Characteristics, Prevention, and Management of Cardiovascular Disease in People Living With HIV: A Scientific Statement From the American Heart Association

Abstract

As early and effective antiretroviral therapy has become more widespread, HIV has transitioned from a progressive, fatal disease to a chronic, manageable disease marked by elevated risk of chronic comorbid diseases, including cardiovascular diseases (CVDs). Rates of myocardial infarction, heart failure, stroke, and other CVD manifestations, including pulmonary hypertension and sudden cardiac death, are significantly higher for people living with HIV than for uninfected control subjects, even in the setting of HIV viral suppression with effective antiretroviral therapy. These elevated risks generally persist after demographic and clinical risk factors are accounted for and may be partly attributed to chronic inflammation and immune dysregulation. Data on long-term CVD outcomes in HIV are limited by the relatively recent epidemiological transition of HIV to a chronic disease. Therefore, our understanding of CVD pathogenesis, prevention, and treatment in HIV relies on large observational studies, randomized controlled trials of HIV therapies that are underpowered to detect CVD end points, and small interventional studies examining surrogate CVD end points. The purpose of this document is to provide a thorough review of the existing evidence on HIV-associated CVD, in particular atherosclerotic CVD (including myocardial infarction and stroke) and heart failure, as well as pragmatic recommendations on how to approach CVD prevention and treatment in HIV in the absence of large-scale randomized controlled trial data. This statement is intended for clinicians caring for people with HIV, individuals living with HIV, and clinical and translational researchers interested in HIV-associated CVD.

Pharmacologic Management of Human Immunodeficiency Virus and Common Chronic Conditions

“…4 In addition to traditional risk factors of atherosclerotic cardiovascular disease (ASCVD), HIV infection is associated with elevated ASCVD risk. 17 Thus, interventions that effectively attenuate risk are of key importance. 3-Hydroxy-3 methyl-glutaryl-coenzyme A reductase inhibitors, also known as statins, have a role in cardiovascular risk reduction.…”

“…There is evidence that statins significantly reduce cardiovascular events in people without HIV with increased inflammation and low levels of low-density lipoprotein cholesterol (LDL-C). 17 Increased systemic and arterial inflammation and persistent immune activation in HIV are predictive of cardiovascular disease and mortality. 17 Thus, anti-inflammatory effects of statins may provide additional rationale for therapy.…”

“…Examples of treatment options for common chronic conditions for each category are listed in Tables 1, 2, and 3. 16,17 NPs should be diligent in reviewing risk profiles and risk categories of commonly prescribed pharmacologic agents before selecting a regimen.…”

Impact of team‐based care on appropriate statin therapy prescribing in ***HIV‐infected patients

“…In PLWH without known CVD, 45% were observed in one study to have angiographic evidence of coronary plaque and 36% had high‐risk morphology coronary plaque . Human immunodeficiency virus‐specific factors believed to contribute to this higher incidence and premature onset of CVD include chronic arterial inflammation, persistent immune activation, endothelial dysfunction, ART‐related metabolic changes, and a higher prevalence of traditional risk factors (ie, smoking) …”

Heart failure in human immunodeficiency virus-infected patients

“…Вопрос о частоте различных изменений ФВ ЛЖ у ВИЧ-инфицированных больных носит дискуссионный характер. В нашем исследовании лишь 6% больных ХСН на фоне ВИЧ-инфекции имени ФВ ЛЖ <40%, 26% -от 40 до 49%, 68% ->50% По европейским данным, среди людей, живущих с ВИЧ-инфекцией, чаще встречается ХСН со сниженной ФВ ЛЖ (40%), в 30% -ХСН с сохраненной ФВ ЛЖ, в 15% -ХСН с промежуточной ФВ ЛЖ, в 15% -диагноз ХСН сомнителен [6]. Отличие частоты встречаемости различных фенотипов ХСН у ВИЧ-инфицированных в нашем исследовании можно объяснить "гипердиагностикой" ХСН при нормальной концентрации NT-proBNP, но при использовании более ранних и точных биомаркеров повреждения миокарда, таких как галектин-3 или sST2, диагноз ХСН был бы подтвержден у каждого третьего больного с нормальным уровнем миокардиального стресса [7].…”