Correlation between Diastolic Function and left ventricular global longitudinal stress (GLS) decline in Hypertensive Patients

Abstract

Heart failure with preserved LVEF is a major cause of morbidity and mortality in hypertensive patients. The close correlation between the impairment of diastolic function and the longitudinal systolic dysfunction has several possible explanations. First the diastole is an energy-dependent process, especially during its first phase, it also includes active systolic components during the isovolumetric relaxation phase; in addition, the achievement of intrinsic myocyte function is part of hypertensive pathology as evidenced by recent studies. Echocardiography was performed in a series of 200 hypertensive patients (25 to 75 years-old). The left ventricular ejection fraction was calculated by biplane method, the indexed left ventricular mass and the relative wall thickness were measured or calculated. In order to differentiate eccentric and concentric LVH, diastolic function analysis and finally study of the LV longitudinal deformation by the speckle tracking technique (GLS calculation) were performed. Patients with secondary hypertension, valve insufficiency or stenosis, arrhythmia, history of coronary insufficiency were excluded from this study. One hundred and seventy-eight patients (89%) of the 200 hypertensive patients had diastolic function impairment, of which 37 patients (18.5%) had high filling pressures. Mean arterial blood pressure was statistically higher in hypertensive patients with high filling pressures than in hypertensives with normal filling diastolic LV pressure. 30 of 37 patients with high filling pressure had low GLS. We reported a significant relationship between the decrease in GLS and the increase in the left ventricular filling pressure. These results suggest that the increase in filling pressures is closely associated with the atrioventricular interaction in hypertensive patients, with a significant correlation with the impairment of longitudinal systolic function and diastolic function. When myocardial fibrosis develops, collagen accumulation increases myocardial rigidity and induces diastolic dysfunction; it also deprives cardiomyocytes of the skeleton necessary for myocardial contraction. Therefore, the degree of myocardial fibrosis can be associated with the defects of systolic and diastolic properties. LVEF is a poorly sensitive indicator of myocardial contractility and subclinical alterations in LV systolic function are already evident in heart failure with preserved LVEF. The decline in the longitudinal function index, despite a preserved LVEF, is well correlated with the increase in filling pressures in hypertensive patients with LVH. The association between HT with LVH and the deterioration of asymptomatic diastolic function is well recognized. A linear relationship is thus established between the increase in left ventricular mass, diastolic dysfunction and LV systolic dysfunction. Finally, the detection of longitudinal systolic dysfunction in an hypertensive patient should impose a therapeutic prevention strategy with the objective of delaying the onset of symptomatic heart failure.