Weber K T
Division of Cardiovascular Diseases, Department of Medicine, University of Tennessee Health Science Center, Memphis, USA.
Hypertension. 2001 Sep;38(3 Pt 2):588-91. doi: 10.1161/01.hyp.38.3.588.
The normal myocardium is composed of a variety of cells. Cardiac myocytes, tethered within an extracellular matrix of fibrillar collagen, represent one third of all cells; noncardiomyocytes account for the remaining two thirds. Ventricular hypertrophy involves myocyte growth. Hypertensive heart disease (HHD) includes myocyte and nonmyocyte growth that leads to an adverse structural remodeling of the intramural coronary vasculature and matrix. In HHD, it is not the quantity of myocardium but rather its quality that accounts for increased risk of adverse cardiovascular events. Structural homogeneity of cardiac tissue is governed by a balanced equilibrium existing between stimulator and inhibitor signals that regulate cell growth, apoptosis, phenotype, and matrix turnover. Stimulators (eg, angiotensin II, aldosterone, and endothelins) are normally counterbalanced by inhibitors (eg, bradykinin, NO, and prostaglandins) in a paradigm of reciprocal regulation. To reduce the risk of heart failure and sudden cardiac death that accompanies HHD, its adverse structural remodeling must be targeted for pharmacologic intervention. Cardioprotective agents counteract the imbalance between stimulators and inhibitors. They include ACE and endopeptidase inhibitors and respective receptor antagonists. Cardioreparative agents reverse the growth-promoting state and regress existing abnormalities in coronary vascular and matrix structure. ACE inhibition has achieved this outcome with favorable impact on vasomotor reactivity and tissue stiffness. Today's management of hypertension should not simply focus on a reduction in blood pressure, it must also target the adverse structural remodeling that begets HHD.
正常心肌由多种细胞组成。心肌细胞束缚于纤维状胶原蛋白的细胞外基质中，占所有细胞的三分之一；非心肌细胞占其余的三分之二。心室肥大涉及心肌细胞生长。高血压性心脏病（HHD）包括心肌细胞和非心肌细胞生长，这会导致壁内冠状动脉血管系统和基质发生不良结构重塑。在HHD中，导致心血管不良事件风险增加的不是心肌的数量，而是其质量。心脏组织的结构同质性由调节细胞生长、凋亡、表型和基质周转的刺激信号和抑制信号之间的平衡来控制。刺激物（如血管紧张素II、醛固酮和内皮素）通常在相互调节的模式下被抑制剂（如缓激肽、一氧化氮和前列腺素）所抵消。为降低HHD伴随的心力衰竭和心源性猝死风险，必须针对其不良结构重塑进行药物干预。心脏保护剂可抵消刺激物和抑制剂之间的失衡。它们包括ACE和内肽酶抑制剂以及各自的受体拮抗剂。心脏修复剂可逆转促生长状态，并使冠状动脉血管和基质结构中的现有异常消退。ACE抑制已实现这一结果，对血管运动反应性和组织硬度产生了有利影响。当今高血压的管理不应仅仅关注血压降低，还必须针对导致HHD的不良结构重塑。
