Kuhn H
Z Kardiol. 1985;74 Suppl 7:179-85.
In contrast to all commonly observed myocardial disorders presenting more or less pronounced hypertrophy in the sense of an adaptation to increased work load, the hypertrophic process in hypertrophic cardiomyopathies is characterized by the unknown etiology and pathogenesis (no adaptation), by the non homogeneous gross anatomic and microscopic picture, by the problems in measuring the muscle mass, by a non dilating ventricular cavity during follow-up, by the lack of experimental models in animals, and by concealed myocardial storage diseases. Methods for the investigation of the regression of hypertrophy include echocardiography, angiocardiography, ECG and myocardial biopsy. The studies are based on changes of hypertrophy in the natural course and after the application of propranolol, verapamil and surgical management respectively. According to previous available results regression of cardiac hypertrophy could not be proved either during the natural course nor after medical or surgical treatment. The data indicate that clinical and hemodynamic improvements observed after therapeutic interventions are not induced by global or regional decrease of myocardial mass. They may be a consequence of systolic and diastolic improvement of ventricular function, which apparently is independent of regression of cardiac hypertrophy.
与所有常见的心肌疾病不同,这些疾病在适应增加的工作负荷方面或多或少呈现出明显的肥大,肥厚型心肌病中的肥厚过程具有病因和发病机制不明(无适应性)、大体解剖和微观表现不均一、测量肌肉质量存在问题、随访期间心室腔不扩张、缺乏动物实验模型以及隐匿性心肌贮积病等特征。研究肥厚消退的方法包括超声心动图、心血管造影、心电图和心肌活检。这些研究分别基于肥厚在自然病程中的变化以及应用普萘洛尔、维拉帕米和手术治疗后的变化。根据先前可得的结果,无论是在自然病程中还是在药物或手术治疗后,都无法证实心脏肥大的消退。数据表明,治疗干预后观察到的临床和血流动力学改善并非由心肌质量的整体或局部减少所引起。它们可能是心室功能收缩和舒张改善的结果,这显然与心脏肥大的消退无关。