Higher prevalence of detectable troponin I among cocaine-users without known cardiovascular disease.
While cocaine use is an established risk factor for acute cardiovascular complications, associations between cocaine use and markers of cardiac injury outside of acute hospital presentation remain poorly characterized. We leveraged advances in cardiac troponin (cTnI) testing to assess low but clinically meaningful levels of cardiac injury among cocaine users and non-users.



We conducted a case control study comparing cTnI levels by the presence of cocaine among patients presenting for non-cardiac care in an urban safety net hospital. Samples were chosen sequentially among those for which urine drug screens were ordered by providers hospital-wide.



During 2015, 14% of all hospital drug screens ordered were cocaine-positive. Among unique persons providing cocaine-positive (N=100) and cocaine-negative (N=100) samples, 37% were female, 45% were African-American and the median age was 51. Detectable cTnI (> 0.02ng/mL) was observed in 21 samples (11%). It was more common in subjects using cocaine (Adjusted OR=2.81; 95% CI=1.03-7.65), but not other drugs. Moreover, there was a significant correlation between concentrations of cTnI and the cocaine metabolite, benzoylecgonine (Spearman Correlation=0.34, p<0.01).



Among urban safety net hospital patients, 11% had detectable cTnI, and cTnI concentration was significantly correlated with benzoylecgonine concentration. While these preliminary results require additional confirmation, they suggest the potential utility of considering cocaine use as more than just an episodic exposure leading to acute cardiac events. The consideration of cocaine use as an ongoing chronic exposure leading to subclinical cardiac injury may improve risk-stratification and patient outcomes in populations where cocaine use is high.
Division of HIV, Infectious Diseases and Global Health, Department of Medicine, University of California, San Francisco, CA, USA. Electronic address: elise.riley@ucsf.edu.
Elise D
ED
Riley
Division of Cardiology, Department of Medicine, University of California, San Francisco, CA, USA.
Priscilla Y
PY
Hsue
Department of Epidemiology and Biostatistics, University of California, San Francisco, CA, USA.
Eric
E
Vittinghoff
Department of Laboratory Medicine, San Francisco General Hospital, University of California, SanFrancisco, CA, USA.
Alan H B
AH
Wu
Division of HIV, Infectious Diseases and Global Health, Department of Medicine, University of California, San Francisco, CA, USA; San Francisco Department of Public Health, San Francisco, CA, USA.
Phillip O
PO
Coffin
Division of General Internal Medicine, Department of Medicine, University of California, San Francisco, CA, USA; Division of Hospital Medicine, Department of Medicine, San Francisco Veterans Affairs Medical Center, San Francisco, CA, USA.
Peter K
PK
Moore
Department of Laboratory Medicine, San Francisco General Hospital, University of California, SanFrancisco, CA, USA.
Kara L
KL
Lynch
D000328:Adult; D001741:Black or African American; D015415:Biomarkers; D002318:Cardiovascular Diseases / Q000097:blood* / Q000453:epidemiology / Q000209:etiology; D016022:Case-Control Studies; D003042:Cocaine / Q000031:analogs & derivatives / Q000097:blood; D019970:Cocaine-Related Disorders / Q000097:blood* / Q000150:complications / Q000453:epidemiology; D004305:Dose-Response Relationship, Drug; D005260:Female; D006801:Humans; D008297:Male; D008875:Middle Aged; D015995:Prevalence; D019210:Troponin I / Q000097:blood*
D015415:Biomarkers; D019210:Troponin I; C005618:benzoylecgonine; D003042:Cocaine
Benzoylecgonine; Cardiac injury; Cocaine; Troponin; cTnI