Titus Msoka; Rogath, Josephine; Gary Van Guilder; Gibson Kapanda; Smulders, Yvo; et al.

Citation: 
Titus Msoka; Rogath, Josephine; Gary Van Guilder; Gibson Kapanda; Smulders, Yvo; et al.
Publication year: 
2021

Recent estimates indicate there are 1.6 million HIV-infected people in Tanzania (4.6% prevalence).1 Over the last decade, however, Tanzania has made tremendous progress in antiretroviral therapy (ART) coverage. Currently, 75% of people living with HIV in Tanzania are receiving ART. With the increase in successful ART coverage, the favorable effects of ART on the life expectancy of HIV-infected individuals bring on a new challenge: the potential for an increasing incidence of cardiovascular disease (CVD). Indeed, cardio- and cerebrovascular diseases are important non-infectious causes of mortality in HIV-infected patients, particularly in sub-Saharan Africa (SSA) countries, including Tanzania.2 However, significant limitations and inconsistencies in identifying the population at risk for CVD in HIV-infected populations exist.

Assessment of CVD risk is the most suitable way to differentiate between individuals who require intervention and risk modification, and those at low risk, who do not. However, several concerns have been raised when adopting a CVD risk prediction algorithm for clinical assessments of HIV-infected patients.3 Controversies on the magnitude of CVD risk among individuals according to serostatus and specific drugs in ART regimens have been reported both in studies using biomarkers (such as carotid intima-media thickness (cIMT), pulse wave velocity (PWV), and flow-mediated dilatation),4–6 as well as in studies using different CVD risk prediction algorithms/equations. Multiple studies have compared calculated risk between HIV-infected persons (both with and without ART) and controls and found conflicting results; some studies suggesting a similar risk,7,8 others an increased risk due to chronic inflammation of the HIV-infection.9,10 Some studies related this increased CVD risk to the adverse effect of ART due to dyslipidemia.11 Even a decreased risk was found in treated HIV-infected persons compared to uninfected controls.12

The quality of risk prediction in HIV-infected patients is questionable, particularly in SSA countries, because the calculators were neither developed in HIV-infected populations nor in populations from SSA countries. The Framingham risk score (FRS) was established in a predominantly white population.13 Studies have revealed that, in non-white racial groups, the risk scores tend to considerably underestimate CVD risk.11,12 Conversely, the American Heart Association (AHA)–American College of Cardiology (ACC) atherosclerotic cardiovascular disease (ACC/AHA ASCVD) equation incorporates race in the prediction of both the 10-year and lifetime CVD risk of an individual.14 However, the ASCVD algorithm used Afro-Americans to develop the equation, and hence may not work well in blacks living in sub-Saharan Africa. The aim of this study was to compare cardiovascular risk profiles between HIV-infected (with and without ART) and HIV-uninfected adults as predicted by the ACC/AHA ASCVD and the FRS algorithms in HIV-infected and uninfected groups.