Decrements in CRR were related to changes of the coronary microcirculation. Both the decrease in CRR and these changes in the coronary microcirculation were related to the degree of hypertrophy. All these factors might contribute to the well-known occurrence of ischemia in this patient group.

Hypertrophic cardiomyopathy is a benign disease in an unselected population with a low incidence of cardiac death. Syncope was associated with a higher incidence of SCD and patients with a significant LVOT obstruction were more susceptible to clinical deterioration.

Background The purpose of this pilot study was to identify biological risk factors for restenosis after percutaneous transluminal coronary angioplasty (PTCA) to predict the long-term outcome of PTCA before treatment.

Abstract-The development of left ventricular hypertrophy (LVH) in subjects with hypertrophic cardiomyopathy (HCM) is variable, suggesting a role for modifying factors such as angiotensin II. We investigated whether the angiotensin II type 1 receptor (AT 1 -R) A/C 1166 polymorphism, the angiotensin-converting enzyme (ACE) insertion/deletion (I/D) polymorphism, and/or plasma renin influence LVH in HCM. Left ventricular mass index (LVMI) and interventricular septal thickness were determined by 2-dimensional echocardiography in 104 genetically independent subjects with HCM. Extent of hypertrophy was quantified by a point score (Wigle score). Plasma prorenin, renin, and ACE were measured by immunoradiometric or fluorometric assays, and ACE and AT 1 -R genotyping were performed by polymerase chain reactions. The ACE D allele did not affect any of the measured parameters except plasma ACE (PϽ0.04). LVMI was higher (PϽ0.05) in patients carrying the AT 1 -R C allele (190Ϯ8.3 g/m 2 ) than in AA homozygotes (168Ϯ7.2 g/m 2 ), and similar patterns were observed for interventricular septal thickness (23.0Ϯ0.7 versus 21.6Ϯ0.7 mm) and Wigle score (7.0Ϯ0.3 versus 6.3Ϯ0.3). Plasma renin was higher (Pϭ0.05) in carriers of the C allele than in AA homozygotes. Multivariate regression analysis, however, revealed no independent role for renin in the prediction of LVMI. Plasma prorenin and ACE were not affected by the AT 1 -R A/C 1166 polymorphism, nor did the ACE and AT 1 -R polymorphisms interact with regard to any of the measured parameters. We conclude that the AT 1 -R C

In contrast to earlier reports, mean mitral annular systolic velocity and early mitral annular diastolic velocity velocities were not reduced in G+/LVH- subjects, and TDI velocities were not sufficiently sensitive for determination of the affected status of an individual subject. Our findings, however, support the theory that diastolic dysfunction is a primary component of pre-clinical HCM.