Abstract 11069: Sex-Specific Cardio-Protection Against Vulnerable Plaque Composition and Coronary Vascular Dysfunction in Responders to Statin Therapy
Background: Coronary artery distensibility index (CDI) is an endothelial-dependent process, associated with vulnerable-plaque (VP) composition, and development of coronary artery disease (CAD). The effects of statin-therapy on CDI and VP composition are not well studied. This study evaluates the response to statin therapy through CDI, VP and clinical outcome.
Methods: Two hundred and forty eight subjects (aged 65±8 years, 46% women, and 100% statin-therapy) underwent computed tomography angiography (CTA) and were prospectively followed. CDI in left anterior descending artery (LAD) was defined as: [(Early diastole - mid diastole lumen cross section area (CSA))/ (lumen CSA in mid diastole x central pulse pressure) x 1000]. Vulnerable-plaque composite-score (VPS) was measured using semi-quantified plaque volume (none, localized, intermediate, or diffuse) and severity of diseased coronaries (normal, mild, moderate, or severe) in non-calcified and mixed plaques based on American Heart Association 15-segment model. Major adverse cardiac event (MACE) was defined as myocardial infarction or cardiovascular-death. Impaired CDI (0) distinguished non-responders from responders to statin therapy.
Results: During a median of 36-month follow-up, the event Rate was 10.1% (12.1% in men and 6.25% in women). After adjustment for risk factors, the risk of MACE was 628% and 226% higher in impaired CDI and VPS as compared to normal cohort, which were different between genders (p<0.05). Statin therapy reduced the risk of MACE by 46%. The event free survival rate decreased significantly from responders to in non-responders in both gender (p<0.05). The relative risk of MACE was 17.48 and 13.38 in non-responder men and women as compared to corresponding responder cohort (p<0.05). (Figure)
Conclusions: Statin therapy is associated with sex-specific cardio-protective effects by improving CDI and decreasing VPS, and reduces MACE independent of conventional risk factors.
- © 2011 by American Heart Association, Inc.