Overall risk of coronary heart disease

The natural history of HIV disease has changed in countries where people living with HIV have access to cART. The individuals receiving combination ART regimens experience fewer opportunistic AIDS-related diseases and live longer than those without access to cART. These same individuals however develop long-term age-related complications. Cardiac complications have shifted from myocardial and pericardial diseases linked to immunosuppression to atherosclerotic diseases including myocardial infarction and peripheral and cerebrovascular diseases . Several large observational cohorts and cohort collaborations including persons living with HIV have examined their specific causes of mortality. The Antiretroviral Therapy Cohort Collaboration, including patients from Europe and North America, reported that cardiovascular deaths accounted for 6.5% of total deaths . Cardiovascular deaths accounted for 15% of total deaths in the US outpatient HOPS study , for 10% in the French “Mortalité 2010” survey , and for 6% in the Swiss HIV Cohort Study .

Reports from as early as 2007 describe an increased risk of myocardial infarction in HIV-infected versus uninfected populations . Using data from the US health care system-based cohort study, in 2007, Triant et al. put forward an adjusted risk ratio of 1.75 (95% confidence interval [CI] 1.51–2.02) for myocardial infarction in HIV-infected versus uninfected groups . In 2011, using information collected by the Régie de l’Assurance Maladie du Québec (RANQ), Durand et al. estimated the adjusted incidence ratio for myocardial infarction in HIV-infected individuals compared to uninfected individuals was 2.11 (95% CI 1.69–2.63) . Furthermore, in 2013, Freiberg et al. found HIV-positive veterans in the Veterans Aging Cohort Study Virtual Cohort (VACS-VC) had an increased risk of incident myocardial infarction compared with uninfected veterans, with an adjusted hazard ratio (HR) of 1.48 (95% CI 1.27–1.72) .

Based on information drawn from the French Hospital Database on HIV (FHDH), in 2010, Lang et al. found the sex- and age-standardized morbidity ratio of people living with HIV compared to the general population was estimated as 1.5 (95% CI 1.3–1.7) overall . As in several cohorts, the Lang et al.’s study showed that people living with HIV experience myocardial infarction earlier, at around age 50 , while in the uninfected population myocardial infarction commonly occurs after 60 years of age. Such findings suggest a potential acceleration of atherosclerosis in HIV-infected populations. However, before stating that there is a premature aging process, it is crucial to note that the age distribution of HIV-infected and uninfected populations differ. Consequently, it is important to take this variability into account when making comparisons. Recently, Petoumenos et al. observed only limited evidence of accelerating risk of CVD with age in the D:A:D cohort compared with the general population . In any case, if people living with HIV may experience accelerated atherosclerosis development it is possibly the result of their higher exposure to cardiovascular risk factors including tobacco and illicit drugs, higher prevalence of co-morbidities, antiretroviral therapy, and/or the result of the HIV infection per se. This will be discussed later in the article.

Traditional cardiovascular risk factors and clinical presentation

In primary prevention, people living with HIV already have a higher calculated risk of CHD compared to the same-age general population . They are also at higher rate of cardiovascular risk factors, such as smoking and dyslipidemia . Furthermore, HIV-infected individuals seem to be at higher risk of coronary artery disease than the general population. As demonstrated in 2004 by Bergersen et al. , twice as many people living with HIV taking highly active ART had an estimated 10-year CHD Framingham risk > 20% as compared to control participants.

From a cohort of 309 individuals living with HIV, in 2004 Neumann et al. found the risk of cardiovascular events is related to the age of HIV-infected individuals. The overall 10-year probability for cardiovascular events was higher in the oldest group (> 50 years; median 20.5%) than in the youngest group (18–30 years; median 1.9%; P < 0.01). These findings suggest that an increased duration of life due to more effective ART has a significant impact on the rate of cardiovascular events in HIV-infected populations.

Hadigan et al. in 2003 estimated the 10-year CHD risk among 91 men and women living with HIV who experienced fat redistribution, and compared it with the risk estimated for 273 age-, sex-, and body mass index-matched subjects enrolled in the Framingham Offspring Study. The 10-year CHD risk estimate was significantly elevated among HIV-infected individuals with fat redistribution, particularly among men. However, when matched with control subjects by waist-to-hip ratio, the 10-year CHD risk estimate did not differ significantly between groups. In this study, individuals living with HIV presenting no evidence of fat redistribution did not demonstrate elevated 10-year CHD risk estimate compared with control subjects. Also, the CHD risk estimate was greatest in HIV-infected individuals with primary lipoatrophy as compared to those with either lipohypertrophy or mixed fat redistribution. A severe subcutaneous fat loss is recognized as predisposing individuals to insulin resistance, diabetes, and dyslipidemia.

More recently, in 2007, Knobel et al. described the cardiovascular risk factors in a cohort of 760 persons living with HIV. They compared the Framingham, Prospective Cardiovascular Munster [PROCAM] and SCORE equations. The authors observed that the Framingham equation categorized a higher proportion of HIV-infected males with moderate cardiovascular risk and a lower proportion of those with low risk ( P < 0.0001) compared with PROCAM and SCORE. However, regardless of the equation used, the Knobel et al. study showed a high prevalence of HIV-infected individuals at low cardiovascular risk (between 76.6% and 90.1%).

