Pessina A C, Sacchetto A, Rossi G P
Department of Clinical & Experimental Medicine, University of Padua Medical School.
Adv Exp Med Biol. 1997;432:63-9. doi: 10.1007/978-1-4615-5385-4_7.
Left ventricular hypertrophy (LVH) is a common finding in hypertension and represents a detrimental outcome since it is associated with increased morbidity and mortality. For similar elevation of blood pressure the severity and type of LVH vary considerably in relation to several factors. Compelling evidence suggests that both the renin-angiotensin system (RAS) and the aldosterone excess play an important role in the pathogenesis of LVH, since experimentally angiotensin II has been found to cause myocardial cells hypertrophy and/or hyperplasia and excess aldosterone has been related to extracellular matrix and collagen deposition and therefore to myocardial fibrosis. Secondary forms of hypertension offer models for investigating the relative role of the RAS and aldosterone on the heart in humans. Being rare in the population of hypertensive patients, they furnish an example of the so called Bateson's approach to the understanding of diseases "Treasure your exceptions." In this paper, we review the data concerning the LV changes in primary aldosteronism and renovascular hypertension and discuss the insight that they have provided into the pathogenesis of LVH.
左心室肥厚（LVH）是高血压中的常见表现，并且是一种有害的结果，因为它与发病率和死亡率增加相关。对于相似的血压升高，LVH的严重程度和类型因多种因素而有很大差异。有力证据表明，肾素-血管紧张素系统（RAS）和醛固酮过多在LVH的发病机制中均起重要作用，因为实验发现血管紧张素II可导致心肌细胞肥大和/或增生，而醛固酮过多与细胞外基质和胶原沉积有关，进而与心肌纤维化有关。继发性高血压为研究RAS和醛固酮对人类心脏的相对作用提供了模型。它们在高血压患者群体中较为罕见，为理解疾病的所谓贝特森方法“珍视你的例外情况”提供了一个例子。在本文中，我们回顾了有关原发性醛固酮增多症和肾血管性高血压中左心室变化的数据，并讨论了它们对LVH发病机制的启示。
