Mori T, Suda K, Ohnishi M, Kanoh Y, Shiotani H, Yokota Y, Fujitani K, Fukuzaki H, Maeda K
First Department of Internal Medicine, Kobe University School of Medicine.
J Cardiol. 1987 Mar;17(1):35-46.
Thallium-201 (Tl) single photon emission computed tomography (SPECT) after dipyridamole infusion (0.56 mg/kg) was performed in 23 patients with hypertrophic non-obstructive cardiomyopathy (HNCM) and in seven patients with HCM simulating dilated cardiomyopathy (HCM-DCM) to clarify the mechanism and clinical significance of decreased coronary vasodilatory reserve. The coronary vasodilatory reserve in the hypertrophied area assessed by SPECT was compared with the findings of echocardiography, left ventriculography and endomyocardial biopsy. 1. Eleven patients with HNCM had no perfusion defects in the hypertrophied area (group I), but the other 12 patients (52.2%) had such defects (group II). All seven patients with HCM-DCM had perfusion defects in the anterior or septal walls (group III). Redistribution was observed in 11 of the 12 patients in group II and in three of the seven patients in group III. 2. The regional washout rate was relatively low in the upper septum in group II and in the anterior wall and upper septum in group III. Thus, coronary vasodilatory reserve in the hypertrophied area was decreased in groups II and III. 3. Echocardiographically, the degree of hypertrophy did not differ between groups I and II, but the latter had significantly greater left ventricular diastolic dimension (42.3 mm vs 49.5 mm: p less than 0.05) and lower percent fractional shortening (%FS) (43.7% vs 35.6%: p less than 0.05). However, group III showed thinner left ventricular wall, much greater diastolic dimension (60.9 mm vs 49.5 mm: p less than 0.05), and lower %FS (24.0% vs 35.6%: p less than 0.05) than did those of group II. 4. On left ventriculography, those in group II showed larger left ventricular end-diastolic volume index (93.9 ml/m2 vs 79.7 ml/m2: p less than 0.05) than that of group I. Left ventricular ejection fraction showed the same tendency, but this was not statistically significant. 5. On endomyocardial biopsy, the specimens of the patients in group II had significantly higher percent fibrosis than did those of group I (11.4% vs 6.8%: p less than 0.05). These findings suggest that the mechanism of decreased coronary vasodilatory reserve in the hypertrophied area may be related to myocardial fibrosis, and this decrease may induce left ventricular dysfunction and compensatory dilatation.
对23例肥厚型非梗阻性心肌病（HNCM）患者和7例模拟扩张型心肌病的肥厚型心肌病（HCM-DCM）患者进行了双嘧达莫（0.56mg/kg）静脉注射后的铊-201（Tl）单光子发射计算机断层扫描（SPECT），以阐明冠状动脉扩张储备降低的机制及临床意义。通过SPECT评估肥厚区域的冠状动脉扩张储备，并与超声心动图、左心室造影和心内膜活检结果进行比较。1. 11例HNCM患者肥厚区域无灌注缺损（I组），但其他12例患者（52.2%）有此类缺损（II组）。7例HCM-DCM患者前壁或室间隔均有灌注缺损（III组）。II组12例患者中有11例及III组7例患者中有3例出现再分布。2. II组上室间隔及III组前壁和上室间隔的局部洗脱率相对较低。因此，II组和III组肥厚区域的冠状动脉扩张储备降低。3. 超声心动图显示，I组和II组的肥厚程度无差异，但II组左心室舒张末期内径显著更大（42.3mm对49.5mm：p<0.05），射血分数缩短百分比（%FS）更低（43.7%对35.6%：p<0.05）。然而，III组左心室壁更薄，舒张末期内径更大（60.9mm对49.5mm：p<0.05），%FS更低（24.0%对35.6%：p<0.05），均低于II组。4. 左心室造影显示，II组左心室舒张末期容积指数更大（93.9ml/m²对79.7ml/m²：p<0.05）。左心室射血分数有相同趋势，但无统计学意义。5. 心内膜活检显示，II组患者标本的纤维化百分比显著高于I组（11.4%对6.8%：p<0.05）。这些发现提示，肥厚区域冠状动脉扩张储备降低的机制可能与心肌纤维化有关，而这种降低可能导致左心室功能障碍和代偿性扩张。
