CORRESPONDENCE: RESEARCH CORRESPONDENCE
Evidence of Cocaine-Related Coronary Atherosclerosis in Young Patients With Myocardial Infarction
Roberto Patrizi, MD*,
Vincenzo Pasceri, MD,
Alessandro Sciahbasi, MD,
Francesco Summaria, MD,
Giuseppe M.C. Rosano, MD and
Ernesto Lioy, MD
* Catheterization Laboratory, Department of Cardiology, Policlinico Casilino ASL Roma B, Via Lucio Elio Seiano 80 00174, Rome, Italy (Email: patrizi.roberto{at}tin.it).
To the Editor: Cocaine use has increased in the last years reaching in 1999 in the U.S. 30% of all drug-related visits to the emergency department, exceeding morphine and representing the most frequent cause of drug-related deaths (1). One of every four myocardial infarctions (MIs) in people aged 18 to 45 years can be linked to cocaine use (2). Several reports (3) implicated coronary vasospasm in normal coronary arteries as the cause of MI in cocaine users, but other studies revealed the cocaine-related enhanced vasoconstriction at the site of significant stenosis (4). Animal and experimental studies support the proatherosclerotic effects of cocaine (5); this drug may increase concentration of plasminogen-activator inhibitor, endothelial permeability to low-density lipoprotein, and platelet activation and aggregability. Moreover, post-mortem studies have suggested that signs of coronary atherosclerosis can be detected in cocaine users, despite the young age (6), but this observation can be influenced by survival bias. Thus, we studied the prevalence of coronary atherosclerosis in young patients suffering from acute MI with and without evidence of cocaine use.
We enrolled 51 consecutive Caucasian patients (49 men) with MI with persistent ST-segment elevation (STEMI), as first manifestation of coronary artery disease (CAD), age  50 years. A total of 17 patients (16 men) reported non-occasional cocaine use. We excluded from the study occasional cocaine users. No temporal relationship between cocaine use and onset of acute MI was considered among the inclusion criteria, but only a self-reported history of non-occasional use of cocaine. As previously reported (2), regular user was defined as having experienced cocaine in lifetime 10 to 100 times or >100 times, occasional user <10 times. In our study, by angiography, we compared the extent of coronary atherosclerosis in cocaine users versus non-cocaine users with STEMI. We also assessed the number of common risk factors (family history, smoking, overweight, hypertension, diabetes, dyslipidemia) and the acute cardiovascular risk profile by Thrombolysis In Myocardial Infarction risk score (TRS). Coronary angiography was performed according to standard techniques and angiograms reviewed according to the American College of Cardiology/American Heart Association classification. A semiquantitative assay for the primary urinary metabolite of cocaine, benzoylecgonine, was carried out in all patients (Cozart, Oxfordshire, United Kingdom). Data are presented as mean ± SD. Differences between groups were always tested with non-parametric statistics, thus avoiding the need for normalization or transformation of data. Continuous variables were compared with Mann-Whitney U test, while frequencies were compared with Fisher exact test. A p value of <0.05 (two-tailed) was considered as significant.
As compared with the control group, the cocaine users had lower mean age (38.8 ± 5.8 vs. 43.9 ± 3.7, p < 0.01), lower mean number of CAD risk factors (1.4/patient vs. 2.1/patient, p < 0.05), and lower incidence of patients with multiple risk factors (29% vs. 85%, p < 0.01). Cocaine users had also a lower TRS on admission (TRS  3, 18% vs. 56%, p < 0.01). Seven patients (41%), with positive urinary test, had used cocaine in the 24 h before MI. The prevalence of non-significant coronary atherosclerosis was quite low and similar in both groups (12% vs. 9%, p = NS). The prevalence of at least one critical coronary stenosis (70%) was also similar in the two groups (76% vs. 70%, p = NS). However, cocaine users had a higher prevalence of multivessel disease (65% vs. 32%, p < 0.05) and a higher number of coronary artery lesions 50% (2.3/patient vs. 1.6/patient, p < 0.05) (Fig. 1). There were no significant differences in the acute MI treatment (thrombolysis 65% vs. 85%, p = NS; primary PTCA 6% vs. 15%, p = NS; rescue PTCA 18% vs. 24%, p = NS), in the overall rate of coronary revascularization procedures (PTCA 59% vs. 73%, p = NS; coronary artery bypass graft 24% vs. 18%, p = NS), and in the MI culprit vessel (left anterior descending 53% vs. 44%, p = NS; circumflex 18% vs. 21%, p = NS; right 18% vs. 26%, p = NS). No patient died during the hospitalization. No intracranial bleeding was observed, despite the frequent use of thrombolytic therapy in a class of patients considered to have a high hemorrhagic risk, due to hypertensive surge and cerebral vasospasm (7). No patient in the control group had a positive urinary test.
This is the first study that compares the prevalence of coronary atherosclerosis in young patients with STEMI with and without history of cocaine use. We found that significant coronary atherosclerosis is quite common in cocaine users with MI, and can even be more severe and diffuse than in non-cocaine users, even with a more benign risk factor profile.
Cocaine induces vasoconstriction primarily by blocking the pre-synaptic reuptake of norepinephrine and by stimulating alpha-adrenergic receptors; thus, it has been suggested that coronary spasm on otherwise normal coronary arteries may be the main cause of MI in young cocaine users (3). However, only a direct comparison of prevalence of coronary atherosclerosis between cocaine and non-cocaine users, in the same population of young patients with STEMI, as in our study, could support this hypothesis. On the contrary, our findings support the hypothesis that in cocaine users functional factors (including coronary spasm) occur in a significant atherosclerotic background.
In our study, we did not assess the relationship between the duration and frequency of cocaine use and the extent of CAD, because of the limited size of the population. We found that only 41% of the cocaine users had a positive drug urinary test. We did not focus on the immediate causal relationship between cocaine use and onset of MI, but on the relationship between chronic use of cocaine and acceleration of atherosclerosis. The urinary drug screening test was mainly performed to check the patients of the control group, who denied cocaine use in the previous 24 h. Another limit is represented by the fact that low social status (which may be more common in cocaine users) is also an independent CAD risk factor (8), but in our study social class was similar both in cocaine users and in control subjects, all living in the same area near the hospital.
In conclusion, our findings show the proatherosclerotic effects of cocaine in humans. Myocardial infarction with normal coronary arteries is uncommon, whereas significant and severe coronary atherosclerosis, with increased incidence of multivessel disease, is frequent in young regular cocaine users with acute MI.
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