Author(s): Cheung N, Bluemke DA, Klein R, Sharrett AR, Islam FM, Cotch MF, Klein BE, Criqui MH, Wong TY. Retinal arteriolar narrowing and left ventricular remodeling: the Multi-Ethnic Study of Atherosclerosis. J Am Coll Cardiol. 2007 Jul 3;50(1):48-55. Epub 2007 Jun 18. PMID 17601545
Journal: Journal Of The American College Of Cardiology, Volume 50, Issue 1, Jul 2007
OBJECTIVES This study sought to examine the relationships of retinal vascular signs with left ventricular (LV) mass, volume, and concentric remodeling.
BACKGROUND Microvascular disease, reflected as retinopathy lesions, has been shown to predict clinical congestive heart failure. Whether these retinal vascular changes are related to early structural alterations and remodeling of the heart in asymptomatic individuals is unknown.
METHODS A cross-sectional, population-based study of 4,593 participants ages 45 to 85 years, free of clinical cardiovascular disease. Retinal vascular calibers and retinopathy were graded from retinal photographs according to standardized protocols. The LV mass and volume were measured from cardiac magnetic resonance imaging. Extent of LV concentric remodeling was determined by the ratio of LV mass to end-diastolic volume (M/V ratio).
RESULTS After controlling for age, gender, race, center, past and current systolic blood pressure, body mass index, smoking, antihypertensive medications, diabetes, diabetes duration, glycosylated hemoglobin, lipid profile, and C-reactive protein, narrower retinal arteriolar caliber was associated with concentric (highest quintile of M/V ratio) remodeling (odds ratio [OR] 2.06, 95% confidence interval 1.57 to 2.70). This association was seen in men and women, and was present even in those without diabetes, without hypertension, and without significant coronary calcification. In multivariate analysis, the presence of retinopathy (OR 1.31, 95% confidence interval 1.08 to 1.61) was also associated with concentric remodeling.
CONCLUSIONS Narrower retinal arteriolar caliber is associated with LV concentric remodeling independent of traditional risk factors and coronary atherosclerotic burden, supporting the hypothesis that microvascular disease may contribute to cardiac remodeling.