Strauer B E
Department of Medicine, University of Marburg, FRG.
Nephron. 1987;47 Suppl 1:76-86. doi: 10.1159/000184559.
In essential hypertension ventricular function is determined primarily by the degree of hypertrophy (myocardial factor) and by the organic complications in the coronary artery (coronary factor). Ventricular function is inversely correlated with ventricular size and systolic wall stress, inasmuch as ventricular function diminishes when these two variables increase. Even the young hypertensive heart of normal size with no angiographic abnormalities appears to be prone to ischemia, because the coronary reserve is seriously limited even in the absence of coronary stenosis. Unlike ventricular distensibility, myocardial compliance may be normal even in the presence of pronounced myocardial hypertrophy. As myocardial compliance decreases, systolic wall stress increases and ventricular function is reduced. The hypertensive heart, the most common form of an irregular hypertrophy of the ventricular wall, is found in 14% of such cases. Analysis of the degree of hypertrophy shows that the hypertrophy can be inappropriately high (high mass-to-volume ratio, reduced wall stress), appropriate, or inappropriately low (normal mass-to-volume ratio, increased wall stress). Coronary reserve is reduced even in hypertensive hypertrophy without evidence of coronary artery disease. MVO2 per mass unit was directly correlated with systolic wall stress per cross-sectional area of the left ventricular wall. It is concluded that the appropriateness of left ventricular hypertrophy, as a result of mass-to-volume ratio and stress, is a major determinant of left ventricular performance, of coronary blood flow, and of myocardial oxygen consumption. Pharmacotherapeutical means of reversing cardiac hypertrophy (prazosin, clonidine, enalapril, and nifedipine) were analyzed in concentrically, as well as eccentrically, hypertrophied left ventricles. Regression of cardiac hypertrophy, i.e. therapeutic intervention on a critical precursor of hypertensive congestive heart failure, can be obtained by various antihypertensive agents. Prazosin, calcium channel blockers and angiotensin-converting enzyme inhibitors as well as a combined treatment regimen using alpha-receptor blockers together with diuretics and vasodilators can all induce regression of hypertrophy associated with an improvement in left ventricular function. Moreover, an improved coronary reserve may reduce the ischemic risk of the hypertrophied myocardium. However, not all antihypertensive drugs seem equally effective in bringing about coronary regression of left ventricular hypertrophy. No regression or little regression has been found with diuretic monotherapy despite a satisfactory reduction in blood pressure.(ABSTRACT TRUNCATED AT 400 WORDS)
在原发性高血压中,心室功能主要由肥厚程度(心肌因素)和冠状动脉器质性并发症(冠脉因素)决定。心室功能与心室大小和收缩期壁应力呈负相关,因为当这两个变量增加时,心室功能会减弱。即使是没有血管造影异常的正常大小的年轻高血压心脏,似乎也容易发生缺血,因为即使没有冠状动脉狭窄,冠脉储备也会严重受限。与心室扩张性不同,即使存在明显的心肌肥厚,心肌顺应性也可能正常。随着心肌顺应性降低,收缩期壁应力增加,心室功能降低。高血压性心脏是心室壁不规则肥厚最常见的形式,在14%的此类病例中可见。对肥厚程度的分析表明,肥厚可能过高(质量与容积比高,壁应力降低)、适当或过低(质量与容积比正常,壁应力增加)。即使在没有冠状动脉疾病证据的高血压性肥厚中,冠脉储备也会降低。每单位质量的心肌耗氧量与左心室壁每横截面积的收缩期壁应力直接相关。得出的结论是,左心室肥厚的适当性,由质量与容积比和应力决定,是左心室功能、冠脉血流量和心肌耗氧量的主要决定因素。对在向心性和离心性肥厚的左心室中逆转心脏肥厚的药物治疗方法(哌唑嗪、可乐定、依那普利和硝苯地平)进行了分析。心脏肥厚的消退,即对高血压性充血性心力衰竭关键前体的治疗干预,可以通过各种抗高血压药物实现。哌唑嗪、钙通道阻滞剂和血管紧张素转换酶抑制剂,以及使用α受体阻滞剂与利尿剂和血管扩张剂联合的治疗方案,都可以诱导肥厚消退并改善左心室功能。此外,改善的冠脉储备可能降低肥厚心肌的缺血风险。然而,并非所有抗高血压药物在使左心室肥厚发生冠脉消退方面似乎都同样有效。尽管血压得到了令人满意的降低,但利尿剂单一疗法未发现消退或几乎没有消退。(摘要截选至400字)