Cocaine Toxicity ================ þ Ann Emerg Med 2008;51:127-129 - ? beta blockers are actually good - limited study, theoretical reasons to suspect beta blockers bad þ Epidemiology of Cocaine Toxicity: 3,617 cases and 28 deaths in 1989. þ Cocaine Toxicity Treatment: - gastric decontamination only for body packers. - Monitor, seizure precautions. - Use both alpha and beta blocker, i.e. labetalol (). - Hypotension in late phases: dopamine, norepi. þ For asystole: anecdotal reports of large doses of bicarb working: þ "Washed Out" syndrome: - from massive use, can get total depletion of catecholamines and deep coma þ Chest pain from Cocaine: - As only 0.7% to 6% of patients with cocaine-associated chest pain have an MI, risk stratification of these patients in an observation unit may significantly reduce unnecessary admissions and improve resource utilization. - Mittleman et al18 also demonstrated that cocaine users with recent MI were more likely to be male (87%), current cigarette smokers (84%), young (44 years of age), and nonwhite (63%) than a comparable group with MI and no recent cocaine use. These characteristics appear to be similar in most patients presenting with cocaineassociated chest pain, making it exceedingly difficult to predict those at risk for MI, given the low incidence of cocaine-associated MI. - Cocaine-associated MI appears to occur most often soon after cocaine ingestion. In one study, two thirds of MI events occurred within 3 hours of cocaine ingestion. In a survey of 3946 patients with recent MI, 38 patients admitted to cocaine use in the preceding year, and 9 patients reported ingestion in the 60 minutes preceding the onset of MI symptoms. This survey reported a striking 24-fold higher risk of MI in the first hour after cocaine use, with a rapid decrease in risk after this time. - Investigators have noted, however, that the onset of ischemic symptoms could still occur several hours after cocaine ingestion, at a time when the blood concentration is low or undetectable. Amin et al reported an 18-hour median length of time between cocaine use and MI onset among 22 patients presenting with chest pain after cocaine ingestion. This accounted for an unusually high rate of MI of 31% in this retrospective analysis, whereas other studies reported a range extending from 1 minute to up to 4 days. These findings are attributed to cocaine metabolites, which rise in concentrations several hours after cocaine ingestion, persist in the circulation for up to 24 hours, and may cause delayed or recurrent coronary vasoconstriction. - the overall incidence of cocaine-associated MI varies between studies from 0.7% to 6% of those presenting with chest pain after cocaine ingestion. [McCord J, Jneid H, Hollander JE, et al. Management of cocaine-associated chest pain and myocardial infarction: a scientific statement from the American Heart Association Acute Cardiac Care Committee of the Council on Clinical Cardiology. Circulation 2008;117:1897-907.] - In one study, only 44% of 91 patients with cocaine-associated MI reported antecedent chest pain. [Hollander JE, Hoffman RS. Cocaine-induced myocardial infarction: an analysis and review of the literature. J Emerg Med. 1992;10:169 –177.] - In a study of 130 patients with cocaine-associated MI, there was equal distribution between anterior (45%) and inferior (44%) MI, and most were non- Q wave (61%). [Hollander JE, Lozano M, Fairweather P, Goldstein E, Gennis P, Brogan GX, Cooling D, Thode HC, Gallagher EJ. ‘Abnormal’ electrocardiograms in patients with cocaine-associated chest pain are due to ‘normal’ variants. J Emerg Med. 1994;12:199 –205.] - Early repolarization common in this population. - The phenomenon of Cocaine-associated MI is a real one. See Judd Hollander's prospective, multicenter study. It demonstrates the relative low but too-high-to-ignore rule in rate (by CK-MB isoenzymes) of 5.7% in all comers with central or L chest pain and cocaine use. They found 8.6% (12/140) of admitted patients ruled in. The complication rates of 4-12% for ventricular dysrhythmias, 5-7% for CHF, and other badness are reviewed and referenced in his NEJM review on the topic. (Good, concise review!) --Bill Bozeman, M.D. - [Hollander JE, Hoffman RS, Gennis P, Fairweather P, DiSano MJ, Schumb DA, Feldman JA, Fish SS, Dyer S, Wax P, et al Prospective multicenter evaluation of cocaine-associated chest pain. Cocaine Associated Chest Pain (COCHPA) Study Group. Acad Emerg Med 1994 Jul-Aug;1(4):330-9.] Abstract: - [Hollander JE. The Management of Cocaine-associated Myocardial Ischemia. NEJM 1995;333(19):1267-1272.] - A 12-hour observation period is sufficient for cocaine-associated chest pain. [Weber JE, Shofer FS, Larkin GL, Kalaria AS, Hollander JE. Validation of a brief observation period for patients with cocaine-associated chest pain. N Engl J Med 2003; 348:510-7. BACKGROUND: Retrospective studies of patients with cocaine-associated chest pain suggest that a strategy of discharging patients from the emergency department after a 12-hour observation