Purpose of Review Cardiovascular disease (CVD) increasingly afflicts people living with HIV (PLWH) in the contemporary era of antiretroviral therapy (ART). Coronary artery disease (CAD) is the most widely studied cardiovascular problem in PLWH; however, less is known about other clinically relevant subtypes of CVD such as heart failure (HF), cerebrovascular disease, sudden cardiac death, pericardial diseases, and pulmonary hypertension. This paper reviews evidence of other subtypes of CVD as emerging issues in the post-ART era. Recent Findings Recent studies have shown that PLWH have higher risk of HF as well as subclinical impairment of left ventricular (LV) mechanics (systolic and diastolic dysfunction) and myocardial abnormalities (fibrosis and steatosis). The underlying mechanisms, however, are not well-understood. A few studies have also shown higher rates of atrial fibrillation and sudden cardiac death in PLWH. Ischemic stroke is the most common stroke type in the post-ART era, with underlying mechanisms like those identified in CAD: chronic inflammation and associated vasculopathy. Studies of great vessels (carotid artery and aorta) and peripheral arterial disease show heterogeneous results. Small subclinical pericardial effusions are common in PLWH in post-ART era. Pulmonary hypertension continues to be an underdiagnosed and potentially fatal complication of HIV infection. Summary PLWH remain at higher risk for all types of CVD including heart failure, stroke, and arrhythmias in the post-ART era. Chronic inflammation may play an important role in this increased risk. More studies are needed to further elucidate the extent of non-coronary CVD in PLWH and the underlying mechanisms for them.

Purpose of Review Introduction of combination antiretroviral therapy (ART) has increased the life expectancy of patients with HIV infection, allowing them to live longer with this chronic medical condition and consequently experiencing conditions such as cardiovascular diseases (CVDs). Several studies have investigated the increased risk of CVD in people living with HIV (PLWH). However, less is known about the exact mechanisms involved in this increased risk. Also, specific guidelines for management of CVD in PLWH have not been developed yet. In this article, we review the recent literature on the mechanisms involved in pathogenesis of CVD in PLWH, with an emphasis on coronary artery disease (CAD). Recent Findings Although initial studies suspected the increased prevalence of traditional CVD risk factors and side effects of ART to be involved in the increased CVD risk in PLWH, recent studies have uncovered the important role of chronic persistent inflammation in this increased risk. In addition, biomarkers of inflammation have been associated with both CVD events and subclinical CAD in this population. Lastly, recent studies and ongoing clinical trials have been investigating medical interventions that aim to reduce inflammation and cardiovascular events. Summary Different mechanisms of inflammation have been examined in PLWH, including subclinical viremia, microbial translocation, and coinfection with other pathogens such as cytomegalovirus. Although inflammatory biomarkers have been consistently associated with CVD and subclinical CVD outcomes, their prognostic value is unknown. Recent and ongoing trials are exploring the benefits of anti-inflammatory drugs, statins, and antimicrobial translocation drugs on both inflammation and CVD risk among PLWH.

Introduction Clinic-based tracing efforts and public health surveillance data can provide different information about HIV care status for the same patients. The relative yield and how best to use these sources to identify and re-engage out of care patients is unknown. Methods At a large public HIV clinic in San Francisco, we selected a 10% random sample of active patients who were at least 210 days “late” for an HIV primary care visit as of April 1, 2013, for clinic-based outreach. Patients were considered out of care if they did not have an HIV primary care visit in the 210 days prior to April 1, 2013. We then matched the sample with the San Francisco Department of Public Health HIV surveillance registry. Patients with a CD4 or viral load result in the 210-day period were classified as in care. We compared results from both sources and estimated the cumulative incidence of disengagement from care for the full cohort of clinic patients. Results Of 940 patients lost to follow-up, 95 were sampled. Clinic tracing found 60 (63%) in care, 23 (24%) not located, 9 (10%) out of care, 2 (2%) incarcerated, and 1 (1%) had died. Of 42 individuals surveillance classified as out of care, tracing found 22 (52%) were in care. Of 52 patients found to be in care by surveillance, 12 (23%) were out of care by clinic tracing or unable to be located. The naïve estimate of the cumulative incidence of disengagement from care at three years for the active clinic cohort was 41.1% (95% Confidence Interval [CI]: 37.6%–44.5%). The use of surveillance data reduced this estimate to 12.7% (95% CI: 18.2%–25.4%) and when further corrected using tracing outcomes, the estimate dropped to only 6.4% (95%CI: 3.4%–9.4%). Conclusions Clinic-based tracing and surveillance data together provide a better understanding of care status than either method alone. Using surveillance data to inform clinic-based outreach efforts may be an effective strategy, though tracing efforts are most likely to be successful if conducted in real time.

The Affordable Care Act will insure an estimated 20000 more HIV+ patients in California. With a dwindling supply of HIV specialists, many of these patients will be principally cared for by PCPs. PCPs will go to great lengths to ensure that HIV+ patients receive superior care, but they need the support of HIV specialists to expand their skills. Priority should be given to ensuring that expert consultation is widely available to PCPs who find themselves caring for HIV+ patients.