weeks amlodipine -1.3 ml vs atenolol + 10.1 ml; P = 0.05) but between drug effects were not different at 12 weeks. 5 The systemic vascular resistance was reduced on amlodipine (12 weeks: amlodipine -176 dyn s cm-5: P < 0.05) without change on atenolol (atenolol -48 dyn s cm-5: NS). 6 The cardiac stroke work was lowered on amlodipine both at 4 weeks (P < 0.01) and 12 weeks (P < 0.05) and statistically different from the unaltered atenolol values at both time points. 7 Skin nutrient flow or fingertip temperature was not altered by either treatment. 8 These results are consistent with contrasting mechanisms of action -vasodilator for amlodipine and decreased cardiac pumping for atenolol. The greater reduction in cardiac stroke work on amlodipine compared with atenolol warrants further investigation during longer-term studies.
The hemodynamic consequences of blockade at both beta-adrenoceptors and slow calcium channels is of therapeutic importance for patients with angina pectoris. The hemodynamic interaction of a new cardioselective beta blocker, celiprolol, and nifedipine was examined in an acute hemodynamic study using three prospectively matched groups with angiographically confirmed coronary artery disease (n = 10/group). Patients were randomly allocated to intravenous celiprolol (8 mg), sublingual nifedipine (20 mg), or their combination. Rest and exercise (supine bicycle) hemodynamics were determined before and following each therapy. At rest, celiprolol did not alter pumping function; nifedipine reduced diastolic blood pressure and systemic vascular resistance index (SVRI), with a small increase in heart rate. Combination therapy reduced systemic arterial pressure and SVRI; heart rate and cardiac stroke volume index increased. During exercise celiprolol tended to reduce heart rate and cardiac index; nifedipine reduced exercise SVR and cardiac stroke work indices. Combination therapy reduced all components of blood pressure; cardiac stroke work and SVR indices fell. These hemodynamic data suggest that beta blockade with celiprolol may result in a slight depression of cardiac pumping during exercise; however, such effects are offset by the vasodilating actions of nifedipine (reflex sympathetic action offsetting cardiodepression). Thus the acute hemodynamic effects of this combination were seemingly safe in these patients; the longer term effects during maintained therapy should be further assessed.
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