Comparison of hypertensive patients with left ventricular hypertrophy versus hypertensive patients without left ventricular hypertrophy using echocardiography and tissue doppler imaging

Abstract

Background and aim Systemic hypertension (SH) causes a gradual increase in the mass of the left ventricle, resulting in left ventricular hypertrophy (LVH). Derangement of LV function is caused by morphologic changes in the left ventricular (LV) walls, which result in hypertrophy. According to a recent meta-analysis, LVH raises the risk of cardiovascular morbidity and mortality. The aim was to compare between hypertensive patients with LVH and hypertensive patients without LVH regarding LV function (by Simpson’s method) and myocardial performance index (by Tissue Doppler echocardiography). Patients and methods The study included 40 selected hypertensive patients and 20 healthy participants undergoing echocardiographic assessment at the echocardiography unit. The patients were classified into two groups: group I included 20 normotensive healthy control, and group II included 40 hypertensive patients. Group II was further divided into two subgroups according to the absence or presence of echocardiographic signs of LVH: group IIa included 20 hypertensive patients without echocardiographic signs of LVH, and group IIb included 20 hypertensive patients with echocardiographic signs of LVH. Results Regarding systolic and diastolic blood pressures, there was an extremely statistically significant difference between the two groups. Regarding LV mass index, there was a highly statistically significant difference. However, LVMI in subgroup IIa was normal in comparison with subgroup IIb, with an extremely statistically significant difference. Regarding ejection fraction (EF%), there was an extremely statistically significant difference between the two groups. Regarding EF%, there was an extremely statistically significant difference between group I and group IIa. Regarding EF%, there was an extremely statistically significant difference between subgroup IIa and subgroup IIb. Regarding myocardial performance index, there was an extremely statistically significant difference between the two groups (0.36±3.2 in group I vs. 0.51±4.8 in group II). Conclusion First, SH causes a cascade of LV hemodynamic changes that can range from maladaptive hypertrophy to heart failure. Second, Tissue Doppler echocardiography appears to be able to differentiate between the many types and degrees of LV dysfunction in SH, as well as the various stages of the hypertensive disease process. Third, Myocyte apoptosis and collagen deposition in the interstitial space appear to be factors that favor the transition from LVH to heart failure.