title: Hypertension impairs myocardial blood perfusion reserve in subjects without regional myocardial ischemia.
abstract: Quantitative analysis of myocardial perfusion MRI can provide noninvasive assessments of myocardial perfusion reserve (MPR), which is associated with endothelial function. Endothelial function is influenced by various factors, including hypertension, diabetes, dyslipidemia, renal dysfunction and anemia. The purpose of this study was to evaluate which risk factor is the strongest effector of MPR in subjects without regional myocardial ischemia. We studied 110 patients (66 years ±10, male 68%, hypertension 76%, diabetes mellitus (DM) 40% and dyslipidemia 65%) without regional myocardial ischemia. Adenosine triphosphate (ATP) stress and rest first-pass perfusion magnetic resonance (MR) images were acquired with a 1.5-T MR system, and MPR was calculated as the ratio of stress to rest myocardial blood flow (MBF). Average rest MBF in 110 patients was 1.07±0.62 ml min⁻¹ g⁻¹, whereas stress MBF was 3.15±1.93 ml min⁻¹ g⁻¹ and the MPR was 3.33±1.82. Rest MBF correlated significantly with hematocrit, whereas stress MBF showed a strong correlation with estimated glomerular filtration rate (e-GFR). MPR was associated with hypertension, age, e-GFR, hematocrit and left ventricular mass index (LVMI). In multiple regression analysis, hypertension (P=0.003, β=-0.274) showed the strongest correlation with MPR among other risk factors, such as diabetes (P=ns), dyslipidemia (P=ns), e-GFR (P=ns), LVMI (P=0.007, β=-0.248) and hematocrit (P=ns) after adjusting age and gender. Hypertension is the most important effector of MPR in subjects without myocardial ischemia.
authors.affiliation: Department of Cardiology, Mie University Graduate School of Medicine, Tsu, Japan.
authors.forename: Hiroshi
authors.initials: H
authors.lastname: Nakajima
authors.forename: Katsuya
authors.initials: K
authors.lastname: Onishi
authors.forename: Tairo
authors.initials: T
authors.lastname: Kurita
authors.forename: Masaki
authors.initials: M
authors.lastname: Ishida
authors.forename: Motonori
authors.initials: M
authors.lastname: Nagata
authors.forename: Kakuya
authors.initials: K
authors.lastname: Kitagawa
authors.forename: Kaoru
authors.initials: K
authors.lastname: Dohi
authors.forename: Mashio
authors.initials: M
authors.lastname: Nakamura
authors.forename: Hajime
authors.initials: H
authors.lastname: Sakuma
authors.forename: Masaaki
authors.initials: M
authors.lastname: Ito
mesh_terms: D000255:Adenosine Triphosphate / Q000032:analysis; D000319:Adrenergic beta-Antagonists / Q000627:therapeutic use; D000368:Aged; D000806:Angiotensin-Converting Enzyme Inhibitors / Q000627:therapeutic use; D002121:Calcium Channel Blockers / Q000627:therapeutic use; D003287:Contrast Media; D004727:Endothelium / Q000503:physiopathology; D005260:Female; D019786:Gadolinium DTPA; D006321:Heart / Q000503:physiopathology*; D006400:Hematocrit; D006801:Humans; D006973:Hypertension / Q000188:drug therapy / Q000503:physiopathology*; D008297:Male; D008875:Middle Aged; D017202:Myocardial Ischemia / Q000503:physiopathology*; D055414:Myocardial Perfusion Imaging; D012039:Regional Blood Flow / Q000187:drug effects
chemical_list: D000319:Adrenergic beta-Antagonists; D000806:Angiotensin-Converting Enzyme Inhibitors; D002121:Calcium Channel Blockers; D003287:Contrast Media; D000255:Adenosine Triphosphate; D019786:Gadolinium DTPA