Ohtani K, Yutani C, Nagata S, Koretsune Y, Hori M, Kamada T
Department of Internal Medicine, Kobe Ekisakai Hospital, Japan.
J Am Coll Cardiol. 1995 Apr;25(5):1162-9. doi: 10.1016/0735-1097(94)00529-y.
We examined the extent of fibrotic changes in the left atrium of cardiomyopathic human hearts and investigated the relation of mechanical overload caused by left ventricular dysfunction to fibrosis of the left atrium.
Left atrial dysfunction in dilated cardiomyopathy may contribute to progression of heart failure. In contrast to fibrosis of the left ventricle, atrial fibrosis has not been extensively studied in cardiomyopathic hearts.
The extent of fibrosis in the left atrium and left ventricle was determined by an automatic image analyzer in 38 autopsied hearts obtained from 9 patients who died of noncardiac illness (control group), 16 patients with dilated cardiomyopathy, 6 patients with hypertrophic cardiomyopathy with features mimicking dilated cardiomyopathy and 7 patients with a previous myocardial infarction. Transverse sections were obtained at the upper margins of the foramen ovale and left auricle in the left atrium and the median level of the left ventricle.
There were no significant differences in extent of left atrial dilation, left ventricular dysfunction or duration of illness among the three groups with cardiac disease. Percent area of left atrial fibrosis (mean +/- SD) was significantly greater in the specimens from patients with dilated cardiomyopathy (13.1 +/- 6.1%, p < 0.01) and hypertrophic cardiomyopathy mimicking dilated cardiomyopathy (26.5 +/- 9.5%, p < 0.01) than in those from patients with an old myocardial infarction (3.8 +/- 1.1%). Percent area of left ventricular fibrosis in hearts from patients with dilated cardiomyopathy (12.9 +/- 8.6%) was significantly smaller than that in hearts from patients with hypertrophic cardiomyopathy mimicking dilated cardiomyopathy (35.8 +/- 11.9%, p < 0.01) and a previous myocardial infarction (38.4 +/- 8.0%, p < 0.01). Percent area of atrial fibrosis was significantly correlated with left ventricular ejection fraction in the group with a previous myocardial infarction but not in the other groups.
There was a high degree of fibrotic change in the left atrium in the groups with dilated cardiomyopathy and hypertrophic cardiomyopathy mimicking dilated cardiomyopathy. Our findings suggest that atrial fibrosis in these patients may not have been related to mechanical overload of the left atrium but to some other, still unknown mechanisms.
我们研究了心肌病患者心脏左心房纤维化改变的程度，并探讨了左心室功能障碍引起的机械性负荷过重与左心房纤维化之间的关系。
扩张型心肌病中的左心房功能障碍可能会促进心力衰竭的进展。与左心室纤维化不同，心房纤维化在心肌病心脏中尚未得到广泛研究。
使用自动图像分析仪测定了38例尸检心脏左心房和左心室的纤维化程度，这些心脏来自9例死于非心脏疾病的患者（对照组）、16例扩张型心肌病患者、6例具有类似扩张型心肌病特征的肥厚型心肌病患者以及7例曾有心肌梗死的患者。在左心房卵圆孔和左心耳的上缘以及左心室的中间水平获取横切面。
三组心脏病患者在左心房扩张程度、左心室功能障碍或病程方面无显著差异。扩张型心肌病患者（13.1±6.1%，p<0.01）和类似扩张型心肌病的肥厚型心肌病患者（26.5±9.5%，p<0.01）标本中的左心房纤维化面积百分比显著高于陈旧性心肌梗死患者（3.8±1.1%）。扩张型心肌病患者心脏的左心室纤维化面积百分比（12.9±8.6%）显著小于类似扩张型心肌病的肥厚型心肌病患者（35.8±11.9%，p<0.01）和曾有心肌梗死的患者（38.4±8.0%，p<0.01）。在曾有心肌梗死的组中，心房纤维化面积百分比与左心室射血分数显著相关，而在其他组中则无相关性。
在扩张型心肌病组和类似扩张型心肌病的肥厚型心肌病组中，左心房存在高度纤维化改变。我们的研究结果表明，这些患者的心房纤维化可能与左心房的机械性负荷过重无关，而是与其他一些尚不清楚的机制有关。
