Key result
Telmisartan therapy for 12 months reduced LV torsion and torsional rate, and increased mean peak systolic longitudinal strain and strain rate compared to 1-2 months of therapy.
Why the study?
Does telmisartan improve left ventricular longitudinal deformation and torsion in previously untreated patients with hypertension?
Observational (n=37)
Does telmisartan improve left ventricular longitudinal deformation and torsion in previously untreated patients with hypertension?
Telmisartan-induced cardioreparative effects suggest that left ventricular torsion is associated with systolic longitudinal deformation and concentric hypertrophy in hypertensive patients.
Telmisartan-linked LV torsion changes tie to longitudinal strain; leaves open causal mechanisms in hypertensive remodeling.
AIMS: Left ventricular (LV) torsion may be an important component of normal LV systolic function. However, its mechanics remain unresolved. Two-dimensional (2-D) strain imaging is increasingly used to quantify LV torsion in the clinical setting. Telmisartan has cardioreparative effects, including attenuation of subendocardial myocardial fibrosis and improvement of LV remodelling. To clarify the mechanisms of LV torsion, in the present study, we evaluated changes in LV longitudinal deformation and torsion after medication with telmisartan using 2-D strain imaging in patients with hypertension (HT). METHODS AND RESULTS: Telmisartan (20-40 mg daily) was administered to 37 previously untreated patients with HT. Two-dimensional strain echocardiography was performed after medication had been continued for 1-2 months with normal values for blood pressure (BP) (phase I) and for 12 months (phase II). In the phase II, relative LV wall thickness, LV mass index, LV torsion, and torsional rate were reduced, whereas the mean peak systolic longitudinal strain and strain rate were increased, compared to the phase I. LV torsion correlated well with relative LV wall thickness, but not LV mass index. CONCLUSION: Our results obtained from cardioreparative effects of telmisartan suggested that LV torsion is associated with systolic longitudinal deformation related to subendocardial myocardial fibrosis, and/or LV concentric hypertrophy-related difference in torques between the subendocardial and subepicardial sides.
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Mizuguchi et al. (2010) conducted an observational in Hypertension (n=37). Telmisartan vs. Phase I (1-2 months of therapy) was evaluated on Changes in LV longitudinal deformation and torsion. Telmisartan therapy for 12 months reduced LV torsion and torsional rate, and increased mean peak systolic longitudinal strain and strain rate compared to 1-2 months of therapy.
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