LEFT-VENTRICULAR REMODELING IN THE YEAR AFTER 1ST ANTERIOR MYOCARDIAL-INFARCTION - A QUANTITATIVE-ANALYSIS OF CONTRACTILE SEGMENT LENGTHS AND VENTRICULAR SHAPE
LEFT-VENTRICULAR REMODELING IN THE YEAR AFTER 1ST ANTERIOR MYOCARDIAL-INFARCTION - A QUANTITATIVE-ANALYSIS OF CONTRACTILE SEGMENT LENGTHS AND VENTRICULAR SHAPE
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DOI：
10.1016/0735-1097(92)90314-d
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发表时间：
1992-05-01
影响因子：
24
通讯作者：
PFEFFER, MA
中科院分区：
文献类型：
--
作者：
MITCHELL, GF;LAMAS, GA;PFEFFER, MA
心肌梗死后的梗死扩张导致早期心室增大和心室几何形状扭曲。为了描述晚期容量增大的组成部分，我们对52例首次前路心肌梗死后3周和1年的患者进行了双平面左心室造影术。测量双平面舒张周长、收缩段和非收缩段长度。使用球形指数（心室的血管造影体积除以具有相同周长的球体体积）来评估整体几何形状。通过测量心内膜曲率来评估区域几何形状，心内膜曲率是壁张力的重要决定因素。由于收缩节段长度（34 +/- 5至37 +/- 5 cm， p < 0.001）和球度指数（0.74 +/- 0.07至0.76 +/- 0.08,p < 0.001）增加，而非收缩节段长度减少（15 +/- 6至12 +/- 6 cm， p < 0.005），舒张末期容积在基线时增大，并在1年后增加（230 +/- 42至244 +/- 55 ml， p = 0.01）。曲率分析显示，在梗死前基底缘（-6.0 +/- 4.0至-4.5 +/- 3.7,p < 0.01）和下缘（-4.5 +/- 2.0至-3.6 +/- 2.1,p < 0.005）的高张力凹变平，前壁较少隆起（9.4 +/- 2.5至8.2 +/- 2.3,p < 0.001）。选择晚期扩大（舒张容积增加bbb20 ml， n = 19）的患者在1年内收缩节段延长（32 +/- 4至36 4 cm）后，球形度增加（0.75 +/- 0.05至0.80 +/- 0.08,p < 0.005），舒张周长增加（54 +/- 3至56 +/- 4 cm， p < 0.001）。因此，心肌梗死后晚期心室增大是由于收缩节段长度增加和心室几何形状改变所致，而不是进行性梗死扩张的结果。在由于梗塞相关血管的持续闭塞而具有晚期心室增大高风险的患者组中，卡托普利治疗通过防止收缩节段长度和心室几何形状的这些变化来减弱晚期心室增大。
Infarct expansion after myocardial infarction results in early ventricular enlargement and distortion of ventricular geometry. To characterize the components of late volume enlargement, biplane left ventriculography was performed in 52 patients 3 weeks and 1 year after a first anterior myocardial infarction. Biplane diastolic circumference and contractile and noncontractile segment lengths were measured. Global geometry was evaluated by using a sphericity index (angiographic volume of the ventricle divided by the volume of a sphere with the same circumference). Regional geometry was assessed by measurement of endocardial curvature, an important determinant of wall tension.End-diastolic volume was enlarged at baseline and increased at 1 year (230 +/- 42 to 244 +/- 55 ml, p = 0.01) as a result of increases in contractile segment length (34 +/- 5 to 37 +/- 5 cm, p < 0.001) and sphericity index (0.74 +/- 0.07 to 0.76 +/- 0.08, p < 0.001), whereas the noncontractile segment length decreased (15 +/- 6 to 12 +/- 6 cm, p < 0.005). Curvature analysis revealed a flattening of presumably high tension concavity at the anterobasal (-6.0 +/- 4.0 to -4.5 +/- 3.7, p < 0.01) and inferior (-4.5 +/- 2.0 to -3.6 +/- 2.1, p < 0.005) margins of the infarct and less bulging of the anterior wall (9.4 +/- 2.5 to 8.2 +/- 2.3, p < 0.001). Patients selected for late enlargement (diastolic volume increase > 20 ml, n = 19) had an increase in sphericity (0.75 +/- 0.05 to 0.80 +/- 0.08, p < 0.005) and in diastolic circumference (54 +/- 3 to 56 +/- 4 cm, p < 0.001) secondary to elongation of the contractile segment (32 +/- 4 to 36 4 cm, p = 0.001) at 1 year.Thus, late ventricular enlargement after anterior infarction results from an increase in contractile segment length and a change in ventricular geometry and is not a result of progressive infarct expansion. In the group of patients at high risk for late ventricular enlargement because of persistent occlusion of the infarct-related vessel, captopril therapy attenuated late volume enlargement by preventing these changes in contractile segment length and chamber geometry.