Natsume T
Department of Emergency and Critical Care Medicine, Jichi Medical School, Tochigi, Japan.
Eur Heart J. 1993 Jul;14 Suppl D:33-7. doi: 10.1093/eurheartj/14.suppl_d.33.
As a consequence of persistently raised blood pressure, left ventricular hypertrophy (LVH) develops as a compensatory mechanism for wall stress induced by the increase in afterload. Recent advances in the fields of molecular biology and genetics are now clarifying the mechanisms involved in the development of LVH. It has been reported that messenger RNA of oncogenes, such as c-fos and c-myc, increases by stretching; these oncogenes contribute to the progression of LVH, the messenger RNA expression of myosin and contractile protein synthesis in the cardiomyocytes. Vasoactive hormones and vascular contracting factors are also reported to have a progressive effect on LVH. In contrast, some antihypertensive agents have been shown to have pharmacological effects on regression of LVH in animals and man. The mechanisms responsible for LVH progression have been extensively studied. In contrast, the mechanisms of LVH regression have not been defined and require elucidation. This paper outlines the basic recognition of the mechanisms of LVH progression and discusses the varied pharmacological actions of calcium antagonists and angiotensin converting enzyme inhibitors on the regression of LVH in man and rats. Although the role of antihypertensive therapy in regression of LVH remains controversial, the calcium antagonist nicardipine appears to have an important role to play in the treatment of LVH in hypertension and in congestive heart failure.
由于血压持续升高，左心室肥厚（LVH）作为后负荷增加所诱导的壁应力的一种代偿机制而发展。分子生物学和遗传学领域的最新进展正在阐明LVH发生发展所涉及的机制。据报道，诸如c-fos和c-myc等癌基因的信使核糖核酸（mRNA）会因拉伸而增加；这些癌基因有助于LVH的进展、心肌细胞中肌球蛋白的信使核糖核酸表达以及收缩蛋白的合成。血管活性激素和血管收缩因子也被报道对LVH有促进作用。相比之下，一些抗高血压药物已被证明对动物和人类的LVH消退具有药理作用。对LVH进展的机制已进行了广泛研究。相比之下，LVH消退的机制尚未明确，需要阐明。本文概述了对LVH进展机制的基本认识，并讨论了钙拮抗剂和血管紧张素转换酶抑制剂对人类和大鼠LVH消退的不同药理作用。尽管抗高血压治疗在LVH消退中的作用仍存在争议，但钙拮抗剂尼卡地平似乎在高血压和充血性心力衰竭患者LVH的治疗中发挥重要作用。
