CXCR4 gene transfer prevents pressure overload induced heart failure
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Pressure overload
Ventricular remodeling
Pressure overload
Ventricular hypertrophy
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The accumulation of collagen within the myocardium is termed fibrosis. In left ventricular pressure overload a reactive interstitial fibrosis, having distinctive biochemical and structural features, is seen. This reactive fibrosis occurs in the absence of myocyte necrosis, is progressive in nature, and initially is an adaptive response that preserves the force generating capacity, or active (systolic) stiffness, of the hypertrophied myocardium. Later in hypertrophy a reparative (or replacement) fibrosis occurs in response to cell loss, the pathogenesis of which is not clear. Nevertheless, independently of cell loss, interstitial fibrosis can have a detrimental influence on the diastolic and systolic stiffness of the myocardium and can result in pathologic hypertrophy with heart failure. In established hypertrophy with disproportionate collagen matrix remodeling (ie, interstitial heart disease), it would be desirable to retard the continued formation of collagen and, if necessary, degrade collagen fibers that are responsible for impeding the stretching and shortening of muscle fibers. Prevention of interstitial fibrosis in pressure overload hypertrophy with pharmacologic agents with both antihypertensive and antifibrotic properties must also be considered. Future research should address these issues with a view toward developing corrective and preventative forms of therapy. Such advances will require a better understanding of cardiac fibroblast growth, collagen synthesis and the regulation of collagen gene expression in the heart. Am J Hypertens 1989;2:931-940.
Pressure overload
Myocardial fibrosis
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Pressure overload in patients with aortic stenosis (AS) induces an adverse remodeling of the left ventricle (LV) in a sex-specific manner. We assessed whether a sex-specific miR-29b dysregulation underlies this sex-biased remodeling pattern, as has been described in liver fibrosis. We studied mice with transverse aortic constriction (TAC) and patients with AS. miR-29b was determined in the LV (mice, patients) and plasma (patients). Expression of remodeling-related markers and histological fibrosis were determined in mouse LV. Echocardiographic morpho-functional parameters were evaluated at baseline and post-TAC in mice, and preoperatively and 1 year after aortic valve replacement (AVR) in patients with AS. In mice, miR-29b LV regulation was opposite in TAC-males (down-regulation) and TAC-females (up-regulation). The subsequent changes in miR-29b targets (collagens and GSK-3β) revealed a remodeling pattern that was more fibrotic in males but more hypertrophic in females. Both systolic and diastolic cardiac functions deteriorated more in TAC-females, thus suggesting a detrimental role of miR-29b in females, but was protective in the LV under pressure overload in males. Clinically, miR-29b in controls and patients with AS reproduced most of the sexually dimorphic features observed in mice. In women with AS, the preoperative plasma expression of miR-29b paralleled the severity of hypertrophy and was a significant negative predictor of reverse remodeling after AVR; therefore, it may have potential value as a prognostic biomarker.
Pressure overload
Ventricular remodeling
Myocardial fibrosis
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Pressure overload
Concentric hypertrophy
Ventricular remodeling
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Cardiac hypertrophy resulting from pressure overload and from volume overload differ considerably in many respects. For example, pressure overload leads to concentric hypertrophy while volume overload leads to eccentric hypertrophy (1). Systolic contractile function is depressed in pressure overload hypertrophy (2) but is normal in volume overload hypertrophy (3). Studies utilizing experimentally produced pressure overload hy-pertrophied right ventricular papillary muscles of small mammals like cats (3-6) and rabbits (7, 8) have contributed considerably to the understanding of changes in myocar-dial function in cardiac hypertrophy. A surgically produced atrial septal defect in cats has been shown by Cooper et al. (3) to cause volume overload right ventricular hypertrophy which is another useful model for the study of cardiac hypertrophy. However, the surgical technique requires thoracotomy and pericardiotomy. A nonsurgical technique to create an atrial septal defect would facilitate further studies Of vol...
Volume overload
Pressure overload
Thoracotomy
Concentric hypertrophy
Right ventricular hypertrophy
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Pressure overload
Constriction
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Pressure overload
Ventricular hypertrophy
Myocardial fibrosis
Hydroxyproline
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Pressure overload
Concentric hypertrophy
Volume overload
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Hypertrophy can be induced by pressure-overload or treadmill running. Pressure-overload-hypertrophy is associated with distinct changes in gene expression. The regulatory mechanisms in exercise-induced-hypertrophy are largely unknown.
Pressure overload
Myocardial hypertrophy
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