Influence of low high-density lipoprotein cholesterol on left ventricular hypertrophy and diastolic function in essential hypertension.

Background: Left ventricular (LV) hypertrophy and LV diastolic dysfunction, which are common cardiac changes in hypertensive patients, are modified by several nonhemodynamic (eg, genetic, neurohumoral, and metabolic) factors. However, the influence of serum lipids on these LV changes has not been sufficiently studied. Although low high-density lipoprotein (HDL) cholesterol is well known to be a major risk factor for coronary heart disease, it is unclear whether HDL cholesterol plays a role in hypertensive heart disease.

[Eosinophil infiltration in the heart with free-wall rupture following acute myocardial infarction: a case report].

A 90-year-old woman was referred to us due to acute extensive anterior myocardial infarction with cardiogenic shock. Echocardiography revealed akinesis of infarct region, associated with wall thinning. She was treated with catecholamines and diuretics because her hemodynamics were classified in Forrester subset IV.

Fasting plasma glucose is an independent determinant of left ventricular diastolic dysfunction in nondiabetic patients with treated essential hypertension.

Left ventricular (LV) hypertrophy and LV diastolic dysfunction are common cardiac changes in hypertensive patients, and these changes are modified by various factors other than blood pressure. The present study was conducted to investigate the influence of mild abnormalities in glucose metabolism on LV structure and function in essential hypertension. In 193 nondiabetic patients with treated essential hypertension, two-dimensional and Doppler echocardiographic examinations were performed, and relative wall thickness (RWT), LV mass index (LVMI), fractional shortening, and the ratio of the peak velocity of atrial filling to early diastolic filling (A/E) were calculated.