AIM It was the aim of our study to determine whether myocardial fibrosis influences physiologic or non-physiologic left ventricular (LV) hypertrophy in severe aortic stenosis. METHODS Myocardial fibrosis was evaluated using specimens taken from the ventricular septum in 79 patients submitted to aortic valve replacement because of symptomatic aortic stenosis. Patients were considered to have p...

Overexpression and activation of protein kinase C-epsilon (PKCepsilon) results in myocardial hypertrophy. However, these observations do not establish that PKCepsilon is required for the development of myocardial hypertrophy. Thus, we subjected PKCepsilon-knockout (KO) mice to a hypertrophic stimulus by transverse aortic constriction (TAC). KO mice show normal cardiac morphology and function. T...

It is uncertain whether chronic beta-adrenoreceptor (beta-AR)-activation in hypertension could initiate the progression from compensated left ventricular (LV) hypertrophy to pump dysfunction. It is also uncertain if this effect is through adverse LV remodeling (chamber dilatation with wall thinning and pump dysfunction) or intrinsic myocardial contractile dysfunction. We evaluated the effect of...

Both myocardial contractility and contraction duration were assessed load-independently in isolated hypertrophic and control rat hearts. Hemodynamic parameters for isolated isovolumically contracting hearts were compared for 7 Wistar rats with DOCA-salt induced hypertrophy (LVH) and 7 controls. Loads were altered by changing the volume of an intraventricular balloon. Myocardial contractility wa...

Coronary pressure-flow relations during autoregulated and vasodilated flow states were compared between eight dogs with renovascular hypertension and left ventricular hypertrophy and 12 normal dogs. Each relation was constructed from serial steady-state measurements of end-diastolic coronary pressure and flow during perfusion of the circumflex artery by an extracorporeal circuit at controlled d...

Correspondence to: Professor Lennart Bergfeldt, Department of Cardiology, Sahlgrenska University Hospital/S, S-413 45 Gothenburg, Sweden; [email protected] _________________________ L eft ventricular (LV) hypertrophy may reflect physiological adaptation to an increased work load of the heart following intense physical training. However, LV hypertrophy often represents a pathophysiolog...

Cardiac hypertrophy, as a response to hemodynamic stress, is associated with cardiac dysfunction and death, but whether hypertrophy itself represents a pathological process remains unclear. Hypertrophy is driven by changes in myocardial gene expression that require the MEF2 family of DNA-binding transcription factors, as well as the nuclear lysine acetyltransferase p300. Here we used genetic an...

In the previous study, we established a mouse model of cardiac hypertrophy using transverse aortic constriction (TAC) and found that the expression of long non-coding RNAs TINCR was downregulated in myocardial tissue. The present study was designed to determine the potential role of TINCR in the pathogenesis of cardiac hypertrophy. Our results showed that enforced expression of TINCR could atte...

background and aims: there has been scant information concerning antihypertrophic effects of vitamin d specifically on its cellular and molecular mechanisms. sirtuin 1 (sirt1) is regarded as a key deacetylase enzyme in cardiomyocytes which applies potential cardioprotective effects by functional regulation of different proteins. this study aimed to evaluate the effects of 1, 25-dihydroxyvitamin...

Angiotensin-II (Ang-II) plays a key role in myocardial hypertrophy, remodeling and failure. We investigated whether Ang-II-induced cardiomyocyte hypertrophy is dependent on WNT1 inducible signaling pathway protein 1 (WISP1), a pro growth factor. Ang-II induced hypertrophy and WISP1 expression in neonatal rat cardiomyocytes (NRCM), effects that were significantly inhibited by pre-treatment with ...