Hayakawa M, Inoh T, Kawanishi H, Kaku K, Kumaki T, Yokota Y, Fukuzaki H
J Cardiogr. 1982 Sep;12(3):605-12.
In order to evaluate left ventricular function of dilated cardiomyopathy, 24 patients and ten healthy subjects were studied by exercise echocardiography. The patients with dilated cardiomyopathy were classified into 3 groups according to the presence or absence of mitral regurgitation and the severity of left ventricular dilatation: Group I was consisted of five cases with mitral regurgitation. Group II was consisted of seven cases without mitral regurgitation who had marked left ventricular dilatation, where the left ventricular end-diastolic dimension index (DdI) was greater than 46 mm/m2 and left ventricular end-systolic dimension index (DsI) was greater than 40 mm/m2. Group III was consisted of 12 cases without mitral regurgitation who had moderate left ventricular dilatation, where the DdI was less than 46 mm/m2 or DsI was less than 40 mm/m2. The ergometer exercise tests were performed for 3 min at 25 watts in a supine position. There was no significant differences of exercise-induced increases in heart rate, elevations of systolic blood pressure and increases of rate pressure product, respectively, between healthy subjects and each group of dilated cardiomyopathy. In healthy subjects, both DdI and DsI were unchanged on exercise. In Group I, DdI was unchanged but DsI decreased (p less than 0.02), thus percent fractional shortening of the left ventricle (delta D) was increased (p less than 0.05). In Group II, both DdI and DsI were unchanged. In Group III, DdI was increased (p less than 0.05) while DsI was unchanged, thus delta D was increased (p less than 0.02). These results suggested that the left ventricle is able to respond to exercise by its further dilatation (increase of preload) in mild to moderate dilated cardiomyopathy (Group III). On the other hand, in cases with marked left ventricular dilatation (Group II), the further dilatation is not induced. The same was true in dilated cardiomyopathy with mitral regurgitation (Group I), where the left ventricle had almost the same size as in Group II, although changes in DsI and delta D were not evaluated precisely because of the associated regurgitation.
为了评估扩张型心肌病患者的左心室功能,对24例患者和10名健康受试者进行了运动超声心动图研究。根据是否存在二尖瓣反流以及左心室扩张的严重程度,将扩张型心肌病患者分为3组:第一组由5例有二尖瓣反流的患者组成。第二组由7例无二尖瓣反流但有明显左心室扩张的患者组成,其左心室舒张末期内径指数(DdI)大于46 mm/m2,左心室收缩末期内径指数(DsI)大于40 mm/m2。第三组由12例无二尖瓣反流但有中度左心室扩张的患者组成,其DdI小于46 mm/m2或DsI小于40 mm/m2。在仰卧位以25瓦功率进行3分钟的测力计运动试验。健康受试者与扩张型心肌病各亚组之间,运动引起的心率增加、收缩压升高和心率血压乘积增加均无显著差异。在健康受试者中,运动时DdI和DsI均无变化。在第一组中,DdI无变化,但DsI降低(p<0.02),因此左心室短轴缩短率(delta D)增加(p<0.05)。在第二组中,DdI和DsI均无变化。在第三组中,DdI增加(p<0.05),而DsI无变化,因此delta D增加(p<0.02)。这些结果表明,在轻度至中度扩张型心肌病(第三组)中,左心室能够通过进一步扩张(增加前负荷)对运动作出反应。另一方面,在左心室明显扩张的病例(第二组)中,未诱发进一步扩张。伴有二尖瓣反流的扩张型心肌病(第一组)也是如此,尽管由于相关反流未精确评估DsI和delta D的变化,但左心室大小与第二组几乎相同。