Развитие гипертрофии левого желудочка в условиях "метаболического синдрома"

Дан анализ эффектов ингибитора ангиотензинпревращающего фермента на морфофункциональные параметры левого желудочка при гипертензии, развивающейся в условиях метаболических нарушений. Показано, что морфологические различия в ультраструктуре митохондрий отражают функциональные состояния органелл, обусловленные различным уровнем энергетического метаболизма и метаболическим «фоном», а также эффектами ингибитора ангиотензинпревращающего фермента эналаприла (АПФ).

Left ventricular Hypertrophy: effect on "metabolic syndrome"

Hypertension and heart failure arc marked by activation of both the renin-angiotensin-aldosterone system (RAAS) and the sympathetic nervous system. These forms of neurohumoral activation, in turn, have deleterious effects on the heart, kidney, and other target organs, worsening the prognosis in these disease states. Pharmacological agents that interrupt the RAAS are useful in both improving hemodynamics and preventing morbidity and mortality in such patients. In particular, treatment with ACE inhibitors has been shown to improve survival in patients with advanced heart failure and after myocardial infarction. It is hypothesized that ACE inhibitors exert beneficial effects by inhibiting both circulating and cardiac tissue ACE, thus attenuating unfavorable remodeling of the left ventricle (LV), reducing afterload, and improving the balance between thrombotic and thrombolytic factors. It remains unclear whether the dominant mechanism of action of ACE inhibitors in the setting of LV dysfunction relates to their global hemodynamic effects (which result in improved loading conditions), to reduced production of angiotensin (Ang) 11 with subsequent diminished Ang 11 type I (AT, ) receptor activation, or to alteration of other neurohormonal systems, such as the kallikrein-kinin system.