Myocardial infarction cocaine

Serious adverse effects of epinephrine potentially occur when it is given in an excessive dose, or too rapidly, for example, as an intravenous bolus or a rapid intravenous infusion. These include ventricular dysrhythmias, angina, myocardial infarction, pulmonary edema, sudden sharp increase in blood pressure, and cerebral hemorrhage. The risk of epinephrine adverse effects is also potentially increased in patients with hypertension or ischemic heart disease, and in those using (3-blockers (due to unopposed epinephrine action on vascular Ui-adrenergic receptors), monoamine oxidase inhibitors, tricyclic antidepressants, or cocaine. Even in these patients, there is no absolute contraindication for the use of epinephrine in the treatment of anaphylaxis [1,5,6]. 

Increased oxygen demand secondary to increased heart rates and blood pressure has been hypothesized to lead to myocardial infarction (especially in patients with fixed coronary disease) and/or ventricular arrhythmias. In patients with no history of cardiac disease, cocaine is thought to induce acute isehemie complications via vasospasm of the coronaries (Ascher et al. 1988). In addition, Virmani et al. (1988) have reported a 20 percent incidence of myocarditis thought to be secondary to accumulated microvascular injuries. 

One eritical factor that has been neglected in considering mechanisms of cardiac fatalities is the timeframe for various types of toxicities. For example, a majority of cocaine-related fatalities and near fatalities reported from emergency rooms are attributed to one or more types of cardiac ischemic or hypertensive episodes (Isner et al. 1986). Thus, these studies may discount the cocaine-induced arrhythmias and conduction defects as important direct causes of fatalities. Yet, if coroner reports are used as data sources (Virmani et al. 1988 Wetli and Wright 1979 Mittleman and Wetli 1984), there are great numbers of deaths in which pulmonary effusion and lack of evidence for coronary occlusion, acute myocardial infarction, or... 

Ascher, E.K. Stauffer, J-C.E. and Gaasch, W.H. Coronary artery spasm, cardiac arrest, transient electrocardiographic Q waves and stunned myocardium in cocaine-associated acute myocardial infarction. 

Central nervous system toxicity is rarely observed with catecholamines or drugs such as phenylephrine. In moderate doses, amphetamines commonly cause restlessness, tremor, insomnia, and anxiety in high doses, a paranoid state may be induced. Cocaine may precipitate convulsions, cerebral hemorrhage, arrhythmias, or myocardial infarction. Therapy is discussed in Chapter 59 Management of the Poisoned Patient. 

Cardiovascular effects include tachycardia, hypertension, and increased cardiac irritability large intravenous doses can cause cardiac failure. Cardiac dysrhythmias have been ascribed to a direct toxic effect of cocaine and a secondary sensitization of ventricular tissue to catecholamines (17), along with slowed cardiac conduction secondary to local anesthetic effects. Myocardial infarction has increased as a complication of cocaine abuse (7,8). Dilated cardiomyopathies, with subsequent recurrent myocardial infarction, have been associated with long-term use of cocaine, raising the possibility of chronic effects on the heart (18). Many victims have evidence of pre-existing fixed coronary artery disease precipitated by cocaine (SEDA-9, 35) (19-21). However, myocardial infarction has been noted even in young intranasal users with no evidence of coronary disease (22), defined by autopsy or angiography (23,24). If applied to mucous membranes, cocaine causes local vasoconstriction, and, with chronic use, necrosis. 

By one estimate, since the first report in 1982, over 250 cases of myocardial infarction due to cocaine have been reported, mostly in the USA The first report from the UK was published in 1999 (63). Acutely, cocaine suppresses myocardial contractility, reduces coronary caliber and coronary blood flow, induces electrical abnormalities in the heart, and increases heart rate and blood pressure. These effects can lead to myocardial ischemia (36,37). However, intranasal cocaine in doses used medicinally or recreation-ally does not have a deleterious effect on intracardiac pressures or left ventricular performance (38). 

As cocaine use has become more widespread, the number of cocaine-related cardiovascular events has increased (39). Myocardial ischemia and infarction associated with cocaine are unrelated to the route of administration, the amount taken, and the frequency of use. The risk of acute myocardial infarction is increased after acute use of cocaine and it can occur in individuals with normal coronary arteries at angiography. The patients are typically young men and smokers and do not have other risk factors for atherosclerosis. 

Fiberoptic bronchoscopy is often done after intratracheal injection of 2.5% cocaine solution and lidocaine spray. Acute myocardial infarction after fiberoptic bronchoscopy with intratracheal cocaine has been reported (48). 

