title: Effects of blood pressure lowering and metabolic control on systolic left ventricular function in Type II diabetes mellitus.
abstract: Decreased left ventricular long-axis function may be the earliest stage in subclinical heart failure in Type II diabetes. To assess whether a decrease in SBP (systolic blood pressure) or a change in metabolic control would improve the long-axis function, 48 Type II diabetic patients participating in the CALM II (Candesartan and Lisinopril Microalbuminuria II) study were included in the present study. Patients were examined with tissue Doppler echocardiography at baseline and after 3 and 12 months of follow-up. Corresponding blood pressure, fructosamine and HbA(1c) (glycated haemoglobin) values were obtained. During the follow-up period, a decrease in SBP of 8 mmHg was seen (from 141+/-11 mmHg at baseline to 133+/-12 mmHg; P<0.001) and the peak systolic strain rate was significantly improved (from -1.10+/-0.25 at baseline to -1.25+/-0.22; P<0.01). There was a highly significant relationship between the changes in systolic strain rate, HbA(1c) (P<0.001) and fructosamine (P<0.05), and similarly to changes in left ventricular mass (P<0.05), whereas the correlation to the SBP reduction was not significant. Patients with improved glycaemic control, defined as a reduced HbA(1c) value after 12 months of follow-up, had a significantly improved strain rate (from -1.07+/-0.3 s(-1) at baseline to -1.32+/-0.25 s(-1); P<0.01) compared with patients with increases in HbA(1c) (from -1.14+/-0.25 s(-1) at baseline to -1.16+/-0.27 s(-1); P=not significant). The two groups had comparable baseline values of SBP, left ventricular mass, age and disease duration. In conclusion, changes in left ventricular systolic long-axis function are significantly correlated with changes in left ventricular mass, as well as metabolic control, in hypertensive patients with Type II diabetes mellitus.
authors.affiliation: Medical Department M (Diabetes and Endocrinology) and The Medical Research Laboratories, Aarhus University Hospital, DK-8000 Aarhus C, Denmark. holmark@ki.au.dk
authors.forename: Niels H
authors.initials: NH
authors.lastname: Andersen
authors.forename: Steen H
authors.initials: SH
authors.lastname: Poulsen
authors.forename: Per L
authors.initials: PL
authors.lastname: Poulsen
authors.forename: Søren T
authors.initials: ST
authors.lastname: Knudsen
authors.forename: Kjeld
authors.initials: K
authors.lastname: Helleberg
authors.forename: Klavs W
authors.initials: KW
authors.lastname: Hansen
authors.forename: Dines S
authors.initials: DS
authors.lastname: Dinesen
authors.forename: Hans
authors.initials: H
authors.lastname: Eiskjaer
authors.forename: Allan
authors.initials: A
authors.lastname: Flyvbjerg
authors.forename: Carl E
authors.initials: CE
authors.lastname: Mogensen
mesh_terms: D000368:Aged; D000959:Antihypertensive Agents / Q000627:therapeutic use; D001786:Blood Glucose / Q000378:metabolism; D003924:Diabetes Mellitus, Type 2 / Q000097:blood / Q000503:physiopathology*; D003925:Diabetic Angiopathies / Q000097:blood / Q000188:drug therapy / Q000503:physiopathology*; D015150:Echocardiography, Doppler; D005260:Female; D005500:Follow-Up Studies; D019270:Fructosamine / Q000097:blood; D006442:Glycated Hemoglobin / Q000378:metabolism; D006352:Heart Ventricles / Q000473:pathology; D006801:Humans; D006973:Hypertension / Q000097:blood / Q000188:drug therapy* / Q000503:physiopathology; D008297:Male; D008875:Middle Aged; D009929:Organ Size; D018487:Ventricular Dysfunction, Left / Q000097:blood / Q000000981:diagnostic imaging / Q000503:physiopathology*
chemical_list: D000959:Antihypertensive Agents; D001786:Blood Glucose; D019270:Fructosamine; D006442:Glycated Hemoglobin