학술논문

Independent associations of glucose status and arterial stiffness with left ventricular diastolic dysfunction: an 8-year follow-up of the Hoorn Study.
Document Type
Journal Article
Source
Diabetes Care. Jun2012, Vol. 35 Issue 6, p1258-1264. 7p.
Subject
Language
ISSN
0149-5992
Abstract
Objective: To investigate relative contributions of glucose status and arterial stiffness to markers of left ventricular (LV) systolic and diastolic dysfunction after 8 years of follow-up.Research Design and Methods: In the population-based prospective Hoorn Study, 394 individuals with preserved LV systolic and diastolic function participated, of whom 87 had impaired glucose metabolism and 128 had type 2 diabetes. Measurements including arterial ultrasound and echocardiography were performed according to standardized protocols.Results: The presence of type 2 diabetes was associated with more severe LV systolic and diastolic dysfunction 8 years later: LV ejection fraction was 2.98% (95% CI 0.46-5.51) lower, and left atrial (LA) volume index, LV mass index, and tissue Doppler-derived E/e' were 3.71 mL/m(2) (1.20-6.22), 5.86 g/m(2.7) (2.94-8.78), and 1.64 units (0.95-2.33) higher, respectively. Furthermore, presence of impaired glucose metabolism or type 2 diabetes was associated with 8-year increases in LV mass index. More arterial stiffness (measured as a lower distensibility) was associated with LV diastolic dysfunction 8 years later: LA volume index, LV mass index, and E/e' at follow-up were higher. Subsequent adjustments for baseline mean arterial pressure and/or LV diastolic dysfunction did not eliminate these associations. Associations of type 2 diabetes and arterial stiffness with markers of LV diastolic dysfunction were largely independent of each other.Conclusions: Both glucose status and arterial distensibility are independently associated with more severe LV diastolic dysfunction 8 years later and with deterioration of LV diastolic dysfunction. Therefore, type 2 diabetes and arterial stiffness may relate to LV diastolic dysfunction through different pathways. [ABSTRACT FROM AUTHOR]