Marked improvement in left ventricular ejection fraction during long-term β-blockade in patients with chronic heart failure: Clinical correlates and prognostic significance

Metra, Marco; Nodari, Savina; Parrinello, Giovanni; Giubbini, Raffaele; Manca, C; Dei, Livio

doi:10.1067/mhj.2003.105

Cited by 101 publications

(64 citation statements)

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“…In a study by Metra et al, 7 22% of the patients receiving β-blockers had an increase in LVEF of ≥15 absolute unit; more recently, we reported an LVEF>45% after β-blockade in 126 out of 314 patients with LVSD. 8 Although this reverse remodeling has been associated with a better midterm prognosis, its long-term implications are uncertain.…”

Section: Discussionmentioning

confidence: 99%

“…[3][4][5] The mean improvement in LVEF is close to 9% in meta-analyses, 6 and this improvement has been associated with a favorable outcome. 7,8 In some patients, β-blockers may induce a major improvement with an almost normalization of LVEF. These patients with recovered LVEF represent a distinct subgroup of patients, different from patients with heart failure with preserved LVEF.…”

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confidence: 99%

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Long-Term Functional and Clinical Follow-Up of Patients With Heart Failure With Recovered Left Ventricular Ejection Fraction After β-Blocker Therapy

Groote

Fertin

Pentiah

et al. 2014

Circ: Heart Failure

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Background-Some patients with left ventricular systolic dysfunction (LVSD) have a dramatic improvement in left ventricular ejection fraction (LVEF) after β-blockade. No study has analyzed the long-term echocardiographic and clinical follow-up of this subgroup of patients. Methods and Results-We included in this analysis 174 consecutive patients with LVSD who had an LVEF≥45% after β-blockade. We performed a long-term echocardiographic follow-up (median 7.7 [4-9.9] years) and clinical follow-up (median 9.2 [7.2-10.8] years). LVEF improved from 33±8% to 54±6% after β-blockade (P<0.0001). At the last echocardiographic evaluation, 26% of the patients had an LVEF<45% (mean±SD: 34±6%), whereas 74% still had an LVEF≥45% (mean±SD: 54±6%). Independent predictors of LVEF deterioration were a low LVEF, a high left ventricular end-diastolic diameter and a low heart rate after β-blockade, and the presence of a complete left bundle-branch block. In the overall study population, survival rates were 90% at 5 years and 75% at 10 years. Cardiovascular death rate was 9%, noncardiovascular death rate was 11%, and unknown death rate was 3%. Patients with subsequent LVEF deterioration had a higher cardiovascular mortality compared with patients with sustained recovered LVEF (22% versus 4%). Conclusions-The long-term survival of patients with LVSD and with near-normal LVEF after β-blockade is good.However, a quarter of these patients may experience a subsequent degradation of LVEF. These patients are at higher risk of cardiovascular mortality. (Circ Heart Fail. 2014;7:434-439.)

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Section: Discussionmentioning

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Long-Term Functional and Clinical Follow-Up of Patients With Heart Failure With Recovered Left Ventricular Ejection Fraction After β-Blocker Therapy

Groote

Fertin

Pentiah

et al. 2014

Circ: Heart Failure

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“…Although SHIFT emphasized the importance of isolated heart rate reduction on outcomes in patients with HF, several β-blocker trials could not establish any relationship between the baseline heart rate and the efficacy of β-blocker therapy with either nonselective agents 132,133 or selective agents.…”

