title: Possible mechanisms of left ventricular torsion evaluated by cardioreparative effects of telmisartan in patients with hypertension.
abstract: OBJECTIVE
  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).
  
  
  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.
  
  
  CONCLUSIONS
  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.
authors.affiliation: Cardiovascular Section, Higashi Tokushima National Hospital, National Hospital Organization, 1-1 Ohmukai-kita, Ohtera, Itano, Itano, Tokushima 779-0193, Japan. mizuguchi@higasitokusima.hosp.go.jp
authors.forename: Yukio
authors.initials: Y
authors.lastname: Mizuguchi
authors.forename: Yoshifumi
authors.initials: Y
authors.lastname: Oishi
authors.forename: Hirokazu
authors.initials: H
authors.lastname: Miyoshi
authors.forename: Arata
authors.initials: A
authors.lastname: Iuchi
authors.forename: Norio
authors.initials: N
authors.lastname: Nagase
authors.forename: Nusrat
authors.initials: N
authors.lastname: Ara
authors.forename: Takashi
authors.initials: T
authors.lastname: Oki
mesh_terms: D047228:Angiotensin II Type 1 Receptor Blockers / Q000627:therapeutic use*; D000806:Angiotensin-Converting Enzyme Inhibitors / Q000627:therapeutic use*; D001562:Benzimidazoles / Q000627:therapeutic use*; D001565:Benzoates / Q000627:therapeutic use*; D004452:Echocardiography; D005240:Feasibility Studies; D005260:Female; D005355:Fibrosis / Q000188:drug therapy; D006352:Heart Ventricles / Q000000981:diagnostic imaging / Q000187:drug effects / Q000473:pathology*; D006801:Humans; D006973:Hypertension / Q000188:drug therapy*; D017379:Hypertrophy, Left Ventricular / Q000000981:diagnostic imaging / Q000209:etiology* / Q000473:pathology; D008297:Male; D008875:Middle Aged; D013223:Statistics as Topic; D013318:Stroke Volume; D000077333:Telmisartan; D016277:Ventricular Function, Left
chemical_list: D047228:Angiotensin II Type 1 Receptor Blockers; D000806:Angiotensin-Converting Enzyme Inhibitors; D001562:Benzimidazoles; D001565:Benzoates; D000077333:Telmisartan