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Progression of Subclinical Myocardial Dysfunction in Type 2 Diabetes after 5 years Despite Improved Glycemic Control
Author(s) -
Vintila Vlad Damian,
Roberts Aled,
Vinereanu Dragos,
Fraser Alan Gordon
Publication year - 2012
Publication title -
echocardiography
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.404
H-Index - 62
eISSN - 1540-8175
pISSN - 0742-2822
DOI - 10.1111/j.1540-8175.2012.01748.x
Subject(s) - medicine , cardiology , arterial stiffness , subclinical infection , glycemic , diabetes mellitus , pulse wave velocity , ejection fraction , type 2 diabetes , body mass index , blood pressure , insulin , endocrinology , heart failure
Background: Patients with uncomplicated diabetes have reduced left ventricular long‐axis function, related to poor glycemic control and increased conduit arterial stiffness, with increased radial function. It is unknown if improved control of risk factors can reverse these subclinical changes. Patients and methods: We studied 27 patients with type 2 diabetes (18 men) 57 ± 1 months (mean ± SD) after an initial visit when they were compared with healthy age‐ and sex‐matched controls. On both visits patients had detailed echocardiographic studies including tissue Doppler, noninvasive tests of conduit arterial function, and metabolic and lipid profiling. Results: Mean age at this second review was 63.4 ± 8.1 years; 48% of patients received insulin. Mean HbA1c had decreased by 13% to 8 ± 1.6% and cholesterol by 17% to 4.3 ± 1.3 mmol/L (both, P < 0.01), but long‐axis systolic and early diastolic myocardial velocities had also declined, by 13% and 20%, respectively (both, P < 0.001). Body mass index had increased by 4%, arterial pulse pressure by 17% (both P < 0.01), and carotid arterial stiffness by 49% (P < 0.01). Fractional shortening (by 21%, P < 0.001), radial systolic velocity (by 13%, P < 0.05), and ejection fraction (by 9% to 68 ± 7%, P < 0.01) had all declined. Reductions in longitudinal function were best predicted by its baseline measurements, duration of diabetes, fasting triglycerides, and arterial stiffness (epsilon index). Conclusions: Despite improved diabetic control, subclinical left ventricular dysfunction progressed over 5 years. Radial compensation was reversed. Prevention of subclinical myocardial dysfunction in diabetes might require more intensive control of net cardiovascular risk.