Section: Imaging Of Cardiac Sympathetic Nerve Terminalsmentioning

confidence: 99%

The Autonomic Nervous System and Heart Failure

Florea

Cohn

2014

Circulation Research

453

366

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Abstract:The pathophysiology of heart failure (HF) is characterized by hemodynamic abnormalities that result in neurohormonal activation and autonomic imbalance with increase in sympathetic activity and withdrawal of vagal activity. Alterations in receptor activation from this autonomic imbalance may have profound effects on cardiac function and structure. Inhibition of the sympathetic drive to the heart through β-receptor blockade has become a standard component of therapy for HF with a dilated left ventricle because of its effectiveness in inhibiting the ventricular structural remodeling process and in prolonging life. Several devices for selective modulation of sympathetic and vagal activity have recently been developed in an attempt to alter the natural history of HF. The optimal counteraction of the excessive sympathetic activity is still unclear. A profound decrease in adrenergic support with excessive blockade of the sympathetic nervous system may result in adverse outcomes in clinical HF. In this review, we analyze the data supporting a contributory role of the autonomic functional alterations on the course of HF, the techniques used to assess autonomic nervous system activity, the evidence for clinical effectiveness of pharmacological and device interventions, and the potential future role of autonomic nervous system modifiers in the management of this syndrome. (Circ Res. 2014;114:1815-1826.) Key Words: autonomic nervous system ■ heart failure ■ norepinephrine ■ receptors, adrenergicThe Autonomic Nervous System and Heart Failure Viorel G. Florea, Jay N. Cohn This Review is in a thematic series on The Autonomic Nervous System and the Cardiovascular System, which includes the following articles: Role of the Autonomic Nervous System in Modulating Cardiac Arrhythmias [Circ Res. 2014;114:1004-1021 The Autonomic Nervous System and Hypertension [Circ Res. 2014;114:1804-1814 The Autonomic Nervous System and Heart Failure Renal Denervation for the Treatment of Cardiovascular High Risk-Hypertension or Beyond? Original received February 10, 2014; revision received April 29, 2014; accepted April 29, 2014. In March 2014, the average time from submission to first decision for all original research papers submitted to Circulation Research was 12.63 days.From the Minneapolis VA Health Care System, Section of Cardiology (V.G.F.) and Rasmussen Center for Cardiovascular Disease Prevention, Department of Medicine (J.N.C.), University of Minnesota Medical School.Correspondence to Jay N. endocardium. Parasympathetic effects are carried by the right and left vagus nerves, originating in the medulla. The vagus nerve further divides into the superior and inferior cardiac nerves, finally merging with the postganglionic sympathetic neurons to form a plexus of nerves at the base of the heart, known as the cardiac plexus. 1The 2 mediators of the SNS, norepinephrine and epinephrine, derive from 2 major sources in the body: the sympathetic nerve endings, which release norepinephrine directly into the synaptic cleft, and the adren...

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“…In recent years, new evidence has emerged indicating that chronic ␤-blockade in patients suffering from heart failure, including that caused by MI, improves LV dysfunction and reduces the risk of sudden death (21,24). It has been suggested that one of the key cardioprotective roles of ␤-blockers under such conditions is the characteristic decrease in heart rate, leading to improved myocardial blood flow due to a lengthened diastolic perfusion time (4).…”

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Reduction of heart rate by chronic β₁-adrenoceptor blockade promotes growth of arterioles and preserves coronary perfusion reserve in postinfarcted heart