period if they do not have evidence of ischemia should be associated with a very low rate of complications. METHODS: We prospectively evaluated the safety of a 9-to-12-hour observation period in patients with cocaine-associated chest pain who were at low-to-intermediate risk of cardiovascular events. Consecutive patients who reported or tested positive for cocaine use and who received protocol-driven care in a chest-pain observation unit were included. Patients who had normal levels of troponin I, without new ischemic changes on electrocardiography, and who had no cardiovascular complications (dysrhythmias, acute myocardial infarction, or recurrent symptoms) during the 9-to-12-hour observation period were discharged from the unit. The main outcome was death from cardiovascular causes at 30 days. RESULTS: Three hundred forty-four patients with cocaine-associated chest pain were evaluated. Forty-two of these patients (12 percent) were directly admitted to the hospital. The study cohort comprised the remaining 302 patients. During the 30-day follow-up period, none of the patients died of a cardiovascular event (0 percent; 95 percent confidence interval, 0 to 0.99), and only 4 of the 256 patients for whom detailed follow-up data were available had a nonfatal myocardial infarction (1.6 percent; 95 percent confidence interval, 0.1 to 3.1). All four nonfatal myocardial infarctions occurred in patients who continued to use cocaine. CONCLUSIONS: Patients with cocaine-associated chest pain who do not have evidence of ischemia or cardiovascular complications over a 9-to-12-hour period in a chest-pain observation unit have a very low risk of death or myocardial infarction during the 30 days after discharge.] As a young EM resident there are many patients who are difficult to sort out and develop my own best treatment approach using "evidence based medicine" due to the conflicting opinions and approaches of both the literature as well as my seniors and attendings. Cocaine and chest pain has definitely been one of these areas (though hypertensive emergencies/urgencies is still #1). Anyway, after reading some of the cocaine literature I took away some conclusions that differ from Dr. Louzon and welcome any comments and advice. Dr. Louzon's statement: "My own conclusion is that, given the general acceptance that a 5% missed MI rate is acceptable across the board, and that patients who present with cocaine associated chest pain probably have a likelihood of MI considerably less than this, a reasonable strategy is to send them ALL home unless they have very compelling history or ECG findings in the ED." The literature has seems to have some agreement that the rate of MI with pt reported cocaine use and chest pain is about 6% (1,2,3) therefore the rate is already higher than the "accepted missed MI rate" and the rate of cocaine induced MI is actually not "considerably less." To compound the prevalence of cocaine + chest pain, An Annals study (4) found that only 72% of pts with chest pain and cocaine POSITIVE TOX SCREENS actually admitted to cocaine use, so the incidence of cocaine induced chest pain and subsequent MI is being understated anytime pt honesty is relied upon. Furthermore as far as the critique of Hollander et al's study (1) suggesting that since their conclusion was that "no feature or combination of features could be used to seperate out those patients with cocaine 'induced' chest pain who had actually infarcted from those who did not and, thus, that ALL of these patients had to be ruled out for acute MI. Now isn't that special? If this is their best conclusion that they could come to it seems as if they could have just as well omitted doing the study altogether" I took away a different message from this multicenter, prospective study. Since no clinical parameters are available to identify very low risk pts and an ECG is only 36% sensitive in detecting MI, I need to use a different approach with a cocaine-cp pt as it is a different ball-game than traditional cp pt. I need to have a much reduced clinical confidence in using a "normal" ECG and relying clinical parameters to rule out an MI clinically. I do need to maintain a higher index of suspicion for MI in the absence of an overwhelming story/workup in cocaine-cp pts. I also felt that the Arch Int Med paper (5) provided some helpful info as well. Retrospectively looking at 130 pts with cocaine induced MI, they found 64 complication in 49 pts consisting of CHF (9), v-tach (23), svt (6), & brady-dysrhythmias in 26 showing COCAINE INDUCED MI PTS DO HAVE MORBITY. The overall in-hospital mortality was 0%; however, my QUESTION is how do I apply this 0% mortality. WERE THERE IN-HOSPITAL INTERVENTIONS THAT OCCURRED (ie chemical or electrical intervention) THAT WOULD HAVE YIELDED A DIFFERENT OUTCOME IF THE PATIENTS WERE "just sent home??????" (one pt had v-fib & was successfully cardioverted, but that was confounded by the fact that he was undergoing cardiac cath at the time). Anyway, the other take home point from this article was 90% of