Article date: December 1993
By: T.C.K. THAM, N. HERITY, S. GUY, B. SILKE, in Volume 36, Issue 6, pages 555-560
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.
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).
The heart rate fell on atenolol, both at 4 weeks (amlodipine −3 vs atenolol −12 beats min−1; P < 0.05) and 12 weeks (−1 vs −11 beats min−1; P < 0.05), without change on amlodipine.
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.
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).
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.
Skin nutrient flow or fingertip temperature was not altered by either treatment.
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.
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.
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).
The heart rate fell on atenolol, both at 4 weeks (amlodipine −3 vs atenolol −12 beats min−1; P < 0.05) and 12 weeks (−1 vs −11 beats min−1; P < 0.05), without change on amlodipine.
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.
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).
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.
Skin nutrient flow or fingertip temperature was not altered by either treatment.
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.
DOI: 10.1111/j.1365-2125.1993.tb00414.x
View this article