Gradman Alan H, Alfayoumi Fadi
Western Pennsylvania Hospital, Pittsburgh, PA 15224, USA.
Prog Cardiovasc Dis. 2006 Mar-Apr;48(5):326-41. doi: 10.1016/j.pcad.2006.02.001.
Other than age, left ventricular hypertrophy (LVH) is the most potent predictor of adverse cardiovascular outcomes in the hypertensive population, and is an independent risk factor for coronary heart disease, sudden death, heart failure and stroke. Although directly related to systolic blood pressure, other factors including age, sex, race, body mass index and stimulation of the renin-angiotensin-aldosterone and sympathetic nervous systems play an important role in the pathogenesis of LVH. LVH involves changes in myocardial tissue architecture consisting of perivascular and myocardial fibrosis and medial thickening of intramyocardial coronary arteries, in addition to myocyte hypertrophy. The physiologic alterations which occur as a result of these anatomical changes include disturbances of myocardial blood flow, the development of an arrhythmogenic myocardial substrate and diastolic dysfunction. The latter is directly related to the degree of myocardial fibrosis and is the hemodynamic hallmark of hypertensive heart disease. When diastolic dysfunction is present, left ventricular end-diastolic pressure increases out-of-proportion to volume and may be elevated at rest or with exertion leading to clinical heart failure. At least one third of heart failure patients in the United States can be considered to have heart failure related to diastolic dysfunction. Compared to heart failure patients with systolic dysfunction, diastolic heart failure patients are more likely to be older, female, and to be hypertensive at the time of presentation. Although it has been assumed that LVH may lead to systolic dysfunction, evidence is lacking that LVH resulting from hypertension is a major risk factor for systolic heart failure independent of coronary artery disease. Treatment of hypertension greatly attenuates the development of LVH and significantly decreases the incidence of heart failure. In patients with established LVH, regression is both possible and desirable and results in a significant reduction in adverse clinical endpoints.
除年龄外，左心室肥厚（LVH）是高血压人群不良心血管结局最有力的预测指标，并且是冠心病、猝死、心力衰竭和中风的独立危险因素。尽管与收缩压直接相关，但包括年龄、性别、种族、体重指数以及肾素-血管紧张素-醛固酮系统和交感神经系统的刺激等其他因素在LVH的发病机制中起重要作用。LVH除了涉及心肌细胞肥大外，还包括由血管周围和心肌纤维化以及心肌内冠状动脉中层增厚组成的心肌组织结构变化。这些解剖学变化导致的生理改变包括心肌血流紊乱、致心律失常心肌基质的形成和舒张功能障碍。后者与心肌纤维化程度直接相关，是高血压性心脏病的血流动力学标志。当存在舒张功能障碍时，左心室舒张末期压力随容量不成比例增加，可能在静息或运动时升高，导致临床心力衰竭。在美国，至少三分之一的心力衰竭患者可被认为患有与舒张功能障碍相关的心力衰竭。与收缩功能障碍的心力衰竭患者相比，舒张性心力衰竭患者在就诊时更可能年龄较大、为女性且患有高血压。尽管一直认为LVH可能导致收缩功能障碍，但缺乏证据表明高血压导致的LVH是独立于冠状动脉疾病的收缩性心力衰竭的主要危险因素。高血压治疗可大大减轻LVH的发展，并显著降低心力衰竭的发生率。在已确诊LVH的患者中，LVH的逆转是可能且可取的，并且会显著降低不良临床终点的发生率。