In 2003, the French APROCO study group compared the distribution of cardiovascular risk factors in 227 protease inhibitors treated HIV-infected individuals who were aged 35–44 years with 527 HIV-uninfected men from the Multinational MONItoring of trends and determinants in CArdiovascular disease (MONICA) project. Saves et al. found that HIV-1 infected individuals had a lower prevalence of hypertension, a lower mean high-density lipoprotein cholesterol concentration, a higher prevalence of smoking, a higher mean waist-to-hip ratio, and a higher mean triglyceride concentration. They found no difference for total plasma or low-density cholesterol concentrations, or for the prevalence of diabetes. The predicted risk of CHD was greater among HIV-1 infected men (RR 1.20) and women (RR 1.59; P < 10–6 for both) compared with in the uninfected cohort.

In the Swiss HIV Cohort Study , where 8033 individuals completed at least one cardiovascular risk factor questionnaire, Glass et al. found, in 2006, that the most common risk factors were smoking (57.0%), low high-density lipoprotein cholesterol concentration (37.2%), high triglycerides concentration (35.7%), and high blood pressure (26.1%). They reported the 10-year CHD risk as being high (> 20%) in 2.7% of all participants and moderate (10–20%) in 13.8% of all participants. Over 6 years, they found the percentage of smokers decreased from 61.4% to 47.6% and the percentage of individuals with total cholesterol > 6.2 mmol/L decreased from 21.1% to 12.3%. They reported that prevalence of cardiovascular risk factors and CHD was higher in participants currently on ART than in either pre-treated or ART-naive persons.

Among individuals living with HIV, the clinical presentation of CHD is similar to that in the general population, and includes silent ischemia, stable angina, and acute coronary syndrome (ACS). ACS is the main CHD clinical presentation in this young population, particularly ST-segment elevation myocardial infarction ( Table 1 ). In six studies , ( Table 1 ) comparing persons hospitalized for ACS with or without HIV infection, results showed that the most common profile of a person living with HIV presenting an ACS is a young man (90% male, ≤ 50 years), most often treated with ART (varying from 53% to 96%) and mainly taking protease inhibitors (> 59%). When focusing on traditional cardiovascular risk factors, HIV-infected individuals are more frequently smokers and cocaine users, but are less likely to have hypertension or diabetes mellitus ( Table 1 ). In studies looking about cause of sudden cardiac death (SCD) in HIV-infected individuals some discrepancy exists due to differences in definitions used. For example, in 2012 Tseng et al. defined SCD as deaths meeting two criteria: the primary ICD-10 code for all cardiac causes and the World Health Organization stipulation of death within 24 hours of symptoms. However, the same year, Worm et al. limited the time component to death within 6 hours. Subsequently, Tseng et al. found mean SCD rate was 2.6 per 1000 person-years (95%CI 1.8–3.8) with SCDs accounting for 86% of all cardiac deaths while Worm et al. calculated the sudden death rate as 0.33 cases per 1000 person-years (95%CI 0.26–0.41). In light of such issues around traditional cardiovascular risk factors and their clinical presentation, further studies investigating the underlying mechanisms of SCD and providing insight into causes of death are necessary.

Table 1

Summary of studies comparing cardiovascular risk factors in HIV-infected and uninfected individuals with ACS.

First Author Study Period Study Design	HIV+ vs. HIV−			Risk factors HIV+ vs. HIV−, %
	n	Type of ACS, %	Age, y Men, %	Tobacco use	Cocaine use	Premature familial CHD	Hypertension	Diabetes mellitus	Dyslipidemia
Matetzky et al. 1998–2000 Prospective case-control	24 vs. 48	STEMI 58 vs. 58 NSTEMI 42 vs. 42 UA 0	47 ± 9 vs. 48 ± 7 88 vs. 88	58 vs. 48	0	50 vs. 44	29 vs. 44	12 vs. 19	58 vs. 56
Hsue et al. 1993–2003 Database	68 vs. 68	STEMI 29 vs. 35 NSTEMI 25 vs. 37 UA 46 vs. 28 *	50 ± 8 vs. 61 ± 11 90 vs. 62 *	46 vs. 28 *	NA	24 vs. 16	36 vs. 41	9 vs. 28	17 vs. 28 *
Boccara et al. 2003–2006 Prospective case-control	103 vs. 195	STEMI 49 vs. 56 NSTEMI 20 vs. 21 UA 31 vs. 23	48 ± 9 vs. 50 ± 9 93 vs. 94	59 vs. 64	5 vs. 2	20 vs. 27	19 vs. 24	9 vs. 12	45 vs. 46
Perelló et al. 2006–2009 Prospective cohort	44 vs. 583	STEMI 59 vs. 24 * NSTEMI 23 vs. 38 * UA 18 vs. 38 *	47 ± 11 vs. 72 ± 21 92 vs. 67 *	59 vs. 20 *	11 vs. 0.3 *	21 vs. 5 *	18 vs. 65 *	16 vs. 28	36 vs. 49
Pearce et al. 1997–2006 Database	5984 vs. 2,501,904	STEMI 50 vs. 56 * NSTEMI 50 vs. 44 * UA 0	48 ± 0.3 vs. 54 ± 0.02 85 vs. 72 *	25 vs. 30	NA	NA	46 vs. 51 *	20 vs. 28 *	25 vs. 42 *
Lorgis et al. 2005–2009 Retrospective case-control	608 vs. 1216	STEMI 91 vs. 84 * NSTEMI 9 vs. 16 * UA 0	50 ± 10 vs. 68 ± 15 * 89 vs. 66 *	30 vs. 30	NA	NA	17 vs. 22 *	9 vs. 11	31 vs. 29

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