10th International Workshop on Adverse Drug Reactions and Lipodystrophy in HIV


6-8 November 2008, London, UK

ASSOCIATION OF C-REACTIVE PROTEIN AND HIV INFECTION WITH ACUTE MYOCARDIAL INFARCTION

Antiviral Therapy 2008; 13(Suppl. 4):A5 (abstract no. O-05)

VA Triant1,2,3, JB Meigs4 and SK Grinspoon3
1Division of Infectious Diseases, Massachusetts General Hospital, Boston, MA, USA; 2Division of Infectious Diseases, Brigham and Women’s Hospital, Boston, MA, USA; 3Program in Nutritional Metabolism, Massachusetts General Hospital, Boston, MA, USA; 4General Medicine Division, Department of Medicine, Massachusetts General Hospital and Harvard Medical School, Boston, MA, USA

OBJECTIVE: To investigate whether increased C-reactive protein (CRP) levels and HIV infection are independently associated with acute myocardial infarction (AMI) among patients receiving care in a large US healthcare system.

METHODS: Analyses were restricted to patients receiving care in the system between January 1997 and December 2006, with a most recent CRP<3 years and >1 week prior to AMI. A total of 70,357 (487 HIV and 69,870 non-HIV) patients met these criteria from the background population of 1,648,687 patients followed in the system over this time period. Among patients with CRP data available prior to AMI, the percentage of patients with most recent CRP high or not was compared among HIV and non-HIV groups. Multivariate logistic regression analysis was used to test the association of increased CRP and HIV with AMI after adjustment for demographic and other cardiovascular covariates, including hypertension, diabetes and dyslipidaemia, which were more prevalent among the HIV population. Increased CRP was defined based on the normal range of the assay used. Both CRP and high-sensitivity CRP (hsCRP) were included. Sensitivity analyses were performed with CRP restricted to 2 and 1 years before AMI. ICD-9 codes for AMI and other cardiovascular risk factors were validated. Patients with multiple encounters were counted only once and, for those with an AMI event, only the first event was considered.

RESULTS: Among 70,357 patients with CRP data available prior to AMI, the most recent CRP was high in 287 HIV patients (59%) and 26,992 non-HIV patients (39%; P<0.0001). The median time from most recent CRP to first AMI was not significantly different (199 versus 176 days for HIV versus non-HIV patients; P=0.5). In univariate analyses, increased CRP and HIV were each significantly associated with AMI (odds ratio [OR] 2.51; 95% confidence interval [CI] 2.27–2.78; P<0.0001 for increased CRP and OR 2.07; 95% CI 1.31–3.10; P=0.001 for HIV). In a combined model, including CRP category and HIV status, increased CRP (OR 2.50; 95% CI 2.26–2.77; P<0.0001) and HIV (OR 1.74; 95% CI 1.10–2.61; P=0.01) were both independently associated with AMI. In a fully adjusted model, both increased CRP (OR 2.13; 95% CI 1.92–2.37; P<0.0001) and HIV (OR 1.93; 95% CI 1.21–2.93; P=0.004) remained independently associated with AMI, controlling for age, gender, race, diabetes, hypertension and dyslipidaemia. Compared with patients with normal CRP and without HIV, the OR for AMI was increased more than fourfold among patients with HIV and increased CRP.

CONCLUSIONS: Increased CRP and HIV are independently associated with increased AMI risk, and HIV patients with increased CRP have a markedly increased risk of AMI compared with those with neither risk factor. Measurement of CRP may be useful in the cardiovascular risk assessment and prediction of AMI in HIV patients.

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2008-11-06
O-05

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