In conclusion , NVBBs , but not VBBs , determine a lower reduction in cSBP than in pSBP .
However , the difference in treatment-induced SBP amplification changes between NVBB and VBB is nearly abolished after accounting for differences in heart rate changes
β-Blockers are less effective than other antihypertensive drug classes in reducing central systolic blood pressure ( cSBP ) as compared with peripheral SBP ( pSBP ) .
Whether this effect is less pronounced with vasodilating β-blockers ( VBB ) when compared with nonvasodilating β-blockers ( NVBB ) remains unsettled .
Carvedilol reduces aortic wave reflection and improves left ventricular/vascular coupling: a comparison with atenolol (CENTRAL Study).
Blood pressure ( BP ) characteristics , such as central aortic pressure and arterial stiffness , independently predict cardiovascular events . The effects of pharmacologically dissimilar β-blockers on these properties have not been fully eluci date d. Patients with essential hypertension and without significant concomitant cardiovascular disease were r and omly assigned to controlled-release carvedilol , force-titrated to 80 mg ( n=22 ) , or atenolol , force-titrated to 100 mg ( n=19 ) ; each was given once daily for 4 weeks . Baseline characteristics were similar . At the end of week 4 , atenolol and carvedilol  reduced central and brachial systolic and diastolic BP to a similar extent . Central augmentation index was increased in atenolol-treated patients but not carvedilol-treated patients ( atenolol 4.47 % vs carvedilol -0.68 % ; P=.04 ) . Mean augmented central aortic pressure increased slightly during atenolol treatment ( + 1.1 mm Hg ) but decreased slightly during carvedilol treatment ( -1.1 mm Hg ) , although the difference in these changes was not statistically significant ( P=.23 ) . Pulse pressure amplification was reduced more with atenolol at week 4 ( atenolol -10.7 % vs carvedilol -1.8 % ; P=.02 ) . Therefore , we conclude that carvedilol results in more favorable pulse pressure amplification and augmentation index by increasing arterial compliance and reducing the magnitude of wave reflection , respectively , compared with atenolol
In conclusion , NVBBs , but not VBBs , determine a lower reduction in cSBP than in pSBP .
However , the difference in treatment-induced SBP amplification changes between NVBB and VBB is nearly abolished after accounting for differences in heart rate changes
β-Blockers are less effective than other antihypertensive drug classes in reducing central systolic blood pressure ( cSBP ) as compared with peripheral SBP ( pSBP ) .
Whether this effect is less pronounced with vasodilating β-blockers ( VBB ) when compared with nonvasodilating β-blockers ( NVBB ) remains unsettled .