title: Reduced bone mineral density in hypertensive patients is associated with left ventricular diastolic dysfunction, not left ventricular hypertrophy.
abstract: Left ventricular (LV) hypertrophy and diastolic dysfunction are commonly observed in hypertensive patients, and have been demonstrated to be risk factors of chronic heart failure due to LV diastolic dysfunction. Recently, reduced bone mineral density has been found in hypertensive patients compared with healthy controls. However, relationships between bone mineral density and LV hypertrophy and diastolic dysfunction have not been fully assessed. We examined relationships between bone mineral density and both LV hypertrophy and diastolic dysfunction in 38 hypertensive patients (23 males, 15 females; mean age 71 ± 8 y) who had been treated with antihypertensive drugs for at least 1 year. The bone mineral density of the calcaneus was measured with a quantitative ultrasound measurement device (A-1000 EXPRESS/InSight, GE Healthcare, Horten, Norway), and the stiffness index was determined as a parameter of bone mineral density. Echocardiography was performed to measure the left ventricular mass index as a parameter of LV hypertrophy. Left ventricular diastolic dysfunction was also assessed by early diastolic mitral annular velocity (e'), and the ratio of early transmitral flow velocity (E) to e' (E/e'). The bone mineral density did not correlate with left ventricular mass index, but did correlate with e' (r = 0.453, P < .01) and E/e' (r = -0.359, P < .05). Thus, reduced bone mineral density in hypertensive patients is not associated with LV hypertrophy but with LV diastolic dysfunction. Hypertensive patients with reduced bone mineral density may have a high risk of chronic heart failure due to LV diastolic dysfunction as well as bone fractures due to osteoporosis.
authors.affiliation: Department of Integrated Medicine, Kagawa University, Kagawa, Japan. masugata@med.kagawa-u.ac.jp
authors.forename: Hisashi
authors.initials: H
authors.lastname: Masugata
authors.forename: Shoichi
authors.initials: S
authors.lastname: Senda
authors.forename: Koji
authors.initials: K
authors.lastname: Murao
authors.forename: Michio
authors.initials: M
authors.lastname: Inukai
authors.forename: Naohisa
authors.initials: N
authors.lastname: Hosomi
authors.forename: Yasuyoshi
authors.initials: Y
authors.lastname: Iwado
authors.forename: Takahisa
authors.initials: T
authors.lastname: Noma
authors.forename: Masakazu
authors.initials: M
authors.lastname: Kohno
authors.forename: Nobuyuki
authors.initials: N
authors.lastname: Miyatake
authors.forename: Takashi
authors.initials: T
authors.lastname: Himoto
authors.forename: Fuminori
authors.initials: F
authors.lastname: Goda
mesh_terms: D000368:Aged; D000369:Aged, 80 and over; D015519:Bone Density; D003971:Diastole; D005260:Female; D006333:Heart Failure / Q000209:etiology; D006454:Hemoglobins / Q000378:metabolism; D006801:Humans; D006973:Hypertension / Q000150:complications / Q000000981:diagnostic imaging / Q000473:pathology* / Q000503:physiopathology*; D017379:Hypertrophy, Left Ventricular / Q000150:complications / Q000000981:diagnostic imaging / Q000473:pathology*; D016014:Linear Models; D008297:Male; D008875:Middle Aged; D010024:Osteoporosis / Q000150:complications / Q000473:pathology / Q000503:physiopathology; D012307:Risk Factors; D014463:Ultrasonography; D018487:Ventricular Dysfunction, Left / Q000150:complications / Q000503:physiopathology*
chemical_list: D006454:Hemoglobins