Störk T, Möckel M, Danne O, Völler H, Eichstädt H, Frei U
Department of Internal Medicine, Nephrology and Intensive Care Medicine, University Hospital Virchow Klinikum, Berlin, Germany.
Cardiovasc Drugs Ther. 1995 Aug;9 Suppl 3:533-7. doi: 10.1007/BF00877866.
Diastolic dysfunction is an early sign in the temporal sequence of ischemic events in coronary heart disease. The ischemic cascade, beginning with an oxygen demand supply imbalance and metabolic alterations, identifies diastolic disorders of the left ventricle (LV) as an early phenomenon, sometimes before systolic dysfunction, electrocardiographic changes, or chest pain occur. Although the physiology of diastolic function is complex, the factors contributing to diastolic disturbances can be differentiated into intrinsic and extrinsic LV abnormalities. Intrinsic mechanisms include (a) impaired LV relaxation, (b) the complex of LV hypertrophy, and (c) increased LV asynchrony. Myocardial hypertrophy leads to an increase of the myocardial mass/volume ratio, and the degree of hypertrophy is the main determinant of chamber stiffness. The main, if not unique, determinant of myocardial diastolic tissue distensibility is the structure and concentration of the collagen. Consequently, tissue stiffness is increased in coronary disease by reparative interstitial fibrosis or scar following myocardial infarction. In myocardial hypertrophy the LV collagen concentration is elevated due to reactive fibrosis. An increase in regional asynchrony of LV contraction and relaxation is a result of regional ischemia as well as of LV hypertrophy and tissue fibrosis. Factors extrinsic to the LV causing diastolic disorders include (a) increased central blood volume, which will increase left ventricular pressure without altering the LV pressure-volume relation, and (b) ventricular interaction mediated by pericardial restraint, which may cause a parallel upward shift of the diastolic LV pressure-volume relation. Improved insight into the mechanisms of LV relaxation and filling characteristics help in the treatment of LV diastolic dysfunction.
舒张功能障碍是冠心病缺血事件时间序列中的早期迹象。缺血级联反应始于氧供需失衡和代谢改变，将左心室（LV）舒张功能障碍识别为一种早期现象，有时发生在收缩功能障碍、心电图改变或胸痛出现之前。尽管舒张功能的生理学很复杂，但导致舒张功能障碍的因素可分为左心室内在和外在异常。内在机制包括：（a）左心室舒张受损；（b）左心室肥厚复合体；（c）左心室不同步增加。心肌肥厚导致心肌质量/容积比增加，肥厚程度是心室僵硬度的主要决定因素。心肌舒张期组织扩张性的主要（如果不是唯一）决定因素是胶原蛋白的结构和浓度。因此，冠心病时，心肌梗死后的修复性间质纤维化或瘢痕会导致组织僵硬度增加。在心肌肥厚时，反应性纤维化会使左心室胶原蛋白浓度升高。左心室收缩和舒张区域不同步增加是局部缺血以及左心室肥厚和组织纤维化的结果。导致舒张功能障碍的左心室外在因素包括：（a）中心血容量增加，这会增加左心室压力而不改变左心室压力-容积关系；（b）心包约束介导的心室相互作用，这可能导致左心室舒张期压力-容积关系平行向上移位。深入了解左心室舒张和充盈特征的机制有助于治疗左心室舒张功能障碍。
