what is Left ventricular remodeling , acute and chronic remodeling and ‘ stunning ‘???
Ventricular remodeling refers to the changes in LV mass, volume, shape, size, function and composition are regulated by mechanical, neurohormonal, and genetic factors. These de novo changes of the heart that occur following cardiac injury and/or abnormal hemodynamic loading conditions. Remodeling may be physiological and adaptive during normal growth or pathological due to myocardial infarction, cardiomyopathy, hypertension, or valvular heart disease (Figure 1),
Figure 1. Diagrammatic representation of the many factors involved in the pathophysiology of ventricular remodeling. ECM indicates extracellular matrix; RAAS, renin-angiotensin-aldosterone system; CO, cardiac output; SVR, systemic vascular resistance; LV, left ventricular;and AII, angiotensin II.
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driven on a histologic level by a combination of pathologic myocyte hypertrophy, myocyte apoptosis, myoﬁbroblast proliferation, and interstitial ﬁbrosis(fig 3 ) .
Figure 3. Ventricular Remodeling: Gross and Microscopic Architecture Schematic representation of post-myocardial infarction (post-MI) left ventricular remodeling. The early phase is characterized by thinning and elongation of the ﬁbrous scar within the infarcted zone. Subsequent left ventricular dilation, with transition from an elliptical to a more spherical conﬁguration, is driven principally by diffuse myocyte hypertrophy associated with increased apoptosis (not shown) and increases in interstitial collagen. Figure illustration by Craig Skaggs.
LV remodeling may contribute independently to the progression of HF by virtue of the mechanical burdens that are engendered by the changes in the geometry of the remodeled LV.
LV remodeling develops in response to a series of complex events that occur at the cellular and molecular levels. These changes include: (1) myocyte hypertrophy; (2) alterations in the contractile properties of the myocyte; (3) progressive loss of myocytes through necrosis, apoptosis, and autophagic cell death; (4) -adrenergic desensitization; (5) abnormal myocardial energetics and metabolism; and (6) reorganization of the extracellular matrix with dissolution of the organized structural collagen weave surrounding myocytes and subsequent replacement by an interstitial collagen matrix that does not provide structural support to the myocytes.
The myocardium consists of 3 integrated components: myocytes, extracellular matrix, and the capillary microcirculation that services the contractile unit assembly. Consideration of all 3 components provides important insights into the remodeling process and a rationale for future therapeutic strategies. The cardiomyocyte is terminally differentiated and develops tension by shortening. The extracellular matrix provides a stress-tolerant, viscoelastic scaffold consisting of type I and type III collagen that couples myocytes and maintains the spatial relations between the myofilaments and their capillary microcirculation. Myocardial infarction results in the migration of macrophages, monocytes, and neutrophils into the infarct zone; this initiates intracellular signaling and neurohormonal activation, which localizes the inflammatory response. Changes in circulatory hemodynamics are determined primarily by the magnitude of myocyte loss, the stimulation of the sympathetic nervous system and renin-angiotensin-aldosterone system, and the release of natriuretic peptides.
Postinfarction remodeling has been arbitrarily divided into an early phase (within 72 hours) and a late phase (beyond 72 hours). The early phase involves expansion of the infarct zone, which may result in early ventricular rupture or aneurysm formation. Late remodeling involves the left ventricle globally and is associated with time-dependent dilatation, the distortion of ventricular shape, and mural hypertrophy(fig 2 ).
Figure 2. Left ventricular (LV) remodeling after transmural anteroseptal myocardial infarction (MI): 2D echocardiographic evaluation at 1 week and 3 months. Extensive anteroapical akinesis, progressive dilatation, and dysfunction with increased sphericity are evident, as is the development of apical thrombus. EDV indicates end-diastolic volume; ESV, end-systolic volume; and EF, ejection fraction.
The failure to normalize increased wall stresses results in progressive dilatation, recruitment of border zone myocardium into the scar, and deterioration in contractile function.