2010
DOI: 10.1253/circj.cj-09-0989
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Comparative Effects of Carvedilol vs Bisoprolol for Severe Congestive Heart Failure - Special Reference to Atrial Fibrillation -

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Cited by 39 publications
(33 citation statements)
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“…This finding is consistent with a study by Konishi et al, who noted a significant decrease in HR among 110 Japanese patients assigned to a low-dose carvedilol regimen for 18 months. 45 Moreover, in a meta-analysis of HF β-blocker trials, McAlister et al observed a relationship between the extent of the reduction in HR, not the dose of β-blocker, and the magnitude of increased survival. 43 HR reduction is regarded as a marker of sympathetic suppression.…”
Section: Discussionmentioning
confidence: 99%
“…This finding is consistent with a study by Konishi et al, who noted a significant decrease in HR among 110 Japanese patients assigned to a low-dose carvedilol regimen for 18 months. 45 Moreover, in a meta-analysis of HF β-blocker trials, McAlister et al observed a relationship between the extent of the reduction in HR, not the dose of β-blocker, and the magnitude of increased survival. 43 HR reduction is regarded as a marker of sympathetic suppression.…”
Section: Discussionmentioning
confidence: 99%
“…4,5) Among the 3 BBs that have been shown to be effective in systolic HF, ie, carvedilol, bisoprolol, and metoprolol succinate, carvedilol has been used the most all over the world. [6][7][8] The approved maximal dose is 20 mg/day in Japan, whereas its standard dose in the United States and Europe is 50 mg/day. HF guidelines from the US 4) and Europe 5) state that BBs should be titrated as much as tolerated.…”
mentioning
confidence: 99%
“…The polymorphism has gained much attention because, when overexpressed at very high levels KEYWORDS: b-blockers n ADBR1 gene polymorphisms n atrial fibrillation n bisoprolol n carvedilol n heart failure in heterologous cell systems, the Gly389 variant stimulates cAMP synthesis fivefold less than the Arg389 variant, that is, it is a minus variant. Since chronic hyperactivity of b1-adrenoceptors is thought to adversely affect cardiovascular outcome and b-blockade improves it [7,8], it was initially assumed that the homozygous presence of the Arg389 variant would confer a higher risk in patients at high cardiac risk, on the one hand, and better response to b-blockade on the other hand. Indeed, in retrospective clinical analyses, some studies in transgenic mice and isolated human heart muscle preparations reported higher signaling activity of the Arg389 variant and greater responses to b-blockade (see overview in [9,10]).…”
mentioning
confidence: 99%