Echocardiographic studies of regression of left ventricular hypertrophy in hypertension.

Abstract

SUMMARY The availability of echocardiography has allowed direct determinations of left ventricular wall thickness and calculation of left ventricular mass. As a result, the past decade has witnessed a remarkable evolution in our understanding of structural changes in the heart. Moreover, cardiac hypertrophy was found to be reversible by some forms of therapy. In general, reduction of left ventricular mass became evident after 8 to 12 weeks of antihypertensive therapy. Sympatholytics (including methyldopa and reserpine), converting enzyme inhibitors (captopril and enalapril), and calcium entry blockers led to significant regression of left ventricular hypertrophy. On the other hand, arteriolar vasodilators (hydralazine, trimazosin, and minoxidil) were not associated with regression of hypertrophy despite adequate blood pressure control. Finally, data regarding diuretics and /3-blockers are controversial. These differences in results among various antihypertensive drugs reflect the multiplicity of factors modulating left ventricular hypertrophy. T HE past decade has witnessed a remarkable evolution in our understanding of structural changes in the heart and arterial system in hypertension. Not only was cardiac hypertrophy found to occur much earlier in hypertension than previously thought, 1 but it was also clearly demonstrated to be reversible by some forms of therapy within a relatively short period of time.2 This advancement was made possible by the availability of echocardiographic techniques that allowed direct determinations of left ventricular wall thickness and calculation of left ventricular mass. 3 The measurements were shown to be reliable and reproducible over time with adherence to such adequate safeguards as double blind readings, strict application of reading criteria, and use of internal checking measures. 4 The reversibility of left ventricular hypertrophy in humans has been repeatedly demonstrated by many centers.4 " 7 In general, reduction of left ventricular mass became evident after at least 8 to 12 weeks of antihypertensive therapy, 2 ' 5 ' 6 but the ability to induce this regression varied markedly among otherwise equipotent antihypertensive agents. Secondly, most of the centers demonstrated either a lack of or a relatively poor correlation between the degree of blood pressure control and the regression of left ventricular hypertrophy.5 " 9 The correlation between mass and pressure reportedly improved by utilizing averages of 24-hour blood pressure recordings rather than casual blood pressure levels, but even then, the index of determina- Methodological ConsiderationsDifferences in methods may partially account for the diversity of the results among centers. These differences include: age and sex distribution, previous treatment with antihypertensive agents, modes of assessment of hypertrophy by echocardiographic techniques, degree of hypertrophy present at the beginning of the study, reproducibility of results, duration of therapy, presence of control groups, and patient compliance.No sign...

Histopathological Investigation on Salt-Loaded Stroke-Prone Spontaneously Hypertensive Rats, Whose Biochemical Parameters of Renal Dysfunction Were Ameliorated by Administration of Imidapril

“…The occurrence of the myocardial hypertrophy was prevented by the administration of im idapril and enalapril, and the fibrosis was also prevented by enalapril. The development and progression of myo cardial hypertrophy is thought to involve the local renin angiotensin system (9,10,29,30). In addition, there is a report demonstrating that angiotensin II directly stimu lates myocardial protein synthesis (31).…”

Reversion of cardiac hypertrophy and reduced arterial compliance after converting enzyme inhibition in essential hypertension.

“…This is close to the limit of variability attributable to measurement errors. 30,33 diograms in eight subjects (r = 0.98; SD = 28 g) and readings of 24 echocardiograms by two experienced investigators (r= 0.94; SD = 41 g). These results were found to be strikingly similar to the mean difference of 26 g observed between measurements on echocardiograms performed more than a year apart in 53 normal subjects.M They are also smaller than the standard deviation of 43 g obtained in a comparison of echocardiographic and necropsy measurements.…”

Cardiac effects of angiotensin converting enzyme inhibitors

“…Regression of left ventricular hypertrophy in hypertensive patients can be achieved with converting enzyme inhibitors. ACE inhibitors and sympatholytic drugs appear to be more effective than other agents in causing regression of left ventricular hypertrophy, suggesting a role for the renin-angiotensin system in this sequel of hypertension [6][7][8][9].…”