How common are type 1 vs type 2 myocardial infarctions (MIs) among human immunodeficiency virus (HIV)–infected patients, and do patient characteristics differ by MI type?
Among patients with HIV, type 2 MIs occur almost as often as type 1 MIs; sepsis and vasospasm induced by use of cocaine or other illicit drugs are the most common causes of type 2 MIs. Patients with HIV who experience type 2 MIs are younger, with less traditional cardiovascular disease risk factors, than those who experience type 1 MIs.
Type 2 MIs are common among HIV-infected individuals and are caused by heterogeneous clinical conditions; differences in demographic and clinical characteristics among those who experience type 1 and type 2 MIs suggest the need to specifically consider type among HIV-infected individuals to further understand MIs and guide prevention and treatment.
The Second Universal Definition of Myocardial Infarction (MI) divides MIs into different types. Type 1 MIs result spontaneously from instability of atherosclerotic plaque, whereas type 2 MIs occur in the setting of a mismatch between oxygen demand and supply, as with severe hypotension. Type 2 MIs are uncommon in the general population, but their frequency in human immunodeficiency virus (HIV)–infected individuals is unknown.
To characterize MIs, including type; identify causes of type 2 MIs; and compare demographic and clinical characteristics among HIV-infected individuals with type 1 vs type 2 MIs.
Design, Setting, and Participants
This longitudinal study identified potential MIs among patients with HIV receiving clinical care at 6 US sites from January 1, 1996, to March 1, 2014, using diagnoses and cardiac biomarkers recorded in the centralized data repository. Sites assembled deidentified packets, including physician notes and electrocardiograms, procedures, and clinical laboratory tests. Two physician experts adjudicated each event, categorizing each definite or probable MI as type 1 or type 2 and identifying the causes of type 2 MI.
Main Outcomes and Measures
The number and proportion of type 1 vs type 2 MIs, demographic and clinical characteristics among those with type 1 vs type 2 MIs, and the causes of type 2 MIs.
Among 571 patients (median age, 49 years [interquartile range, 43-55 years]; 430 men and 141 women) with definite or probable MIs, 288 MIs (50.4%) were type 2 and 283 (49.6%) were type 1. In analyses of type 1 MIs, 79 patients who underwent cardiac interventions, such as coronary artery bypass graft surgery, were also included, totaling 362 patients. Sepsis or bacteremia (100 [34.7%]) and recent use of cocaine or other illicit drugs (39 [13.5%]) were the most common causes of type 2 MIs. A higher proportion of patients with type 2 MIs were younger than 40 years (47 of 288 [16.3%] vs 32 of 362 [8.8%]) and had lower current CD4 cell counts (median, 230 vs 383 cells/µL), lipid levels (mean [SD] total cholesterol level, 167  vs 190  mg/dL, and mean (SD) Framingham risk scores (8% [7%] vs 10% [8%]) than those with type 1 MIs or who underwent cardiac interventions.
Conclusions and Relevance
Approximately half of all MIs among HIV-infected individuals were type 2 MIs caused by heterogeneous clinical conditions, including sepsis or bacteremia and recent use of cocaine or other illicit drugs. Demographic characteristics and cardiovascular risk factors among those with type 1 and type 2 MIs differed, suggesting the need to specifically consider type among HIV-infected individuals to further understand MI outcomes and to guide prevention and treatment.
Crane HM, Paramsothy P, Drozd DR, Nance RM, Delaney JAC, Heckbert SR, Budoff MJ, Burkholder GA, Willig JH, Mugavero MJ, Mathews WC, Crane PK, Moore RD, Eron JJ, Napravnik S, Hunt PW, Geng E, Hsue P, Rodriguez C, Peter I, Barnes GS, McReynolds J, Lober WB, Crothers K, Feinstein MJ, Grunfeld C, Saag MS, Kitahata MM, for the Centers for AIDS Research Network of Integrated Clinical Systems (CNICS) Cohort. Types of Myocardial Infarction Among Human Immunodeficiency Virus–Infected Individuals in the United States. JAMA Cardiol. 2017;2(3):260-267. doi:10.1001/jamacardio.2016.5139