title: Hypertension attenuates the efficacy of hypoglycemic therapy for preserving coronary flow reserve in patients with type 2 diabetes.
abstract: Impairment of coronary flow reserve (CFR) in patients with type 2 diabetes has been generally demonstrated; however, there have been few studies investigating CFR in cases of relatively well-controlled diabetes, in distinction to the influence of hypertension. The purpose of the present study was to evaluate the influence of diabetes and hypertension upon CFR in relatively well-controlled patients. This study included 12 healthy controls (C group) and 57 patients with type 2 diabetes (DM) and/or essential hypertension who were divided into three groups as follows: patients with DM (DM group; n = 24), patients with essential hypertension (HT group; n = 15), and patients with both DM and essential hypertension (DM+HT group; n = 18). We excluded patients with evidence of coronary artery disease and/or left ventricular hypertrophy. We performed transthoracic Doppler recording of diastolic coronary flow velocity (CFV) in the left anterior descending coronary artery at rest and after maximal vasodilation by adenosine infusion (140 microg/kg/min for 3 min) CFR was defined as the ratio of hyperemic to averaged basal peak CFV. The CFR (2.92 +/- 0.46) of the DM group was not decreased compared to that of the C group (2.96 +/- 0.58), although the CFR of the HT (2.33 +/- 0.25) and DM+HT (2.35 +/- 0.25) groups were significantly reduced. Left ventricular mass index, relative wall thickness, and diastolic function were worse in the HT and DM+HT groups than in the C and DM groups. Subjects with concentric left ventricular remodeling had a lower CFR than those with normal left ventricular geometry. In conclusion, adequate hyperglycemic control prevented the progression of coronary microcirculatory disturbance, but concomitant hypertension attenuated the effect.
authors.affiliation: Department of Geriatric Medicine, Osaka University Graduate School of Medicine, Suita, Japan.
authors.forename: Shin
authors.initials: S
authors.lastname: Takiuchi
authors.forename: Hiromi
authors.initials: H
authors.lastname: Rakugi
authors.forename: Tohru
authors.initials: T
authors.lastname: Masuyama
authors.forename: Hiroshi
authors.initials: H
authors.lastname: Ikegami
authors.forename: Tomoko
authors.initials: T
authors.lastname: Nishikage
authors.forename: Maki
authors.initials: M
authors.lastname: Shintani
authors.forename: Norio
authors.initials: N
authors.lastname: Komai
authors.forename: Michiko
authors.initials: M
authors.lastname: Nagai
authors.forename: Kei
authors.initials: K
authors.lastname: Kamide
authors.forename: Jitsuo
authors.initials: J
authors.lastname: Higaki
authors.forename: Toshio
authors.initials: T
authors.lastname: Ogihara
mesh_terms: D000241:Adenosine; D000255:Adenosine Triphosphate / Q000009:adverse effects; D000368:Aged; D003326:Coronary Circulation / Q000187:drug effects*; D003924:Diabetes Mellitus, Type 2 / Q000188:drug therapy* / Q000503:physiopathology*; D003925:Diabetic Angiopathies / Q000000981:diagnostic imaging / Q000503:physiopathology*; D004452:Echocardiography; D005260:Female; D006439:Hemodynamics; D006801:Humans; D006973:Hypertension / Q000000981:diagnostic imaging / Q000503:physiopathology*; D007004:Hypoglycemic Agents / Q000627:therapeutic use*; D008297:Male; D008875:Middle Aged; D014665:Vasodilator Agents
chemical_list: D007004:Hypoglycemic Agents; D014665:Vasodilator Agents; D000255:Adenosine Triphosphate; D000241:Adenosine