[运动心肌显像评估肥厚性心肌病的洗脱率]。

Journal of cardiography Pub Date : 1986-12-01
A Genda, Y Igarashi, S Mizuno, N Sugihara, Y Kita, T Suematsu, M Shimizu, R Takeda, H Bunko, K Hisada
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引用次数: 0

摘要

本研究从冠状动脉微循环紊乱的角度阐明了非比例肥厚的发病机制。28例冠状动脉造影正常的肥厚性心肌病(HCM)患者,根据左心室和双心室造影肥厚的分布分为四组:(1)室间隔肥厚,(2)室间隔和尖前壁肥厚,(3)尖前壁肥厚,(4)非特异性全壁肥厚。28例HCM患者和10例正常志愿者均采用运动心肌显像检测,计算机处理心肌周长图,将冲洗率与非比例肥厚相联系。HCM组与对照组周向剖面的平均曲线和平均节段值的比较表明,HCM组的平均初始摄取值在根尖段和前间隔段的下部相对较低,代表了这些节段的不成比例的肥大。前间隔段的上段是三维心肌最大的部分,其平均值明显升高。HCM组各节段的平均洗脱率均显著降低,尤其是那些反映不成比例肥大的节段。这一趋势也出现在初始摄入量增加的细分市场。在比较所有组的节段值时,在28例HCM患者中有12例的剖面中观察到初始摄取和/或洗脱率的节段值为对照组的平均值- 2SD。这些都降低了冲洗率。在25个HCM患者的总节段中,初始摄取率和/或洗脱率低于正常限度;其中21个节段的冲洗率下降,16个节段属于不成比例的肥厚壁。这些结果表明,非比例肥厚壁冲洗率下降是HCM的特征。初步认为,由于冠状动脉微循环紊乱,导致初始摄食量减少,洗脱率下降。此外,洗脱率的降低而初始摄取的减少不仅是由于冠状动脉微循环的紊乱引起的,也是由于心肌细胞的代谢紊乱引起的。此外,这两种紊乱都与不成比例肥大的发病机制密切相关。
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[Washout rate in hypertrophic cardiomyopathy assessed by exercise myocardial scintigraphy].

The present study clarified the pathogenesis of disproportional hypertrophy in terms of disturbed coronary microcirculation. Twenty-eight patients with hypertrophic cardiomyopathy (HCM) who had normal coronary angiograms were categorized in four groups according to distributions of disproportional hypertrophy on left ventriculography and biventriculography: (1) Interventricular septal hypertrophy, (2) septal and apico-anterior wall hypertrophy, (3) apico-anterior hypertrophy, and (4) nonspecific hypertrophy of the entire wall. All 28 HCM patients and 10 normal volunteers were tested using exercise myocardial scintigraphy, and the circumferential profiles were processed by computer to relate the washout rate and disproportional hypertrophy. Comparison of the mean curves and mean segmental values of the circumferential profiles of the HCM groups with those of the control group showed that the mean initial uptake values of the HCM groups were to be relatively low in the apical segment and in the lower portion of the anteroseptal segment representing disproportional hypertrophy of these segments. The mean values were significantly elevated in the upper portion of the anteroseptal segment which was projected as the largest amount of the myocardium three-dimensionally. The mean washout rates in the HCM groups were significantly decreased in all segments, especially in those segments which reflected disproportional hypertrophy. This trend was also observed in the segments with increased initial uptakes. On comparing the segmental values of all groups, the segments with initial uptakes and/or washout rates with having the mean value minus 2SD of the control group were observed in the profiles of 12 of the 28 HCM patients. These all had decreased washout rates. In 25 of the total segments of the HCM patients, the initial uptakes and/or washout rates were below the normal limit; 21 of these segments had only decreased washout rates, and 16 of these 21 segments belonged to disproportionally hypertrophic wall. These results indicate that the decreased washout rate in the disproportionally hypertrophic wall is characteristic of HCM. It is suggested that the decreased washout rate with the decreased initial uptake is caused by disturbance of the coronary microcirculation. In addition, the decreased washout rate without a decreased initial uptake is caused not only by disturbance of coronary microcirculation, but by a metabolic disturbance of the myocardial cells as well. Furthermore, both disturbances are closely related to the pathogenesis of disproportional hypertrophy.

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