<原著>心筋梗塞症における拡張期左室壁伸展障害に関する臨床的研究

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Left ventricular volume and segment length of the left ventricular wall were calculated in order to investigate the relaxation characteristics of the infarcted myocardium in 27 patients with old myocardial infarction (MI) and in 22 patients whose coronary artery and hemodynamics were diagnosed as normal. Left ventricular volume was calculated by using the biplane left ventricular cineangiogram. Segment length was calculated by measuring a spatial length between two points which were identified as a junction of ramifying branch on the left coronary arteries on the infarcted and non-infarcted walls by using the biplane coronary cineangiogram. The rapid and slow filling volume of the left ventricle was significantly reduced in the patients with myocardial infarction as compared to the normals (Normal 38±6 (mean±SD) ml/m^2 vs MI 30±7 ml/m^2 : p<0.01), while the filling volume by atrial contraction remained not significantly different (Normal 15±4 ml/m^2 vs MI 17±5 ml/m^2). The lengthening of segmental wall during the rapid and slow filling period at infarcted portion was 5.0±2.9% which was also significantly decreased as compared with that at non-infarcted portion which was 9.6±4.2%. The extents of lengthening by atrial contraction were not different between the two portions (non-infarcted portion 3.8±1.1%, infarcted portion 3.5±1.2%). The above finding indicates that left ventricular filling before the beginning of atrial contraction is reduced in myocardial infarction, resulting in a relative increase of the left ventricular filling by atrial contraction. The reason for the reduced left ventricular filling volume during rapid and slow filling period in these patients is considered to be a reduction of left ventricular wall compliance caused by myocardial fibrosis and incomplete relaxation which causes asynchronous relaxation of the left ventricle. The increase of left ventricular pressure by atrial contraction was 9.5±4.1 mmHg in the patients with myocardial infarction which was significantly greater than that in the normals (5.5±1.9 mmHg). In spite of the same increment of left ventricular volume by atrial contraction, the greater increase of the pressure was recognized in the patients with myocardial infarction. This phenomenon may be explained by two mechanisms. One is that the increase of pressure is greater compared with the increase of muscle length since infarcted portion is stiffer than normal portion. The other reason is that left atrial contraction will be augmented according to the Frank-Starling law, because blood volume moved from the left atrium into the left ventricle before atrial contraction is decreased, resulting in an increased blood volume left at the onset of atrial contraction. This study suggests that an increased stiffness of the infarcted myocardial wall may lead to a reduction of diastolic expansion before the onset of atrial contraction which contributes to a major cause to decrease stroke volume in the patients with myocardial infartion.
1984-03-25

<原著>心筋梗塞症における拡張期左室壁伸展障害に関する臨床的研究

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