Abstract 216: Identification of Secondary Cardiovascular Risk in Patients with Familial Hypercholesterolemia after Coronary Artery Disease from a US Database

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Background: Despite extensive research on health impact of hypercholesterolemia (HC), the cardiovascular (CV) risk in pts with familial hypercholesterolemia (FH) is not well understood. This study was performed to identify the secondary CV risk in pts with FH after coronary artery disease (CAD). Methods: Statin users between Jan 2004 and Jun 2010 were identified from the US IMPACT health insurance claims database. Two groups of FH pts with CAD were identified according to Simon Broome criteria: High-LDL FH (HFH) LDL-C ≥200 mg/dL; Moderate-LDL FH (MFH) 190≤ LDL-C <200 mg/dL. A non-FH cohort was identified as HC+ CAD, with 100< LDL-C <190 mg/dL. Secondary CV event rates (including stoke, myocardial infarction, unstable angina) were assessed in the 3 cohorts against the most recent LDL-C value prior to the CV event. Results: Secondary CV event rate was 7.5/100 pt-yrs in HFH (n=1277, age 59 yrs, 49% male, mean baseline LDL-C 189 mg/dL), 6.1/100 pt-yrs in MFH (n=549, 59 yrs, 48% male, LDL-C 149 mg/dL) and 4.6/100 pt-yrs in Non-FH (n=4484, 61 yrs, 60% male, LDL-C 126 mg/dL). CV event rate increased 63% in HFH (rate ratio (RR)=1.63, p<0.01) and 33% in MFH (RR=1.33, p=0.02) compared to the Non-FH cohort. Furthermore, CV risk continued to rise with LDL-C across all 3 cohorts (8% per every additional 20 mg/dL LDL-C, p<0.01), even in the HFH cohort that had the highest base CV event rate (5% per 20 mg/dL LDL-C, p=0.02). Older age, male gender and more comorbidities were associated with increased CV risk, while ezetimibe+statin and atorvastatin were associated with a lower CV risk compared to simvastatin. Conclusions: Secondary CV event risk increased with LDL-C levels across the FH and non-FH cohorts identified from the US managed care insurance claims database. Compared with non-FH, FH pts are at a significantly higher CV risk. CV risk continues to rise with LDL-C levels even within the high LDL FH cohort. These findings suggest a prominent clinical gap especially in the high LDL FH pts that require appropriate identification for effective therapy.