Kahan T
Karolinska Institute at Danderyd Hospital, Division of Internal Medicine, Sweden.
J Hypertens Suppl. 1998 Sep;16(7):S23-9.
Hemodynamic and non-hemodynamic factors contribute to the development of left ventricular hypertrophy (LVH). The presence of LVH is an important independent risk factor for total mortality and for cardiovascular morbidity and mortality. Direct cardiac effects of LVH include an increased risk of developing of congestive heart failure, an increased risk of arrhythmic events, and a reduced coronary flow reserve, promoting myocardial ischemic episodes. In addition, hypertension may promote the development of coronary artery atherosclerosis. The prognostic implications of LVH underscore the importance of diagnostic procedures. The electrocardiogram has a high specificity to identify patients with LVH but the sensitivity is fairly low. Echocardiography provides higher sensitivity and also gives important information, such as the pattern of left ventricular geometry, which is of prognostic importance, and the presence of diastolic dysfunction, which is an early abnormality in the evolution of hypertensive LVH. Reversal of LVH appears to improve prognosis. Reduction of blood pressure is one important component in the regression of LVH. Important quantitative differences exist between drug classes in the reversal of cardiac hypertrophy despite similar antihypertensive effects, suggesting other factors to be of importance in the regression of left ventricular mass. LVH is reduced more by angiotensin-converting enzyme inhibitors than by other antihypertensive drug classes, suggesting an effect on structural myocardial changes beyond that provided by the reduction of blood pressure. Recent data suggest that angiotensin II receptor antagonists (AIIRAs) have quantitatively similar effects on left ventricular mass as do angiotensin-converting enzyme inhibitors. A comparative trial of the AIIRA irbesartan and the beta-blocker atenolol demonstrated that despite similar reductions in blood pressure, the reductions attained in left ventricular mass with irbesartan were progressive and numerically greater than those attained with atenolol. Taken together, these findings provide circumstantial evidence for an important role of angiotensin II acting on angiotensin type 1 (AT1) receptors in the development or maintenance of cardiac hypertrophy. Confirmation of the favorable effects of angiotensin-converting enzyme inhibitors and AIIRAs on left ventricular mass in larger trials, including those assessing cardiovascular morbidity and mortality, will be of major importance in the future treatment of hypertension.
血流动力学和非血流动力学因素都与左心室肥厚（LVH）的发生有关。LVH的存在是全因死亡率以及心血管疾病发病率和死亡率的重要独立危险因素。LVH对心脏的直接影响包括发生充血性心力衰竭的风险增加、心律失常事件的风险增加以及冠状动脉血流储备减少，从而促发心肌缺血发作。此外，高血压可能会促进冠状动脉粥样硬化的发展。LVH的预后意义凸显了诊断程序的重要性。心电图对识别LVH患者具有较高的特异性，但敏感性相当低。超声心动图具有更高的敏感性，还能提供重要信息，如具有预后重要性的左心室几何形态模式，以及舒张功能障碍的存在情况，舒张功能障碍是高血压LVH演变过程中的早期异常表现。LVH的逆转似乎能改善预后。降低血压是LVH逆转的一个重要组成部分。尽管各类药物的降压效果相似，但在逆转心脏肥厚方面存在重要的定量差异，这表明其他因素在左心室质量逆转中也很重要。与其他降压药物类别相比，血管紧张素转换酶抑制剂对LVH的降低作用更大，这表明其对心肌结构变化的影响超出了单纯降低血压的作用。最近的数据表明，血管紧张素II受体拮抗剂（AIIRAs）对左心室质量的影响在数量上与血管紧张素转换酶抑制剂相似。一项对AIIRA厄贝沙坦和β受体阻滞剂阿替洛尔的比较试验表明，尽管血压降低程度相似，但厄贝沙坦使左心室质量的降低是渐进性的，且在数值上大于阿替洛尔所达到的降低程度。综上所述，这些发现间接证明了血管紧张素II作用于1型血管紧张素（AT1）受体在心脏肥厚的发生或维持中起重要作用。在包括评估心血管疾病发病率和死亡率的更大规模试验中，证实血管紧张素转换酶抑制剂和AIIRAs对左心室质量的有益作用，将对未来高血压治疗具有重要意义。
