A scientific statement from the American Heart Association (AHA) was published in Circulation, with the purpose of providing a thorough review of available evidence on HIV-associated cardiovascular disease (CVD), particularly atherosclerotic CVD , as well as practical guidelines for how best to approach the prevention of CVD and the treatment of HIV considering the lack of large-scale randomized controlled trial data.
The use of early, effective antiretroviral therapy (ART) has allowed HIV to transition “from a progressive, fatal disease to a chronic, manageable disease marked by an elevated risk for chronic comorbid diseases, including CVDs.” People living with HIV (PLWHIV) have significantly higher rates of heart failure (HF), myocardial infarction (MI), stroke, and other manifestations of CVD, including hypertension and sudden cardiac death, compared with uninfected individuals.
This elevated risk persists despite HIV viral suppression and effective ART and after accounting for clinical and demographic risk factors. Although long-term outcomes for CVD in people with HIV are limited as a results of the recent transition of HIV from a fatal disease to a chronic one, these risks may be partly attributable to immune dysregulation and chronic inflammation.
Scientific understanding of the pathogenesis, prevention, and treatment of HIV is based on randomized controlled trials that are underpowered to detect cardiovascular end points, large observational studies, and small interventional studies that examine surrogate CVD end points. This document provides a review of existing evidence and offers guidelines for the prevention and management of these comorbid conditions.
HIV-Associated Atherosclerotic CVD
A range of recent international studies report that PLWHIV have an excess risk of MI and stroke. In fact, PLWHIV who achieve and sustain HIV viral suppression and have few or no CVD risk factors, demonstrate a continued increased risk for MI, compared with people without HIV. In Sub-Saharan African HIV-endemic populations, HIV is the leading risk factor for stroke in young cohorts, with both HIV viremia and immunosuppression appearing to be risk factors for stroke.
PLWHIV also have a 1.5- to 2-fold elevated risk of HF after adjusting for relevant confounders. Moreover, a >1.5-fold higher risk for HF persists in PLWHIV even after adjusting for prior MI.
Other Manifestations of CVD
Although fewer studies of HIV and CVD manifestations concern sudden cardiac death, atrial fibrillation, and peripheral artery disease, 1 study reports a 4-fold greater risk of sudden cardiac death among PLWHIV. This study also found that low CD4 counts are associated with increased incidence and prevalence of atrial fibrillation, and several other studies have reported increased risk for peripheral artery disease among PLWHIV compared with individuals without HIV.
Other risk factors in the development of atherosclerotic CVD include hypertension and cigarette smoking. A meta-analysis conducted between 2011 and 2016 demonstrated that the prevalence of hypertension in PLWHIV receiving ARTs was 35%, meanwhile in PLWHIV not receiving ARTs, the prevalence was 13%.
Elevated pulmonary artery systolic pressure has also been associated with HIV. The increased risk for pulmonary arterial hypertension (PAH), on the other hand, has been well-described since the 1990s, and the prevalence of HIV-associated PAH has not changed with ART. Considering the associations between sleep disorders such as sleep apnea and CVD, it should also be noted that HIV is generally associated with sleep impairments.
This article originally appeared on Infectious Disease Advisor