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Clin Infect Dis. 2018 Mar 5;66(6):886-892. doi: 10.1093/cid/cix910.

The Relationship Between Latent Tuberculosis Infection and Acute Myocardial Infarction.

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Department of Internal Medicine, Division of Infectious Diseases, University of Cincinnati College of Medicine, Ohio.
Department of Medicine, Division of Infectious Diseases, University of Kentucky College of Medicine, Lexington.
Department of Infectious Diseases and Tropical Medicine, Hospital Nacional Dos de Mayo.
Department of Internal Medicine, Universidad Nacional Mayor de San Marcos.
Department of Cardiology, Hospital Nacional Edgardo Rebagliati Martins, Lima, Peru.
Departments of Biostatistics and Statistics, University of Kentucky Colleges of Public Health and Arts & Sciences, Lexington.
Department of Internal Medicine, Division of Infectious Diseases, Wake Forest University School of Medicine, Winston-Salem, North Carolina.
Department of Medicine, Division of Infectious Diseases, Vanderbilt University School of Medicine, Nashville, Tennessee.
Department of Microbiology, Immunology and Molecular Genetics, University of Kentucky College of Medicine, Lexington.



Tuberculosis has been associated with an increased risk of cardiovascular disease (CVD), including acute myocardial infarction (AMI). We investigated whether latent tuberculosis infection (LTBI) is associated with AMI.


We conducted a case-control study in 2 large national public hospital networks in Lima, Peru, between July 2015 and March 2017. Case patients were patients with a first time diagnosis of type 1 (spontaneous) AMI. Controls were patients without a history of AMI. We excluded patients with known human immunodeficiency virus infection, tuberculosis disease, or prior LTBI treatment. We used the QuantiFERON-TB Gold In-Tube assay to identify LTBI. We used logistic regression modeling to estimate the odds ratio (OR) of LTBI in AMI case patients versus non-AMI controls.


We enrolled 105 AMI case patients and 110 non-AMI controls during the study period. Overall, the median age was 62 years (interquartile range, 56-70 years); 69% of patients were male; 64% had hypertension, 40% dyslipidemia, and 39% diabetes mellitus; 30% used tobacco; and 24% were obese. AMI case patients were more likely than controls to be male (80% vs 59%; P < .01) and tobacco users (41% vs 20%; P < .01). LTBI was more frequent in AMI case patients than in controls (64% vs 49% [P = .03]; OR, 1.86; 95% confidence interval [CI], 1.08-3.22). After adjustment for age, sex, hypertension, dyslipidemia, diabetes mellitus, tobacco use, obesity, and family history of coronary artery disease, LTBI remained independently associated with AMI (adjusted OR, 1.90; 95% CI, 1.05-3.45).


LTBI was independently associated with AMI. Our results suggest a potentially important role of LTBI in CVD.

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