Remodelling and adverse remodelling in CAD
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enner · G. Ertl Department of Internal Medicine I/Comprehensive Heart Failure Center, University Hospital Würzburg, Würzburg
Remodelling and adverse remodelling in CAD Introduction At the end of the before last century, German anatomists (Krehl, Romberg, Aschoff, Tawara, Linzbach) already discussed disease-related alterations in cardiac morphology [1]. In 1982, Hochman and Buckey used the term ‘remodelling’ to describe the replacement of necrotic debris by healing tissue after myocardial infarction [2]. Janice A. Pfeffer characterized the dilatation of left ventricular cavity in the rat model of myocardial infarction as ‘remodelling’ in 1985 [3]. In 1990, Mark A. Pfeffer and Eugene Braunwald reviewed ventricular dysfunction resulting from remodelling after acute myocardial infarction [4]. Ten years later, the International Forum on Cardiac Remodelling defined cardiac remodelling as altered genome expression resulting in molecular, cellular and interstitial changes with clinical manifestations in size, shape and function of the heart in response to cardiac load or injury [5]. According to this definition, cardiac remodelling has been observed in a variety of physiological and pathological conditions (. Tab. 1). Reversion of cardiac remodelling with restoration to normal left ventricular size and function has been shown when the underlying stressor has released [6], and bears witness to the enormous cardiac plasticity [7, 8]. Cardiac remodelling may represent an adaptive process to maintain the function of the heart when challenged by effort, volume expansion, overload or injury [7, 9]. Its continuation may turn into a maladaptive process with deterioration of cardiac function. Indicators for the transition from adaptive to maladaptive remod-
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Herz 6 · 2012
elling are unknown and the time course may vary greatly depending on the underlying myocardial damage and stressor intensity. However, maladaptive or adverse cardiac remodelling represents the final pathway of all the conditions causing the heart failure syndrome. This article focuses on cardiac remodelling in coronary artery disease.
Remodelling in coronary artery disease Pfeffers and Braunwald contributed fundamental work on cardiac remodelling post myocardial infarction [3, 4, 10]. Remodelling is initiated by one or several serial ischemic injuries. Loss of contractility in the infracted region increases residual volume and diastolic wall tension. In response, hypercontractility of the noninfracted region is induced to maintain stroke volume. The resulting interaction between hypokinetic and hyperkinetic myocardium redistributes the intracavital
wall tension of the ventricle. Due to anatomy of the coronary arteries, the ventricular apex is at the highest risk of being affected by ischemia. In this case, wall stress increases from base to apex ([11], . Fig. 1). Additionally, the infiltration of inflammatory cells contributes to wall thinning and dilatation until collagen type III is replaced by matured collagen type I [11] and scar formation is complet
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