title: Left ventricular hypertrophy determines the severity of diastolic dysfunction in patients with nonvalvular atrial fibrillation and preserved left ventricular systolic function.
abstract: Regression of left ventricular (LV) hypertrophy (LVH) is known to be related to a lower incidence of stroke in hypertensive patients with nonvalvular atrial fibrillation (NV-AF). However, its mechanism remains controversial. Recently, diastolic dysfunction (DD) was reported to be correlated with ischemic stroke in NV-AF. We hypothesized that hypertension (HTN) and resultant LVH might be associated with the severity of DD in NV-AF. Two hundred and ninety-four patients (204 males, age 66 ± 12 y) with NV-AF with preserved LV systolic function were included. Clinical and echocardiographic data were compared between patients with enlarged left atrial (LA) volume (n = 237) and patients with normal LA. Age (60 ± 12 vs. 67 ± 11 years), sex (male; 81 vs. 62%), duration of NV-AF (4.1 ± 7.8 vs. 45.7 ± 49.0 months), brain natriuretic peptide (108.3 ± 129.3 vs. 236.1 ± 197.0 pg/mL), right ventricular systolic pressure (24.5 ± 5.5 vs. 33.1 ± 11.1 mmHg), mitral inflow velocity (E [77.4 ± 22.2 vs. 88.3 ± 22.0 cm/s]), LV mass index (LVMI [87.6 ± 22.2 vs. 105.1 ± 23.2 g/m(2)]), peak systolic mitral annular velocity (S' [7.2 ± 2.0 vs. 5.8 ± 1.8 cm/s]), and mitral inflow velocity to diastolic mitral annular velocity (E/E' [9.8 ± 3.4 vs. 12.1 ± 4.4]) were significantly different between the two groups, respectively (P < 0.05). In multivariate analysis, LVMI was independently correlated with increased LA volume (OR: 1.037 [95% CI: 1.011-1.063], P < 0.05), whereas HTN was not. LA enlargement, which reflects the severity and chronicity of DD, is independently associated with LVH in patients with NV-AF. Therefore, regression of LVH with anti-hypertensive treatment may lead to improvement of diastolic function and favorable clinical outcomes in hypertensive patients with NV-AF.
authors.affiliation: Cardiology Division, Yonsei Cardiovascular Center, Yonsei University College of Medicine, Seoul, Republic of Korea.
authors.forename: Jeonggeun
authors.initials: J
authors.lastname: Moon
authors.forename: Se-Joong
authors.initials: SJ
authors.lastname: Rim
authors.forename: In Jeong
authors.initials: IJ
authors.lastname: Cho
authors.forename: Sang-Hak
authors.initials: SH
authors.lastname: Lee
authors.forename: Seonghoon
authors.initials: S
authors.lastname: Choi
authors.forename: Wook-Jin
authors.initials: WJ
authors.lastname: Chung
authors.forename: Young-Sup
authors.initials: YS
authors.lastname: Byun
authors.forename: Sung-Kee
authors.initials: SK
authors.lastname: Ryu
authors.forename: Wook-Bum
authors.initials: WB
authors.lastname: Pyun
authors.forename: Jong-Youn
authors.initials: JY
authors.lastname: Kim
mesh_terms: D000368:Aged; D000959:Antihypertensive Agents / Q000627:therapeutic use; D001281:Atrial Fibrillation / Q000150:complications* / Q000503:physiopathology*; D016022:Case-Control Studies; D003971:Diastole; D005260:Female; D006801:Humans; D006973:Hypertension / Q000150:complications* / Q000188:drug therapy / Q000503:physiopathology*; D017379:Hypertrophy, Left Ventricular / Q000150:complications* / Q000188:drug therapy / Q000503:physiopathology; D008297:Male; D008875:Middle Aged; D012189:Retrospective Studies; D012307:Risk Factors; D013599:Systole; D018487:Ventricular Dysfunction, Left / Q000150:complications* / Q000188:drug therapy / Q000503:physiopathology*; D016277:Ventricular Function, Left / Q000187:drug effects
chemical_list: D000959:Antihypertensive Agents