REVIEW ARTICLES
Cardiac remodeling—concepts and clinical implications: a consensus paper from an international forum on cardiac remodeling
Jay N. Cohn, MD*,
Roberto Ferrari, MD ,
Norman Sharpe, MD on Behalf of an International Forum on Cardiac Remodeling
* Department of Medicine, Cardiovascular Division, University of Minnesota Medical School, Minneapolis, Minnesota, USA
Cattedra di Cardiologia, Universita degli Studi di Ferrara, Ferrara, Italy
Department of Medicine and Health Sciences, University of Auckland School of Medicine, Auckland, New Zealand
Manuscript received June 3, 1999;
revised manuscript received October 15, 1999,
accepted November 18, 1999.
Reprint requests and correspondence: Dr. Jay N. Cohn, Cardiovascular Division, Department of Medicine, University of Minnesota Medical School, 420 Delaware Street, SE—Box 508 UMHC, Minneapolis, Minnesota 55455
Cardiac remodeling is generally accepted as a determinant of the clinical course of heart failure (HF). Defined as genome expression resulting in molecular, cellular and interstitial changes and manifested clinically as changes in size, shape and function of the heart resulting from cardiac load or injury, cardiac remodeling is influenced by hemodynamic load, neurohormonal activation and other factors still under investigation.
Although patients with major remodeling demonstrate progressive worsening of cardiac function, slowing or reversing remodeling has only recently become a goal of HF therapy. Mechanisms other than remodeling can also influence the course of heart disease, and disease progression may occur in other ways in the absence of cardiac remodeling.
Left ventricular end-diastolic and end-systolic volume and ejection fraction data provide support for the beneficial effects of therapeutic agents such as angiotensin-converting enzyme (ACE) inhibitors and beta-adrenergic blocking agents on the remodeling process. These agents also provide benefits in terms of morbidity and mortality. Although measurement of ejection fraction can reliably guide initiation of treatment in HF, opinions differ regarding the value of ejection fraction data in guiding ongoing therapy. The role of echocardiography or radionuclide imaging in the management and monitoring of HF is as yet unclear.
To fully appreciate the potential benefits of HF therapies, clinicians should understand the relationship between remodeling and HF progression. Their patients may then, in turn, acquire an improved understanding of their disease and the treatments they are given.
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Abbreviations and Acronyms
| | ACE | = angiotensin-converting enzyme | | AIRE | = Acute Infarction Ramipril Evaluation Study | | ANP | = atrial natriuretic peptide | | ANZ | = Australia/New Zealand Collaborative Group | | CIBIS II | = Cardiac Insufficiency Bisoprolol Study | | ECG | = electrocardiogram | | HF | = heart failure | | LV | = left ventricular | | MDC | = Metropol Dilated Cardiomyopathy trial | | MERIT-HF | = Metoprolol CR/XL Randomized Intervention Trial in Heart Failure | | MI | = myocardial infarction | | MRI | = magnetic resonance imaging | | NO | = nitric oxide | | RAS | = renin angiotensin system | | SAVE | = Survival and Ventricular Enlargement Study | | SNS | = sympathetic nervous system | | SOLVD | = Studies of Left Ventricular Dysfunction | | TBARS | = thiobarbituric acid reactive substances | | TNF | = tumor necrosis factor | | TRACE | = Trandolapril Cardiac Evaluation Study | | V-HeFT I and V-HeFT II | = Vasodilator Heart Failure Trials |
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