Hypertrophic cardiomyopathy and diastolic dysfunction.

Effects of increasing afterload on early diastolic dysfunction in hypertrophic non-obstructive cardiomyopathy.

The effects of increasing afterload on early diastolic dysfunction in 10 patients with hypertrophic non-obstructive cardiomyopathy were studied by computer assisted analyses of digitised M mode echocardiograms. Infusion of angiotensin II increased the end systolic pressure by a mean (SD) of 36.2 (10.3) mm Hg. As the afterload increased early diastolic dysfunction tended to become more normal: t...

AMERICAN JOURNAL OF PHYSIOLOGY-HEART AND CIRCULATORY PHYSIOLOGY (2006) 290(3):H1064-H1070. Tachycardia-induced myocardial ischemia and diastolic dysfunction potentiate secretion of ANP, not BNP, in hypertrophic cardiomyopathy

Assessment of regional systolic and diastolic dysfunction in familial hypertrophic cardiomyopathy using MR tagging.

Diastolic and systolic left ventricular (LV) dysfunction often significantly contribute to disabling symptoms in familial hypertrophic cardiomyopathy (FHC). This study compares regional LV function (midwall circumferential strain) during systole and diastole in eight FHC patients and six normal volunteers (NVs) using MR tagging. A prospectively-gated fast gradient-echo sequence with an echo-tra...

Assessment of diastolic function from velocity-encoded cardiac magnetic resonance data in patients with hypertrophic cardiomyopathy

Background Diastolic dysfunction evaluation may be relevant for early diagnosis of hypertrophic cardiomyopathy (HCM) and subsequent risk assessment. The aim of our study was to assess phase contrast cardiac magnetic resonance (PCCMR) diastolic parameters obtained with a semi-automated method in relation to left ventricular (LV) remodeling and late gadolinium enhancement (LGE) in patients with HCM.

Cardiac dysfunction in hypertrophic cardiomyopathy mutant tropomyosin mice is transgene-dependent, hypertrophy-independent, and improved by beta-blockade.

Familial hypertrophic cardiomyopathy (FHC) has been linked to mutations in proteins of the cardiac contractile apparatus, including alpha-tropomyosin (Tm). Mice expressing alphaTm in the heart were developed to determine the effects of FHC mutant Tm on cardiac structure and function from single cardiac myocytes to whole organ function in vivo. Expression of E180G mutant Tm did not produce cardi...