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Abstract 12216: Age-Related Macular Degeneration as a Predictor of Incidence and Progression of Subclinical Cardiovascular Disease and Cardiovascular Outcomes: The Multi-Ethnic Study of Atherosclerosis
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Introduction:
Age-related macular degeneration (AMD) is a leading cause of vision loss in US adults and shares many similarities with CVD pathophysiology.
Hypothesis:
We assessed the hypothesis that the presence of AMD would independently predict the incidence and progression of subclinical CVD and CVD events in the Multi-Ethnic Study of Atherosclerosis (MESA).
Methods:
Our cohort consisted of 5,803 adults free of known CVD who had retinal photographs taken during the first follow-up examination of the MESA (Exam 2; Aug 2002-Jan 2004). Photographs were evaluated for AMD using the Wisconsin age-related maculopathy grading system. Coronary artery calcium (CAC), carotid intima-media thickness (cIMT), ankle brachial index (ABI), and brachial artery flow-mediated dilation (FMD) were assessed at baseline (Exam 1; July 2000-Aug 2002). Changes in CAC and cIMT from Exam 1 were determined at follow-up Exam 5 (April 2010-Dec 2011). Incident CVD events were ascertained from 2002 through 2012.
Results:
Participants were categorized as AMD+ (n = 244) or AMD- (n = 5,559). Groups did not differ at baseline for cIMT, ABI, or FMD (P>0.19). At Exam 5, 92 AMD+ and 2684 AMD- participants had CAC scores. In those with CAC = 0 at baseline, CAC incidence did not differ between AMD+ (n = 21) and AMD- groups (n = 761). In those with CAC>0, CAC progression was greater in the 46 AMD+ vs. the 1170 AMD- participants after a mean follow-up of 10.4 ± 2.4 years using multivariable-adjusted models (530 ± 537 vs. 339 ± 426 Agatston units, P = 0.004). Ten year cIMT progression (P = 0.85) and incident CVD events (multivariable-adjusted HR (95% CI) = 1.3 (0.9, 1.8); P = 0.20) did not differ between groups.
Conclusions:
In conclusion, the presence of AMD in a diverse population without known CVD was independently associated with higher 10-year CAC progression in participants with baseline CAC>0. AMD was not associated with CAC incidence, other subclinical CVD markers or CVD events. The association between AMD and CAC progression suggests that AMD is associated with a greater degree of atherosclerosis. Longer follow up of individuals with AMD is warranted to clarify whether greater CAC progression increases risk of CVD events.
Ovid Technologies (Wolters Kluwer Health)
Title: Abstract 12216: Age-Related Macular Degeneration as a Predictor of Incidence and Progression of Subclinical Cardiovascular Disease and Cardiovascular Outcomes: The Multi-Ethnic Study of Atherosclerosis
Description:
Introduction:
Age-related macular degeneration (AMD) is a leading cause of vision loss in US adults and shares many similarities with CVD pathophysiology.
Hypothesis:
We assessed the hypothesis that the presence of AMD would independently predict the incidence and progression of subclinical CVD and CVD events in the Multi-Ethnic Study of Atherosclerosis (MESA).
Methods:
Our cohort consisted of 5,803 adults free of known CVD who had retinal photographs taken during the first follow-up examination of the MESA (Exam 2; Aug 2002-Jan 2004).
Photographs were evaluated for AMD using the Wisconsin age-related maculopathy grading system.
Coronary artery calcium (CAC), carotid intima-media thickness (cIMT), ankle brachial index (ABI), and brachial artery flow-mediated dilation (FMD) were assessed at baseline (Exam 1; July 2000-Aug 2002).
Changes in CAC and cIMT from Exam 1 were determined at follow-up Exam 5 (April 2010-Dec 2011).
Incident CVD events were ascertained from 2002 through 2012.
Results:
Participants were categorized as AMD+ (n = 244) or AMD- (n = 5,559).
Groups did not differ at baseline for cIMT, ABI, or FMD (P>0.
19).
At Exam 5, 92 AMD+ and 2684 AMD- participants had CAC scores.
In those with CAC = 0 at baseline, CAC incidence did not differ between AMD+ (n = 21) and AMD- groups (n = 761).
In those with CAC>0, CAC progression was greater in the 46 AMD+ vs.
the 1170 AMD- participants after a mean follow-up of 10.
4 ± 2.
4 years using multivariable-adjusted models (530 ± 537 vs.
339 ± 426 Agatston units, P = 0.
004).
Ten year cIMT progression (P = 0.
85) and incident CVD events (multivariable-adjusted HR (95% CI) = 1.
3 (0.
9, 1.
8); P = 0.
20) did not differ between groups.
Conclusions:
In conclusion, the presence of AMD in a diverse population without known CVD was independently associated with higher 10-year CAC progression in participants with baseline CAC>0.
AMD was not associated with CAC incidence, other subclinical CVD markers or CVD events.
The association between AMD and CAC progression suggests that AMD is associated with a greater degree of atherosclerosis.
Longer follow up of individuals with AMD is warranted to clarify whether greater CAC progression increases risk of CVD events.
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