Longitudinal Strain and Torsion Assessed by Two-Dimensional Speckle Tracking Correlate with the Serum Level of Tissue Inhibitor of Matrix Metalloproteinase-1, a Marker of Myocardial Fibrosis, in Patients with Hypertension

Abstract

We hypothesized that the alterations of myocardial collagen turnover in patients with hypertension may be involved in the early changes of regional contractile function assessed by a new speckle tracking method. In 56 patients with untreated hypertension (48 +/- 11 years, ejection fraction > 55%) and 20 age-matched control subjects, the serum levels of aminoterminal propeptide of procollagen I/III and tissue inhibitor of matrix metalloproteinase (TIMP)-1 were measured by radioimmunoassay and enzyme immunoassay. To assess the regional contractile function, the average of negative longitudinal strain of 6 segments at apical 4-chamber view (longitudinal epsilon), the average of radial strain (radial epsilon) and the average of circumferential strain (circumferential epsilon) of 6 mid-left ventricular (LV) segments, and basal-to-apical torsion were obtained by 2-dimensional speckle tracking imaging. Compared with control group, longitudinal epsilon was significantly decreased (-20.4 +/- 3.0% vs -22.1 +/- 2.2%, P = .030) and basal-to-apical torsion was increased (20.5 +/- 5.7 degrees vs 17.4 +/- 3.7 degrees, P = .013) in patient group. The serum level of log TIMP-1 was higher in the patients (3.6 +/- 0.6 vs 3.0 +/- 0.5, P < .001). The serum log TIMP-1 significantly correlated with longitudinal epsilon (r = 0.405, P = .015), basal-to-apical torsion (r = 0.331, P = .017), and the LV mass (r = 0.266, P = .047). In multivariate analysis, longitudinal epsilon (beta = 0.326, P = .015) and basal-to-apical torsion (beta = 0.402, P = .003) independently correlated with the serum TIMP-1 level. In patients who are hypertensive with normal ejection fraction, impaired longitudinal epsilon and increased LV torsion correlated with serum TIMP-1, which suggests that the change in collagen turnover and the myocardial fibrotic process may affect the early contractile dysfunction of LV.