the complications presented < 12 hours after presentation which seems to be a consistent theme in Hollander & Hoffman's publications. A 1995 New England Journal review By Hollander (6) seems to suggest that the best approach, which would identify 94-100% of infarctions in these pts, is by the use of 1) electrocardiography 2) serial creatinine kinase MB measurements, and 3)observation for 12 hours. This seems to me, based on the literature, what the "status quo" approach to cocaine induced chest pain pts should be despite the fact that it will be costly and time consuming. All of this being said, my question for further discussion to the group is, again, what is the reasonable "standard of care" in both community and academic centers. Do I need to watch these pts for 12 hrs or can I send them out before then (I have no intention of developing a practice style of "spineless EM" admitting everybody because I am afraid to make a clinical decision about a pt, on the other hand the evidence in the literature seems to suggest a 12hr obs period). Finally, aspiring to be an EM physician who combines "evidence based medicine," clinical experience, and "gut feeling" to determine "who is sick and who is not sick" at what point can I determine that a cocaine-chest pain patient is not sick? Any comments and input will be well appreciated Nathan Shapiro, MD 1) Hollander JE, Hoffman RS, Gennis P, et al. Prospective multicenter evaluation of cocaine associated chest pain. Acad Emerg Med 1994;1:330-9. 2)Tokarski GF, Paganussi P, Urbanski R, et al. An evaluation of cocaine induced chest pain. Ann Emerg Med 1990; 19:1088-92. 3) Zimmerman JL, Dellinger RP, Majid PA. Cocaine associated chest pain. Ann Emerg Med 1991; 20:611-615. 4) Hollander JE, Todd KH, Green G et al. Chest pain associated with cocaine: an assessment of prevalence in suburban and urban emergency departments. Ann Emerg Med 1995; 26:671-676. 5) Hollander JE, Hoffman RS, Burstein JL et al. Cocaine associated myocardial infarction. Mortality and complications. Arch Int Med 1995 May 22; 155(10): 1081-6. 6) Hollander JE. The management of cocaine associated myocardial ischemia. New Eng J Med 1995; 333:1267-1272. ---------------------- Instead of rehashing what has already been stated let me see if we can make any headway by analyzing our areas of agreement. Currently the missed MI rate is about 5 - 7% across the board. It is geneally conceded that this number may be halved by improving ECG reading skills and and by not sending home patinets who are CONCEDED to have ischemia at rest. What I was suggesting was that if we adopted a policy of indescriminantly discharging patients with cocaine associated chest pain irrespective of their presentation then the rate of missed MI would be no worse than what is generally accepted. I mentioned 5% but some studies have concluded that rates of up to 7% are acceptable on a cost effectiveness basis. I am talking here about 'order of magnitude' estimates and not exact numbers. Of course, this is a worst case senario which I am not advocating. SELECTIVELY admitting patients with cocaine associated chest pain (as I suggested) would certainly capture some of these MIs don't you think? And as a consequnce it is fair to assume that the rate of missed MI would be considerbaly less than 5%. On the other hand, let me grant you this 5% rate of acute MI in cocaine associated chest pain (which after all the ballots are counted I don't believe for one minute). The rate of acute MI in chest pain UNassociated with cocaine is about 30%. Please answer the following question: Are you now know going to advocate that we lower our standards for admitting NONcociane associated chest pain to the point where our rule in rate is only 5%? Why not? Why are we admitting chest pain temporally related to the use of cocaine at a rate that is 6 times higher than what is considered prudent care for non drug addicts? One final observation. Any study that concludes that patients with chest pain of any etiology should be indiscriminantly ruled out is a gutless wonder. --------------------- One further observation, Nathan. Let's assume, for arguments sake, that an acceptable rate of missed MI is 5% and that the rate of rule in across the board for cocaine associated chest pain is 6% (your numbers I believe). If we admit on average only 1 patient out of 6 with cocaine associated chest we have met our 'quota'. The question then becomes *which* patients to admit. Well, that's easy. If we accept Hollander's et. als. conclusion that there is no way to differentiate which patients will have an MI we can admit these people at random. One way of doing this is to hold up the ECG, like Carnan the Magnificent, to one's temporal area and do it telepathically. Of course this argument is absurd but no more so, I should point out, than the conclusions of the COCHPA study group which, in my opinion, represents the low water mark in the annals of chest pain studies. Its always convenient to selectively choose a certain study to drive home your point but