Cardiac remodeling—concepts and clinical implications: a consensus paper from an international forum on cardiac remodeling

Abstract

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.

Significance of myocardial tenascin‐C expression in left ventricular remodelling and long‐term outcome in patients with dilated cardiomyopathy

“…The outcome of DCM varies greatly among individual cases and is closely associated with the degree of LV remodelling and whether cardiac function is improved by conventional therapy, including β‐blockers and ACE‐inhibitors 13, 14. Left ventricular remodelling is affected by various kinds of neurohumoral and local factors such as the renin–angiotensin–aldosterone system, the adrenergic nervous system, increased oxidative stress, proinflammatory cytokines, and endothelin 13, 14, 15, 16, 17.…”

“…Left ventricular remodelling is affected by various kinds of neurohumoral and local factors such as the renin–angiotensin–aldosterone system, the adrenergic nervous system, increased oxidative stress, proinflammatory cytokines, and endothelin 13, 14, 15, 16, 17. However, the precise mechanisms that cause LV remodelling are still unclear.…”

Adiponectin protects against the development of systolic dysfunction following myocardial infarction

“…Progressive cardiac hypertrophy that occurs in response to MI is known to increase risk of heart failure, although it is believed to be compensatory at the initial stages of remodeling [43]. In this regard, some experimental studies have shown that the development of heart failure can be inhibited by genetic alterations that inhibit cardiac hypertrophy [44].…”

The immune system and cardiac repair

“…Infarct healing results in profound changes in ventricular architecture and geometry, also referred to as "ventricular remodeling" [3], [4]. The molecular and cellular changes associated with ventricular remodeling affect both the necrotic zone and the non-infarcted segments of the ventricle and manifest clinically as chamber dilation, cardiac hypertrophy, increased sphericity of the ventricle and worsened cardiac function [5]. Remodeling is linked to heart failure progression and is associated with poor prognosis following myocardial infarction.…”