Beta-Blockers for Primary Prevention of Heart Failure in Patients With Hypertension

Bangalore, Sripal; Wild, David; Parkar, Sanobar; Kukin, Marrick; Messerli, Franz H.

doi:10.1016/j.jacc.2008.05.057

Cited by 87 publications

(53 citation statements)

References 49 publications

(44 reference statements)

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“…[24][25][26] To date, with the advent of effective drugs to lower blood pressure, concern is now shifting toward how to manage the causal complications typified by hypertensive heart failure with extremely poor prognosis. [24][25][26] Cardiac fibrosis is highly correlated with cardiac dysfunction in patients with a hypertensive heart. 27 Therefore, the reduction or improvement of cardiac fibrosis might be a useful treatment for heart failure.…”

Section: Discussionmentioning

confidence: 99%

Hepatocyte Growth Factor Reduces Cardiac Fibrosis by Inhibiting Endothelial-Mesenchymal Transition

et al. 2012

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Abstract-The purpose of this study was to investigate the effect of hepatocyte growth factor (HGF) on the pathogenesis of cardiac fibrosis induced by pressure overload in mice. Although cardiac fibrosis is attributed to excess pathological deposition of extracellular matrix components, the mechanism remains unclear. Recent reports revealed that ␣-smooth muscle actin-expressing myofibroblasts are primarily responsible for fibrosis. It is believed that myofibroblasts are differentiated from resident fibroblasts, whereas the transformation of vascular endothelial cells into myofibroblasts, known as endothelial-mesenchymal transition, has been suggested to be intimately associated with perivascular fibrosis. Thus, we hypothesized that HGF prevents cardiac fibrosis by blocking these pathways. We analyzed the pressureoverloaded HGF-transgenic mouse model made by transverse aortic constriction. Human coronary artery endothelial cells and human cardiac fibroblasts were examined in vitro after being treated with transforming growth factor-␤1 or angiotensin II with or without HGF. The amount of cardiac fibrosis significantly decreased in pressure-overloaded HGF-transgenic mice compared with pressure-overloaded nontransgenic controls, particularly in the perivascular region. This was accompanied by a reduction in the expression levels of fibrosis-related genes and by significant preservation of echocardiographic measurements of cardiac function in the HGF-transgenic mice (PϽ0.05). The survival rate 2 months after transverse aortic constriction was higher by 45% (PϽ0.05). HGF inhibited the differentiation of human coronary artery endothelial cells into myofibroblasts induced by transforming growth factor-␤1 and the phenotypic conversion of human cardiac fibroblasts into myofibroblasts. We conclude that HGF reduced cardiac fibrosis by inhibiting endothelialmesenchymal transition and the transformation of fibroblasts into myofibroblasts. 1 The number of cardiovascular deaths has been reduced, but in spite of a marked development in recent devices and medicines, cardiovascular disease still impacts the mortality rate in almost all nations.2 Cardiac fibrosis is often present in end-stage heart failure and is caused by various factors, such as ischemia, 3 pressure overload, 4 and cardiomyopathy, 5 so antifibrotic therapy is believed to be beneficial in preventing heart failure. Although fibrosis, which is attributed to an excess deposition of extracellular matrix (ECM) components, is one of the most common pathological changes found in various organs, including the heart, the detailed mechanism remains unclear. It is worth noting that myofibroblasts are characterized by ␣-smooth muscle actin (␣-SMA) expression and appear to play a major role in the pathogenesis of fibrosis by secreting numerous cytokines, growth factors, and ECM proteins. 6 Myofibroblasts were originally thought to be differentiated from resident fibroblasts activated by acute or chronic stimuli, such as myocardial infarction and pressure overload. On the other ...

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Section: Discussionmentioning

confidence: 99%

Hepatocyte Growth Factor Reduces Cardiac Fibrosis by Inhibiting Endothelial-Mesenchymal Transition

et al. 2012

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“…2 In fact, in patients with risk factors alone, β-blocker use was associated with higher risk of primary outcome (composite of cardiovascular death, MI, or stroke; hazards ratio [HR], 1.18; 95% confidence interval [CI], 1.02-1.36; P=0.02), with a strong trend of a higher risk of stroke (HR, 1.22; 95% CI, 0.99-1.52; P=0.06), 2 a finding consistent with that of data from randomized trials. 3,4 However, in those with more recent MI (≤1 year) in REACH, β-blocker use was associated with a lower incidence of composite cardiovascular outcomes including hospitalization for cardiovascular causes. 2 Although there are advantages to such data derived from a large real-world registry, including the large sample size and reflect real-world practice patterns there are potential limitations of registry data including selection bias and lack of rigorous collection/adjudication of outcomes.…”

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confidence: 99%

β-Blockers and Cardiovascular Events in Patients With and Without Myocardial Infarction

Bangalore

Bhatt

Steg

et al. 2014

Circ: Cardiovascular Quality and Outcomes

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Background-The long-term efficacy of β-blockers in patients with and without myocardial infarction (MI) is controversial. Methods and Results-This is post hoc analysis from the Clopidogrel for High Atherothrombotic Risk and IschemicStabilization, Management, and Avoidance (CHARISMA) trial of 4772 patients with prior MI, 7804 patients with known atherothrombosis, and 2101 patients with risk factors alone but without heart failure. Primary outcome was a composite of nonfatal MI, stroke, or cardiovascular mortality. The cohorts were divided into 2 groups based on baseline β-blocker use.In the propensity score-matched prior MI cohort, after 28 months of follow-up, β-blocker use was associated with a 31% 20).In the known atherothrombotic disease and the risk factors alone cohorts, β-blocker use was not associated with lower ischemic outcomes, whereas a trend toward a higher risk of stroke (3.5% versus 1.5%; hazards ratio, 2.13; 95% confidence interval, 0.92-4.92; P=0.079) was observed in the risk factors alone cohort. This higher stroke risk was significant in the regression model adjusted to the propensity score (hazards ratio, 2.69; 95% confidence interval, 1.33-5.44; P=0.006) and in the multivariable models. Conclusions-β-blocker use in patients with prior MI but no heart failure was associated with a lower composite cardiovascular outcome driven by lower risk of recurrent MI with no difference in mortality. However, β-blocker use was not associated with lower cardiovascular events in those without MI, with a suggestion of inferior outcome with regard to stroke risk. Clinical Trial Registration-URL: http://www.clinicaltrials.gov. Unique identifier: NCT00050817.(Circ Cardiovasc Qual Outcomes. 2014;7:872-881.)

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“…22 Carvedilol and other beta-1 blockers were found to be non-inferior to other classes of antihypertensive drugs with regard to primary prevention of heart failure. 23 DHPs may not be superior with regard to primary prevention of heart failure. 24 Hence, carvedilol in patients with chronic renal failure may be preferred in this regard.…”

Section: Discussionmentioning

confidence: 99%

Carvedilol as nephroprotective agent: a meta-analysis of randomized controlled trials

Hiremath

Lokikere

2016

Int J Basic Clin Pharmacol

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Beta-Blockers for Primary Prevention of Heart Failure in Patients With Hypertension

Cited by 87 publications

References 49 publications

Hepatocyte Growth Factor Reduces Cardiac Fibrosis by Inhibiting Endothelial-Mesenchymal Transition

Hepatocyte Growth Factor Reduces Cardiac Fibrosis by Inhibiting Endothelial-Mesenchymal Transition

β-Blockers and Cardiovascular Events in Patients With and Without Myocardial Infarction

Carvedilol as nephroprotective agent: a meta-analysis of randomized controlled trials

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