Global Cardiovascular Risk in Patients with HIV Infection: Concordance and Differences in Estimates According to Three Risk Equations (Framingham, SCORE, and PROCAM)

Abstract

To compare cardiovascular risk stratification according to Framingham, PROCAM (Prospective Cardiovascular Münster), and SCORE (Systematic Coronary Risk Evaluation) equations in patients with HIV infection, a cross-sectional study of a well-characterized cohort of 760 HIV-infected adults managed at the outpatient Infectious Disease Unit in 2003 was conducted. Cardiovascular risk score was examined and patients were classified as having low, moderate, or high risk using Framingham and PROCAM (<10%, 10%-20%, and <20%, respectively) and SCORE (<3%, 3%-4%, and >/=5%, respectively) equations. The prevalence of patients with low, moderate and high cardiovascular risk was 76.6%, 15.1%, and 8.3% by the Framingham, respectively, 90.1%, 4.9%, and 5% by the PROCAM, respectively, and 88.6%, 3%, and 8.4% by SCORE, respectively. Concordance between these three risk functions was significant, but globally moderate (Framingham and PROCAM, kappa 0.36, p < 0.0001; Framingham and SCORE, kappa 0.32, p < 0.0001; PROCAM and SCORE, kappa 0.46, p < 0.0001). The Framingham equation categorized a higher proportion of HIV-infected male patients with moderate cardiovascular risk and a lower proportion of those with low risk (p < 0.0001) compared with PROCAM and SCORE. The present study showed a high prevalence of HIV-infected patients at low cardiovascular risk regardless of the assessed coronary risk system used. However, compared with PROCAM and SCORE, Framingham risk equation in HIV-infected patients identified a higher number of male patients with moderate cardiovascular risk.

Nonconcordance between subclinical atherosclerosis and the calculated Framingham risk score in HIV‐infected patients: relationships with serum markers of oxidation and inflammation

“…Because there is still controversy regarding the application of these population-derived CVD risk scores to HIVinfected patients [12][13][14][15], we decided to assess the agreement of the FRS with the presence of subclinical atherosclerosis in a representative sample of this HIVinfected patient population. We found a good concordance between the estimated FRS and atherosclerosis (as measured by CIMT) in patients with FRS 10%.…”

“…A follow-up of patients within the D:A:D study reported that HIV-infected patients receiving antiretroviral treatment had a risk of developing myocardial infarction that was similar to, or somewhat higher than, that predicted by the FRS [11]. In addition, more recent reports suggest that FRS may underestimate the real CVD risk in HIV-infected patients [12][13][14][15].…”

Higher levels of circulating monocyte–platelet aggregates are correlated with viremia and increased sCD163 levels in HIV-1 infection

“…[22][23][24] Increased immune activation of monocytes was reported to be involved in HIV-1 pathogenesis and thus associated with CVD risk. 17,28,29 In the present study, we demonstrated that in contrast to the decreased percentage of CD14 high CD16 2 monocyte subset, CD14 dim CD16 1 and CD14 high CD16 1 monocyte subsets were expanded during both primary and chronic HIV-1 infection.…”

“…18 MPA is regarded as a more sensitive marker of platelet activation than P-selectin (CD62P), a molecule that binds to Pselectin glycoprotein ligand-1 (PSGL-1) on monocytes, and is closely correlated with thromboembolic events. [19][20][21] Cardiovascular risks are increased in HIV-1-infected patients, [22][23][24] and this increase may be due to a mechanism involving monocyte subset distribution, activation, and MPA formation disorders. Increased MPA formation was previously reported in HIV-1-infected patients receiving antiretroviral therapy and in simian immunodeficiency virus infection.…”

Endothelial Dysfunction in HIV

“…A cross-sectional study of HIV-1 infected patients in a Spanish outpatient setting demonstrated that the traditionally used Framingham risk calculation score identified a higher proportion of HIV-1 infected men with a moderate cardiovascular risk compared to other available risk stratification tools (Knobel et al, 2007). However, this tool may not be equally applicable to all populations -for example, in a study which examined the predicted cardiovascular risk in an HIV-1 infected Thai population, the Framingham calculation over estimated the risk of cardiovascular disease compared to other cardiovascular risk equations (Edwards-Jackson et al, 2011).…”