🏳️‍🌈✝️ HIV-Infected Patients Have Higher Rates of Type 2 Myocardial Infarctions

By Caroline Gamse, PhD

Reviewed by Mark Wainberg, PhD, Director, McGill University AIDS Centre, 

Montreal, Quebec, Canada

02/28/2017

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About 50% of myocardial infarctions (MIs) in HIV-infected patients in the United States are Type 2MIs, not related to traditional cardiovascular disease factors, according to a new study by Heidi Crane, MD, from the University of Washington School of Medicine, and colleagues, in JAMA Cardiology.¹

In the general population, most acute myocardial infarctions (MIs) are Type 1 MIs (T1MI), which result from spontaneous instability or erosion of atherosclerotic plaques. In contrast, Type 2 MIs (T2MI) are rare in the general population (<10% of all MIs), and result from an imbalance in cardiac oxygen supply and demand, usually in the setting of hypotension, hypoxia, and vasospasm.

While it is known that HIV-infected individuals suffer a 50% increased risk of acute MI relative to their uninfected peers,² it has been unclear whether this is primarily due to altered cardiovascular risk, or if other mechanisms are involved.

HIV-induced inflammation and immune activation result in higher incidence of coronary artery disease (CAD) in this population, while various drugs used in antiretroviral therapy (ART) are associated with development of dyslipidemia, insulin resistance, and endothelial dysfunction.³ Combined, these factors result in higher rates of atherosclerosis.


Study design and results

Using the Centers for AIDS Research Network of Integrated Clinical Systems (CNICS) Cohort database, researchers retroactively analyzed data from HIV-infected patients receiving care at 6 US centers who presented with an MI between 1996 and 2014. Using electrocardiograms (ECGs), imaging studies, laboratory tests, and physician notes, independent adjudicators categorized the types of MI and compared the incidence rates of Type 1 versus Type 2 MIs in this diverse HIV-infected population; they also identified potential causes of T2MIs based on the clinical information provided. Names of antiviral medications were redacted to prevent bias during adjudications. Cardiac biomarker and lipid values were available, and all other medications including those used to treat diabetes, dyslipidemia, and hypertension were included.

A total of 571 patients with MIs were identified (430 men, 141 women; median age, 49 years [interquartile range, 43-55 years]) A total of 283 T1MIs (49.6%) and 288 T2MIs (50.4%) were included.

The most common causes of T2MI in these patients were bacteremia/sepsis (34.7%), vasospasm induced by illicit drug use (13.5%) and hypertensive emergency (9.7%), with respiratory failure, noncoronary cardiac conditions, and hypotension responsible for the rest. Relative to HIV-infected patients presenting with T1MIs, a higher proportion of those with T2MIs were (T2% vs T1%): younger than 40 (16.3% vs 8.8%), female (28.1% vs 19.1%), African American (70.1% vs 43.1%), not receiving antiretroviral therapy (46.5% vs 25.1%), and injection drug users (37.2% vs 21.5%). T2MI patients also had higher viral loads (1808 vs 116 cells/mL) and lower CD4 T cell counts (230 vs 383 cells/µL).

Rates of diabetes and hypertension were similar in patients with both types of MI. Compared to persons with T1MI, those with T2MI had lower lipid levels (mean [SD] total cholesterol, 167 [63] vs 190 [54]), and lower Framingham coronary heart disease (CHD) scores (mean (SD) score, 8% [7%] vs 10% [8%]).

Taken together, these data suggest that the opportunistic infections associated with HIV infection, as well as particular behavioral choices, may contribute to the susceptibility of HIV-infected patients to T2MIs. Importantly, the significant demographic and clinical differences present between HIV-infected patients with Type 1 versus Type 2 MI suggest the existence of distinct physiological mechanisms leading to each, requiring different prevention and treatment interventions.

Future research needs

“This is an important finding that needs to be validated in cohorts of HIV-infected individuals and uninfected controls. The study's findings suggest that a portion of the elevated rates of MI in HIV-infected populations may be explained by severe systemic illness, such as severe infections, although certainly intrinsic dysfunction of the heart itself also seems to play a role,” Matthew Feinstein, MD, of Northwestern University Feinberg School of Medicine, told MedPage Today. “As such, it will be important to determine whether particular HIV-induced factors predispose infected individuals to T2MIs, and if so, through what mechanism.”

Recent research has suggested that HIV-infected patients have higher rates of myocardial scarring associated with coronary artery disease, which may be due to lower levels of CD4 T-cell mediated myocardial repair.⁴ Data such as these suggest that the hearts of HIV-infected individuals may be particularly susceptible to ischemic injury. Similarly, another recent study suggests that chronic inflammation induced by HIV infection changes the composition and stability of atherosclerotic plaques, which may account for higher rates of T1MIs as well as other vascular effects.⁵ Research into methods to downregulate immune activation using chemotherapies and newer biological agents may also help unveil the mechanism of T2MI in HIV-infected individuals.

References:

1. Crane HM, Parasmothy P, Drozd D, et al. Type of myocardial infarction among human immunodeficiency virus-infected individuals in the United States. JAMA Cardiology. Epub ahead of print Jan 4, 2017: E1-E8.
2. Freiberg MS, Chang C, Lewis K, et al. HIV infection and the risk of acute myocardial infarction. JAMA Intern Med. 2013;173:614-622.
3. Vachiat A, McCutcheon K, Tsabedze N, et al. HIV and ischemic heart disease. J Am Coll Cardiol. 2017;69:73-82.
4. Feinstein MJ, Mitter SS, Yadlapati A, et al. HIV-related myocardial vulnerability to infarction and coronary artery disease. J Am Coll Cardiol. 2016;68:2026-2027.
5. O’Dwyer EJ, Bhamra-Ariza P, Rao S, et al. Lower coronary plaque burden in patients with HIV presenting with acute coronary syndrome. BMJ Open Heart. 2016;3:1-7.

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