The Journal of heart and lung transplantation : the official publication of the International Society for Heart Transplantation · 2002
Effects of pre-existing left ventricular hypertrophy on ventricular dysfunction and remodeling following myocardial infarction in rats.
Оценочное исследованиеСтатьяПоддержка службы здравоохранения СШАНазвание и аннотация: Перевод в очереди
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Nass Omar, Yang Xiao-Ping, Liu Yun-He, Carretero Oscar A, Khaja Fareed, Goldstein Sidney, Sabbah Hani N
Аннотация
BACKGROUND: Myocardial hypertrophy is a characteristic component of left ventricular (LV) remodeling that may, at least initially, have a beneficial effect on LV function following myocardial infarction (MI). In the present study, we examine the effects of pre-existing left ventricular hypertrophy (LVH) on LV function and chamber enlargement following MI in inbred Lewis rats.
METHODS: The one-kidney, one-clip model (1K1C) of hypertension was used to produce LVH. Four weeks after 1K1C, rats were randomized to left anterior descending coronary artery ligation (LVH + MI group, n = 8) or sham ligation (LVH group, n = 11). Another group of rats underwent sham 1K1C. Four weeks later, they were randomized to coronary ligation (MI group, n = 12) or sham ligation (Sham group, n = 12). LV end-diastolic pressure (EDP, mm Hg), end-diastolic volume (EDV, ml), end-systolic volume (ESV, ml) and ejection fraction (EF) (determined by angiography) were measured in all groups 2 months after MI.
RESULTS: LV EDP was 20 +/- 2 mm Hg in the LVH + MI group compared with 9 +/- 1 mm Hg in the MI group (p < 0.05). LV EDV and ESV were significantly greater with LVH + MI than with MI alone (EDV 0.90 +/- 0.03 vs 0.75 +/- 0.02 ml; ESV 0.68 +/- 0.02 vs 0.50 +/- 0.03 ml; p < 0.05). Pre-existing LVH resulted in a greater reduction in EF following MI (25 +/- 2% for LVH + MI vs 34 +/- 2% for MI alone; p < 0.05).
CONCLUSIONS: Pre-existing LVH is an important determinant of progressive LV dysfunction and remodeling following MI in Lewis inbred rats.
METHODS: The one-kidney, one-clip model (1K1C) of hypertension was used to produce LVH. Four weeks after 1K1C, rats were randomized to left anterior descending coronary artery ligation (LVH + MI group, n = 8) or sham ligation (LVH group, n = 11). Another group of rats underwent sham 1K1C. Four weeks later, they were randomized to coronary ligation (MI group, n = 12) or sham ligation (Sham group, n = 12). LV end-diastolic pressure (EDP, mm Hg), end-diastolic volume (EDV, ml), end-systolic volume (ESV, ml) and ejection fraction (EF) (determined by angiography) were measured in all groups 2 months after MI.
RESULTS: LV EDP was 20 +/- 2 mm Hg in the LVH + MI group compared with 9 +/- 1 mm Hg in the MI group (p < 0.05). LV EDV and ESV were significantly greater with LVH + MI than with MI alone (EDV 0.90 +/- 0.03 vs 0.75 +/- 0.02 ml; ESV 0.68 +/- 0.02 vs 0.50 +/- 0.03 ml; p < 0.05). Pre-existing LVH resulted in a greater reduction in EF following MI (25 +/- 2% for LVH + MI vs 34 +/- 2% for MI alone; p < 0.05).
CONCLUSIONS: Pre-existing LVH is an important determinant of progressive LV dysfunction and remodeling following MI in Lewis inbred rats.