it cuts both ways. I could also point out the fact that, although, complications were observed in Hollander's study they observed that "All cases requiring intervention were evident upon presentation." To me that is the best argument for *selective* rather than indiscriminate admission of these patients contrary to the authors conclusions. ----------------------- In response to the three replies from Dr. Louzon let me start of by saying that by making the posting the intention was not to disarm his original post and advocate that all patients with cocaine-chest pain be admitted and receive a complete million dollar work-up. I am not on a crusade to admit all cocaine-cp pts (this is not what I personally believe), nor am I tying to endorse Hollander's studies as doctrine. I was simplying commenting on studies in the literature which suggest using a more conservative approach with cocaine-chest pain patients as they do not behave in the same way that routine chest pain pts do. My intention was to promote further discussion with the goal of helping to shape my approach to the cocaine -chest pain patient because in my opinion Hollander's literature seems too conservative (or "gutless" as you've put it);however, evaluating these pts as you would a normal pt will cause MIs to be missed. The question is where is the middle ground i.e. by what "selection" criteria should we use to "selectively" admit or observe these patients. (my original post which follows this post) Anyway, in response to Harvey's queries here goes: 1) First of all, if you re-read the original post, my conclusions about the Hollander article (4) were not that pts with chest pain of any etiology should be admitted and ruled out , but that what I took (again, my observation, not the conclusion and not my universal acceptance of the conclusions) from the paper was that our approach to traditional chest pain pts may not have the same diagnostic implications when evaluating cocaine-cp pts as they may behave differently (i.e. have ECGs less sensitive for detecting risk for MI than non-cocaine pts). >"Since no clinical parameters are available to identify very low risk pts and an ECG >is only 36% >sensitive in detecting MI, I need to use a different approach with a >cocaine-cp pt as it is a different ball-game than traditional cp pt. I need to have a much reduced >clinical confidence in using a "normal" >ECG and relying clinical parameters to rule out an MI >clinically. I do need to maintain a higher index of >suspicion for MI in the absence of an >overwhelming story/workup in cocaine-cp pts. 2) As far as the Carnan the magnificent allegations, again I believe that you have overstated my post by assuming that I whole-heartedly advocate the "rule-everyone out theory" However, for the sake of discussion, IF our overall goal is to achieve a 5% missed MI rate than you are certainly right that this can be easily done using stringent selection criteria. I would like to support your argument here (which is actually more clear to me know). If instead of using Carnan the Magnificient, we simply admitted all pts with the ECGs suggesting ischemia, which though were insensitive (36%) were specific (90%) then right there we would have improved our 6% MI to about 4% even though as you stated we were on the same 'order of magnitude' to begin with. However, the theoretical and idealistic question is (and I am sincere with this because I don't know the answer, and I am not trying to be snide): Is our goal to manage these pts to a level consistent with the average missed MI rate, or is it to fully maximize our treatment treatment plan (and potentially surpass that missed MI rate) to provide optimal patient care while keeping in mind the clinical and econimical cost/benefit ratios. (I am sincere with this question and not trying to be snide, I am unsure of the true answer) 3) As far as the remarks on the following: > Nathan Shapiro wrote: >To compound the prevalence > of cocaine + chest pain, An Annals study (4) found that only 72% of pts with > chest pain and cocaine POSITIVE TOX SCREENS actually admitted to cocaine use, > so the incidence of cocaine induced chest pain and subsequent MI is being > understated anytime pt honesty is relied upon. > Dr. Louzon's response: >Of course this observation is completely *irrelvant* to what *percentage* >of patients with cocaine associated chest pain actually have an MI. The >implication of the above statement is somehow that while patients who >admit to using cocaine rule in 6% of the time those who deny it but use it >nonetheless rule in more often. On the basis of what literature (I'm >almost afraid to ask) do you think that the act of denial >increases the risk of MI on a percentage basis in these patients? I totally agree that the observation is irrelevent to the percentage of pts with cocaine induced CP that go on to have MIs and that is not what was written on my part, so further assumptions about implications of pts denying cocaine use having increased MI rate are obviously invalid and I