title: Olmesartan ameliorates myocardial function independent of blood pressure control in patients with mild-to-moderate hypertension.
abstract: Angiotensin II receptor blockers (ARBs) are suggested to be protective against myocardial hypertrophy and fibrosis, although such beneficial effects remain to be elucidated in the human heart. The aim of the present study was to examine the effect of a novel ARB, olmesartan, on myocardial function of the left ventricle in patients with mildto-moderate hypertension. We investigated 10 patients (6 men and 4 women, 62 +/- 7 years of age) who were stable with a single regimen of amlodipine, which was switched to olmesartan. Before and 8 months after changing medications, patients underwent echocardiographic examination and blood sampling, including measurement of the plasma high-sensitivity C-reactive protein (hsCRP) level. Peak velocities at the mitral annulus were determined by tissue Doppler imaging and used as measures of myocardial function. Olmesartan did not significantly alter blood pressure (BP) (systolic BP, 122 +/- 12 to 121 +/- 8 mmHg, P = 0.9; diastolic BP, 79 +/- 6 to 75 +/- 4 mmHg, P = 0.06) or parameters of global left ventricular systolic and diastolic function. Tissue Doppler imaging, however, revealed significant increases in the systolic (8.2 +/- 1.3 to 8.9 +/- 1.1 cm/s, P < 0.01) and early diastolic (6.7 +/- 0.9 to 7.6 +/- 1.0 cm/s, P = 0.02) velocities at the mitral annulus. This was associated with decreases in the left ventricular mass index (83 +/- 15 to 73 +/- 19 g/m2, P = 0.09) and hsCRP (683 +/- 555 to 655 +/- 450 ng/ml, P = 0.07). In conclusion, olmesartan improves myocardial function independent of BP reduction in hypertensive patients. Attenuated inflammatory changes as well as myocardial hypertrophy may play an important role.
authors.affiliation: Third Department of Internal Medicine, Osaka Medical College, 2-7 Daigaku-cho, Takatsuki, Osaka 569-8686, Japan.
authors.forename: Rie
authors.initials: R
authors.lastname: Futai
authors.forename: Takahide
authors.initials: T
authors.lastname: Ito
authors.forename: Yasunori
authors.initials: Y
authors.lastname: Kawanishi
authors.forename: Fumio
authors.initials: F
authors.lastname: Terasaki
authors.forename: Yasushi
authors.initials: Y
authors.lastname: Kitaura
mesh_terms: D000368:Aged; D017311:Amlodipine / Q000627:therapeutic use; D047228:Angiotensin II Type 1 Receptor Blockers / Q000627:therapeutic use*; D015415:Biomarkers / Q000097:blood; D001794:Blood Pressure / Q000187:drug effects*; D002097:C-Reactive Protein / Q000378:metabolism; D002121:Calcium Channel Blockers / Q000627:therapeutic use; D018618:Echocardiography, Doppler, Color; D005260:Female; D005355:Fibrosis; D006801:Humans; D006973:Hypertension / Q000000981:diagnostic imaging / Q000188:drug therapy* / Q000503:physiopathology; D017379:Hypertrophy, Left Ventricular / Q000000981:diagnostic imaging / Q000188:drug therapy* / Q000503:physiopathology; D007093:Imidazoles / Q000627:therapeutic use*; D007249:Inflammation / Q000188:drug therapy / Q000503:physiopathology; D008297:Male; D008875:Middle Aged; D009206:Myocardium / Q000473:pathology; D012720:Severity of Illness Index; D013777:Tetrazoles / Q000627:therapeutic use*; D013997:Time Factors; D016896:Treatment Outcome; D016277:Ventricular Function, Left / Q000187:drug effects*
chemical_list: D047228:Angiotensin II Type 1 Receptor Blockers; D015415:Biomarkers; D002121:Calcium Channel Blockers; D007093:Imidazoles; D013777:Tetrazoles; D017311:Amlodipine; C437965:olmesartan; D002097:C-Reactive Protein