SERIAL ECHOCARDIOGRAPHIC-DOPPLER ASSESSMENT OF LEFT-VENTRICULAR GEOMETRY AND FUNCTION IN RATS WITH PRESSURE-OVERLOAD HYPERTROPHY - CHRONIC ANGIOTENSIN-CONVERTING ENZYME-INHIBITION ATTENUATES THE TRANSITION TO HEART-FAILURE
SERIAL ECHOCARDIOGRAPHIC-DOPPLER ASSESSMENT OF LEFT-VENTRICULAR GEOMETRY AND FUNCTION IN RATS WITH PRESSURE-OVERLOAD HYPERTROPHY - CHRONIC ANGIOTENSIN-CONVERTING ENZYME-INHIBITION ATTENUATES THE TRANSITION TO HEART-FAILURE
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DOI：
10.1161/01.cir.91.10.2642
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发表时间：
1995-05-15
期刊：
影响因子：
37.8
通讯作者：
DOUGLAS, PS
中科院分区：
文献类型：
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作者：
LITWIN, SE;KATZ, SE;DOUGLAS, PS
背景：尽管慢性压力超负荷可进展为左心衰，但这一转变的病理生理学机制尚不清楚。此外，慢性血管紧张素转换酶(ACE)抑制对这一转变的影响在很大程度上尚不清楚。方法与结果研究了升主动脉缩窄所致左心室肥厚大鼠(n=22)和年龄匹配的假手术大鼠(n=6)在主动脉缩窄后6、12和18周时左室结构和功能的变化。记录二维引导下经胸M型超声心动图和二尖瓣多普勒频谱，以评估左室构型以及收缩和舒张期功能。超声心动图检查结束后，左心室肥厚大鼠随机分为不治疗组(n=10)或给予血管紧张素转换酶抑制剂福辛普利(50 mg/kg/d，n=12)治疗。结扎后6周，LVH大鼠左室壁厚度增加，腔内径正常，心内膜收缩短缩超常。然而，中壁缩短被轻度抑制，并且存在限制性的舒张期充盈模式。经过18周未经治疗的压力超负荷后，左室壁厚度没有变化，但腔内扩张、心内膜短轴缩短率下降、舒张期充盈进一步恶化。与未治疗的LVH大鼠相比，福辛普利治疗的大鼠左室舒张腔大小没有改变，收缩和舒张期功能也没有恶化或改善。18周时，LVH组和LVH-福辛普利组大鼠的关闭胸腔左心室收缩压无差异(197对198 mm Hg)，尽管未经治疗的大鼠的舒张末压较高(18对11 mm Hg)。计算的左心室收缩期壁应力在福辛普利治疗组比未治疗的左心室肥厚大鼠低。LV舒张期充盈异常的严重程度与操作LV腔僵硬程度密切相关(r=0.88，P
Background Although chronic pressure overload may progress to left ventricular (LV) failure, the pathophysiology of this transition is not well understood. In addition, the effects of chronic angiotensin-converting enzyme (ACE) inhibition on this transition are largely undefined.Methods and Results To examine changes in LV structure and function during the transition to heart failure, rats with LV hypertrophy due to banding of the ascending aorta (LVH, n=22) and age-matched sham-operated rats (n=6) were studied 6, 12, and 18 weeks after aortic banding. Two-dimensionally guided transthoracic M-mode echocardiograms and transmitral Doppler spectra were recorded for assessment of LV geometry and systolic and diastolic functions. LVH rats were randomized to no treatment (n=10) or treatment with the ACE inhibitor fosinopril (50 mg/kg per day, n=12) after the baseline echocardiogram. Six weeks after banding, LVH rats had increased LV wall thickness with normal cavity dimensions and supranormal endocardial systolic shortening. However, midwall shortening was mildly depressed, and a restrictive diastolic filling pattern was present. After 18 weeks of untreated pressure overload, LV wall thickness was unchanged, but cavity dilation, a fall in endocardial shortening, and further deterioration of diastolic filling were evident. In contrast to untreated LVH rats, the fosinopril-treated rats showed no change in LV diastolic cavity dimension, and systolic and diastolic functions did not deteriorate or improved. Closed chest LV systolic pressures at 18 weeks were not different in LVH or LVH-fosinopril rats (197 versus 198 mm Hg), although end-diastolic pressure was higher in the untreated rats (18 versus 11 mm Hg). Calculated LV systolic wall stress was lower in fosinopril-treated than untreated LVH rats. The severity of LV diastolic filling abnormalities correlated strongly with operating LV chamber stiffness (r=.88, P