OBJECTIVE: Postsystolic shortening is associated with hypertensive heart disease, and the degree of postsystolic shortening can be measured by postsystolic strain index (PSI) of the left ventricle (LV) derived from speckle tracking echocardiography. We studied the association between PSI with delayed diastolic lengthening and diastolic dysfunction in hypertension. METHODS: This study recruited 46 patients (mean age 56 ± 13 years, 24 men) with untreated hypertension, and 26 normal individuals (mean age 55 ± 11 years, 9 men) as controls. Hypertension patients were further divided into two groups based on the presence of diastolic dysfunction. PSI was calculated as [(postsystolic peak longitudinal strain - end-systolic strain)/end-systolic strain] × 100%. Timing of left-ventricular diastolic lengthening was determined by measurements of time to onset of early diastolic mitral annulus lengthening by tissue Doppler imaging. RESULTS: Total PSI was significantly higher in patients with diastolic dysfunction (252 ± 257 vs. 98 ± 72%, P = 0.002). After multivariate analysis, PSI was independently associated with diastolic dysfunction in hypertension [every 10% increment of PSI, odds ratio (OR) 1.13, 95% confidence interval (CI) 1.01-1.27, P = 0.036]. PSI was independently correlated with serum procollagen type I carboxyterminal propeptide (beta = 0.382, P = 0.028) after multivariable analysis, and time delay from onset of early mitral inflow to onset of early diastolic medial (beta = 0.405, P = 0.004) or lateral (beta = 0.582, P < 0.001) annulus lengthening. CONCLUSIONS: Increased PSI was associated with increased procollagen type I carboxyterminal propeptide and diastolic dysfunction in hypertension. Postsystolic shortening was associated with delayed diastolic lengthening which contributed to diastolic dysfunction in hypertension.
OBJECTIVE: Postsystolic shortening is associated with hypertensive heart disease, and the degree of postsystolic shortening can be measured by postsystolic strain index (PSI) of the left ventricle (LV) derived from speckle tracking echocardiography. We studied the association between PSI with delayed diastolic lengthening and diastolic dysfunction in hypertension. METHODS: This study recruited 46 patients (mean age 56 ± 13 years, 24 men) with untreated hypertension, and 26 normal individuals (mean age 55 ± 11 years, 9 men) as controls. Hypertensionpatients were further divided into two groups based on the presence of diastolic dysfunction. PSI was calculated as [(postsystolic peak longitudinal strain - end-systolic strain)/end-systolic strain] × 100%. Timing of left-ventricular diastolic lengthening was determined by measurements of time to onset of early diastolic mitral annulus lengthening by tissue Doppler imaging. RESULTS: Total PSI was significantly higher in patients with diastolic dysfunction (252 ± 257 vs. 98 ± 72%, P = 0.002). After multivariate analysis, PSI was independently associated with diastolic dysfunction in hypertension [every 10% increment of PSI, odds ratio (OR) 1.13, 95% confidence interval (CI) 1.01-1.27, P = 0.036]. PSI was independently correlated with serum procollagen type I carboxyterminal propeptide (beta = 0.382, P = 0.028) after multivariable analysis, and time delay from onset of early mitral inflow to onset of early diastolic medial (beta = 0.405, P = 0.004) or lateral (beta = 0.582, P < 0.001) annulus lengthening. CONCLUSIONS: Increased PSI was associated with increased procollagen type I carboxyterminal propeptide and diastolic dysfunction in hypertension. Postsystolic shortening was associated with delayed diastolic lengthening which contributed to diastolic dysfunction in hypertension.