Dedkov¹,

Christensen²,

Weiß³

et al. 2005

American Journal of Physiology-Heart and Circulatory Physiology

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Dedkov, Eduard I., Lance P. Christensen, Robert M. Weiss, and Robert J. Tomanek. Reduction of heart rate by chronic ␤1-adrenoceptor blockade promotes growth of arterioles and preserves coronary perfusion reserve in postinfarcted heart. Am J Physiol Heart Circ Physiol 288: H2684 -H2693, 2005. First published January 28, 2005 doi:10.1152/ajpheart.01047.2004.-Adequate growth of coronary vasculature in the remaining left ventricular (LV) myocardium after myocardial infarction (post-MI) is a crucial factor for myocyte survival and performance. We previously demonstrated that post-MI coronary angiogenesis can be stimulated by bradycardia induced with the ATP-sensitive K ϩ channel antagonist alinidine. In this study, we tested the hypothesis that heart rate reduction with ␤-blockade may also induce coronary growth in the post-MI heart. Transmural MI was induced in 12-mo-old male Sprague-Dawley rats by occlusion of the left anterior descending coronary artery. Bradycardia was induced by administration of the ␤-adrenoceptor blocker atenolol (AT) via drinking water (30 mg/day). Three groups of rats were compared: 1) control/sham (C/SH), 2) MI, and 3) MI ϩ AT. In the MI ϩ AT rats, heart rate was consistently reduced by 25-28% compared with C/SH rats. At 4 wk after left anterior descending coronary ligation, infarct size was similar in MI and MI ϩ AT rats (67.1 and 61.5%, respectively), whereas a greater ventricular hypertrophy occurred in bradycardic rats, as indicated by a higher ventricular weight-to-body weight ratio (3.4 Ϯ 0.1 vs. 2.8 Ϯ 0.1 mg/g in MI rats). Analysis of LV function revealed a smaller drop in ejection fraction in the MI ϩ AT than in the MI group (ϳ24 vs. ϳ35%). Furthermore, in MI ϩ AT rats, maximal coronary conductance and coronary perfusion reserve were significantly improved compared with the MI group. The better myocardial perfusion indexes in MI ϩ AT rats were associated with a greater increase in arteriolar length density than in the MI group. Thus chronic reduction of heart rate induced with ␤-selective blockade promotes growth of coronary arterioles and, thereby, facilitates regional myocardial perfusion in post-MI hearts. myocardial infarction; angiogenesis; coronary circulation; resistance vessels; capillaries A LARGE TRANSMURAL MYOCARDIAL infarction (MI) of the left ventricle (LV) causes the sudden loss of a substantial number of cardiac myocytes, which leads to increased diastolic wall stress and chronic functional overload of the remaining portion of LV myocardium. As a result, the LV undergoes progressive structural remodeling, consisting of thinning and scarring of the infarcted region, chamber dilation, and eccentric hypertrophy of the surviving portion of the LV myocardium (1,27,30).Because scar tissue is not capable of contracting, LV function after MI is entirely dependent on the hypertrophied portion of the surviving LV myocardium. However, to accommodate an increased O 2 demand in the surviving overloaded cardiac myocytes, an adaptation of the vascular bed is necessary. Two basic me...

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Marked improvement in left ventricular ejection fraction during long-term β-blockade in patients with chronic heart failure: Clinical correlates and prognostic significance

Cited by 101 publications

References 25 publications

Long-Term Functional and Clinical Follow-Up of Patients With Heart Failure With Recovered Left Ventricular Ejection Fraction After β-Blocker Therapy

Long-Term Functional and Clinical Follow-Up of Patients With Heart Failure With Recovered Left Ventricular Ejection Fraction After β-Blocker Therapy

The Autonomic Nervous System and Heart Failure

Reduction of heart rate by chronic β₁-adrenoceptor blockade promotes growth of arterioles and preserves coronary perfusion reserve in postinfarcted heart

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Marked improvement in left ventricular ejection fraction during long-term β-blockade in patients with chronic heart failure: Clinical correlates and prognostic significance

Cited by 101 publications

References 25 publications

Long-Term Functional and Clinical Follow-Up of Patients With Heart Failure With Recovered Left Ventricular Ejection Fraction After β-Blocker Therapy

Long-Term Functional and Clinical Follow-Up of Patients With Heart Failure With Recovered Left Ventricular Ejection Fraction After β-Blocker Therapy

The Autonomic Nervous System and Heart Failure

Reduction of heart rate by chronic β1-adrenoceptor blockade promotes growth of arterioles and preserves coronary perfusion reserve in postinfarcted heart

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Reduction of heart rate by chronic β₁-adrenoceptor blockade promotes growth of arterioles and preserves coronary perfusion reserve in postinfarcted heart