never did nor never would try to support such claims. (especially by using literature) However, what this study found was that of the people with proven cocaine use through tox screens, only 72% of them admitting to usage. What this does mean to me? 1) The problem of cocaine causing chest pain is epidemiologically somewhat understated because for roughly every 4 pts who really use cocaine and get chest pain as a result, 1/4 of them will deny ever using cocaine. The chest pain will be ascribed to some etiology other than cocaine use. Therefore, we are seeing pts w/CP caused by cocaine and missing the true cause of the problem. (Note I am not advocating a tox screen on all pts, I am just suggesting that maybe the problem is slightly worse than we think) 2) In any study such as the retrospective Hollander Arch Int Med that states "we identified 136 cocaine associated MI in 130 pts in 117 hospital years" by looking at pts who admit to cocaine use and concurrent MI, they are missing some pts who had cocaine induced MI because there are pts with chest pain who deny cocaine use in the ED , and (some of whom go on to have MIs) whose etiology was cocaine related, but not recognized as such. Again, the point is that the situation of cocaine causing chest pain may be a little bit more prevalent than we think. Overall, I would like to again conclude with the final paragraph of my original post: All of this being said, my question for further discussion to the group is, again, what is the reasonable "standard of care" in both community and academic centers. Do I need to watch these pts for 12 hrs or can I send them out before then (I have no intention of developing a practice style of "spineless EM" admitting everybody because I am afraid to make a clinical decision about a pt, on the other hand the evidence in the literature seems to suggest a 12hr obs period). Finally, aspiring to be an EM physician who combines "evidence based medicine," clinical experience, and "gut feeling" to determine "who is sick and who is not sick" at what point can I determine that a cocaine-chest pain patient is not sick? Any comments and input will be well appreciated Thanks again, Nathan Shapiro, MD ----------- I know that we've discussed this before but you can never have enough of a good thing. And anyway I just read an article in an Int Med journal on this subject. Let's start with a confessional: some patients who use cocaine do indeed go on to suffer an acute MI. As of 1991 when about 5 million people were using cocaine in America there were 65 documented cases in the literature (1). (By the way, a large percentage of these people did not actually want to snort it but a CIA agent inserted it into their nose). While I'm in a penitant mood I might also concede that seperating the wheat from the chaff in these cases is a diffiuclt undertaking as many of them, demographically, fall into a group that has a high incidence of the benign variant of early repolarization and many also have elevations in serum CK levels postulated to be due to skeletal rhabdomyolysis (1,2). On a percentage basis about 30% of patients across the board who are admitted to CCUs with chest pain will be found to have suffered an acute MI. By contrast only about 5% of admitted cocaine associated chest pain is found to have an MI. Many of the admitted conventional rule-outs have associated conditions such as unstable angina. By contrast the prognosis in cocaine associated chest pain is almost uniformly good (1), even when infarction has occured (4). In a consqutive series of 101 patients with cocaine asspciated chest pain who were admitted to the hospital the incidence of acute MI was precisely zero (1). Clearly we are using a different criterion in these people and cocaine is acquiring a notoriety for causing ischemia that it does not deserve. What does the EM literature have to say about his? Well, a group with the rather presumtuous name of 'Cocaine Associated Chest Pain (COCHPA) Study Group' concluded that no feature or combination of features could be used to seperate out those patients with cocaine 'induced' chest pain who had actually infarcted from those who did not and, thus, that ALL of these patients had to be ruled out for acute MI (5). Now isn't that special? If this is the best conclusion that they could come to it seems as if they could have just as well omitted doing the study altogether. What they are suggesting is a policy of indiscriminately ruling out all of these people which in many institutions, for all practical purposes, means bringing them into the hospital for, at least a short-stay admission. Which brings me (mercifully) to my conclusion. Dr. James Feldman adressing a meeting of the American Federation of Clinical Reaearch was quoted as observing that "Our findings support the approach of not universally admitting [cocaine users with chest pain] to the coronary care unit." In a multicenter study that he participated in they looked a total of 293 patients who were admitted with cocaine associated chest pain. Only 