Schwartzkopff B, Motz W, Vogt M, Strauer B E
Medical Clinic and Policlinic B, University of Duesseldorf, Germany.
Circulation. 1993 May;87(5 Suppl):IV66-72.
Arterial hypertension leads to left ventricular hypertrophy. In proportion to increased left ventricular systolic pressure, left ventricular hypertrophy is considered to be of adaptive nature from the point of view of wall stress regulation. In the beginning, left ventricular function is normal, whereas diastolic filling is already compromised by the process of hypertrophy and altered ventricular geometry. In case of ventricular dilation and wall thinning, wall stress increases and leads to an increment in myocardial oxygen demand and a decrease of left ventricular ejection fraction. This is followed by a further decline in intrinsic myocardial contractility and a decrease in the elastic material properties of the myocardium. The structure of the myocardium is characterized by myocyte hypertrophy, a process of reactive and reparative fibrosis and alterations of the coronary microcirculation. Coronary vasodilator reserve is markedly impaired and is likely to initiate a process of malperfusion and malnutrition under increased metabolic demands. Particularly, the combined involvement of myocytes, interstitium, and intramyocardial vasculature appears to predispose to late heart failure after prolonged exposure to chronic pressure overload in arterial hypertension.
动脉高血压会导致左心室肥厚。与左心室收缩压升高成比例，从壁应力调节的角度来看，左心室肥厚被认为具有适应性。起初，左心室功能正常，而舒张期充盈已经因肥厚过程和心室几何形状改变而受损。在心室扩张和室壁变薄的情况下，壁应力增加，导致心肌需氧量增加和左心室射血分数降低。随后，心肌固有收缩力进一步下降，心肌弹性物质特性降低。心肌结构的特征是心肌细胞肥大、反应性和修复性纤维化过程以及冠状动脉微循环改变。冠状动脉扩张储备明显受损，在代谢需求增加的情况下可能引发灌注不良和营养不良的过程。特别是，心肌细胞、间质和心肌内血管系统的联合受累似乎使动脉高血压患者在长期暴露于慢性压力超负荷后易发生晚期心力衰竭。
