Early detection of asymptomatic left ventricular systolic dysfunction in hypertensive patients

Abstract

Background: Hypertension is a potent risk factor for congestive heart failure (CHF). Development of overt CHF may be preceded by a phase of asymptomatic left venrticular systolic dysfunction. The aim of this study was early detection of alteration in left ventricular systolic function. Methods: 120 hypertensive patients, with preserved ejection fraction (EF), were divided in three groups according LVDD: normal (n=40), abnormal relaxation (Grade I, n=37) and pseudonormal (Grade II, n=43). Left atrial volume index (LAVI), left ventricular mass index (LVMI), left ventricular dimensions and volume inexes (LVEDV/BSA and LVESV/BSA) and EF were estimated by echocardiography. We measured coresponding velocities from tissue Doppler at the level of the septal mitral annulus (Em, Am, Sm), including E/Em and tissue Doppler myocardial performance index (tMPI). The same measurements were repeated after three years. Results: Close correlations were found between Sm and EF (r=0.349; p=0.0009), LVMI (r= -0.222; p=0.015), LVEDV/BSA (r =-0.317; p=0.0004) and LVESV/BSA (r =-0.472; p=0.0005). Levels of LVEDV/BSA (89.3 vs 103.8 vs 101.7; p=0.009), LVESV/BSA (34.0 vs 42.9 vs 44.0; p=0.0004), LVMI (104.3 vs 112.5 vs 123.0; p=0.0004), LAVI (32.0 vs 35.5 vs 44.5; p=0.0001) and MPI (61.7 vs 72.1 vs 76.3; p=0.036) progressively increased from the normal group through LVDD Grade I and II groups. Significantly different values of EF (63 vs 61 vs 59; p=0.003) and Sm (0.074 vs 0.067 vs 0.059; p=0.003) were obtained between groups too, but with progressively decrease from the normal group through LVDD Grade I and II groups. General linear model for repeated measures showed increase of LVEDV/BSA (F=50.009; p<0.001), LVESV/BSA (F=34.258; p<0.001), LVMI (F=27.648; p<0.001), LAVI (F=17.083; p<0.001) and tMPI (F=35.842; p<0.001) during three years, with significant time difference, but withot significant difference between groups, these parameters enarged in all groups almost at the same manner. Sm also significantly changed during three years with significant time difference (F=128.24; p<0.001) and with significant difference between groups (F=4.597; p< 0,012), Sm decrease in all groups, but most expressed in LVDD Grade II group. Conclusion: Left ventriculae EF was not sensitive indicator for the detection of subclinical systolic dysfunction, but decrease of Sm appeared as the first sign of systolic abnormalities following established diastolic dysfunction and was the clear reflection of LV remodeling process. This suggests that Sm may aid in the identification of patients at high risk for development of CHF who need preventive treatment.