7 (2.4%) were diagnosed with acute coronary insufficieny and only 2 (0.7%) had an acute MI!. Unless they have a ' very compelling medical history' all other cocaine users with chest pain "can be sent home after limited observation." My own conclusion is that, given the general acceptance that a 5% missed MI rate is acceptable across the board, and that patients who present with cocaine associated chest pain probably have a likelihood of MI considerably less than this, a reasonable strategy is to send them ALL home unless they have very compelling history or ECG findings in the ED. H. Louzon MD (1) Gitter et. al. Cocaine and Chest Pain: Clinical Features and Outcome of Patients Hospitalized to Rule Out Myocardial Infarction. Ann Int Med 1991;115:277-282 (2) Tokarski et. al. An Evaluation of Cocaine-Induced Chest Pain. Ann EM 1990;19:1088-1092 (4) Hollander JE, Hoffman RS, Burstein JL, Shih RD, Thode HC Jr Cocaine-associated myocardial infarction. Mortality and complications. Cocaine-Associated Myocardial Infarction Study Group. Arch Intern Med 1995 May 22;155(10):1081-6 BACKGROUND: The frequency of complications in patients with cocaine-associated myocardial infarction is unknown. This study was performed to determine the short-term morbidity and mortality secondary to cocaine-associated myocardial infarction. METHODS: We performed a retrospective cohort study at 29 hospital centers throughout the United States. Patients with cocaine-associated myocardial infarction that occurred between 1987 and 1993 were identified through record review. The primary outcome measures were in-hospital mortality and the incidence and timing of major cardiovascular complications. RESULTS: Cocaine-associated myocardial infarction was identified 136 times in 130 patients. Patients were generally young (mean age, 38 years), nonwhite (72%), tobacco smokers (91%) with a history of cocaine use in the past 24 hours (88%). The initial electrocardiogram disclosed infarction in 44% and ischemia in an additional 18% of patients. Myocardial infarctions were evenly distributed between anterior (45%) and inferior (44%) and were most often non-Q-wave (61%). Complications occurred 64 times in 49 patients (36%; 95% confidence interval, 28% to 44%), including congestive heart failure in nine patients, ventricular tachycardia in 23 patients, supraventricular tachycardia in six patients, and brady-dysrhythmias in 26 patients. Most patients who had complications (90%) had them within 12 hours of presentation. Acute in-hospital mortality was 0% (95% confidence interval, 0% to 2%). CONCLUSIONS: The mortality of patients hospitalized with cocaine-associated myocardial infarction was low. The majority of complications occurred within 12 hours of presentation. (5) Hollander JE, Hoffman RS, Gennis P, Fairweather P, DiSano MJ, Schumb DA, Feldman JA, Fish SS, Dyer S, Wax P, et al Prospective multicenter evaluation of cocaine-associated chest pain. Cocaine Associated Chest Pain (COCHPA) Study Group. Acad Emerg Med 1994 Jul-Aug;1(4):330-9 OBJECTIVE: To describe a large cohort of patients who had chest pain following cocaine use, and to determine the incidence of and clinical characteristics predictive for myocardial infarction in this group of patients. METHODS: A prospective observational cohort study of consecutive patients with cocaine-associated chest pain was conducted in six municipal hospital emergency departments (EDs). Demographic variables, drug abuse patterns, medical histories, chest pain characteristics, ECG results, and laboratory data were recorded. Myocardial infarction was the primary endpoint. RESULTS: Fourteen of 246 patients (5.7%; 95% confidence interval [CI], 2.7-8.7%) had myocardial infarction, as diagnosed by elevated CK-MB isoenzyme levels. There were two deaths (0.8%). The patients had a median age of 33 years. The majority were male (71.5%), non-white (83.3%), cigarette smokers (83.3%) who used cocaine regularly. Chest pain began a median of 60 minutes after cocaine use and persisted for a median of 120 minutes. Chest pain was most frequently described as substernal (71.3%) and pressure-like (46.7%). Shortness of breath (59.3%) and diaphoresis (38.6%) were common. There was no clinical difference between patients who had myocardial infarctions and those who did not. Twelve patients had arrhythmias and four had congestive heart failure. All cases requiring intervention were evident upon presentation. An ECG revealing ischemia or infarction had a sensitivity of 35.7% for predicting a myocardial infarction. The specificity, positive predictive value, and negative predictive value of the ECGs were 89.9%, 17.9%, and 95.8%, respectively. CONCLUSIONS: Myocardial infarction in patients who have cocaine-associated chest pain is not uncommon. No clinical parameter available to the physician can adequately identify patients at very low risk for myocardial infarction. Therefore, all patients with cocaine-associated chest pain should be evaluated for myocardial infarction. H. Louzon MD --------------------------