A 73-year-old man with a history of breathlessness, cough, and weight loss had some ill-defined peripheral shadow in the upper zones of a chest X-ray. He had fiberoptic bronchoscopy with cocaine and lidocaine and 5 minutes later became distressed, with dyspnea, chest pain, and tachycardia. Electrocardiography showed an evolving anterior myocardial infarction. Coronary angiography showed a stenosis of less than 25% in the proximal left anterior descending artery with coronary artery spasm. He made an uneventful recovery. 

During the hour after cocaine is used, the risk of myocardial infarction is 24 times the baseline risk (53). Cocaine users have a lifetime risk of non-fatal myocardial infarction that is seven times the risk in non-users, and cocaine use accounts for up to 25% of cases of acute myocardial infarction in patients aged 18 15 years (54). In 2000, there were 175 000 cocaine-related visits to emergency departments in the USA (55), with chest discomfort in 40% of the patients (56), 57% of whom were admitted to the hospital and had an admission lasting an average of 3 days (57), involving huge costs (58). 

Based on a retrospective study of 344 patients with cocaine-associated chest pain, it has been suggested that patients who do not have evidence of ischemia or cardiovascular complications over 9-12 hours in a chest-pain observation unit have a very low risk of death or myocardial infarction during the 30 days after discharge (59). Nevertheless, patients with cocaine-associated chest pain should be evaluated for potential acute coronary syndromes those who do not have recurrent symptoms, increased concentrations of markers of myocardial necrosis, or dysrhythmias can be safely discharged after 9-12 hours of observation. A protocol of this sort should incorporate strategies for treating substance abuse, since there is an increased likelihood of non-fatal myocardial infarction in patients who continue to use cocaine. 

The incidence of acute myocardial infarction in cocaine-associated chest pain is small but significant (60). The electrocardiogram has a higher false-positive rate in these patients. A normal electrocardiogram reduces the likelihood of myocardial injury but does not exclude it. 

Cocaine use may account for up to 25% of acute myocardial infarctions among patients aged 18-45 years. The safety of a 12-hour observation period in a chest pain unit followed by discharge in individuals with cocaine-associated chest discomfort who are at low risk of cardiovascular events has been evaluated in 302 consecutive patients aged 18 years or older (66% men, 70% black, 84% tobacco users) who developed chest pain within 1 week of cocaine use or who tested positive for cocaine (59). Cocaine use was self-reported by 247 of the 302 subjects and rest had urine positive for cocaine 203 had used crack cocaine, 51 reported snorting, and 10 had used it intravenously. Of the 247 who reported cocaine use, 237 (96%) said they had used it in the week before presentation and 169 (68%) within 24 hours before presentation. Follow-up information was obtained for 300 subjects. There were no deaths from cardiovascular causes. Four patients had a non-fatal myocardial infarction during the 30-day period all four had continued to use cocaine. Of the 42 who were directly admitted to hospital, 20 had acute coronary syndrome. The authors suggested that in... 

In a review of 114 cases, coronary anatomy, defined either by angiography or autopsy, was normal in 38% of chronic cocaine users who had had a myocardial infarction (23). The authors of another review concluded that the vast majority of patients dying with cocaine toxicity, either have no pathological changes in the heart, or only minimal changes (24). There can be a delay between the... 

Although percutaneous revascularization for cocaine-associated myocardial infarction is the preferred method of treatment (74), the feasibility and safety of multivessel... 

A healthy 33-year-old man with prior cocaine use had a small myocardial infarction and, 36 hours later, having inhaled cocaine, developed a dissection of the left main coronary artery, extending distally to the left anterior descending and circumflex arteries. There was marked anterolateral and apical hypokinesis. 

A woman who inappropriately used cocaine on the nasal mucosa to treat epistaxis had a myocardial infarction (69). 

A patient who was treated with intranasal cocaine and phenylephrine during a general anesthetic had a myocardial infarction and a cardiac arrest due to ventricular fibrillation (SEDA-20,128). 

There has been a recent report of a myocardial infarct in a full-term infant born to a 28-year-old woman who had used cocaine 2-3 times per week and methadone 40 mg/ day (319). 

Minor RL Jr, Scott BD, Brown DD, Winniford MD. Cocaine-induced myocardial infarction in patients with normal coronary arteries. Ann Intern Med 1991 115(10) 797-806. 

Villota JN, Rubio LF, Flores JS, Peris VB, Burguera EP, Gonzalez VB, Banuls MP, Escorihuela AL. Cocaine-induced coronary thrombosis and acute myocardial infarction. Int J Cardiol 2004 96 481-2. 

Osula S, Stockton P, Abdelaziz MM, Walshaw MJ. Intratracheal cocaine induced myocardial infarction an unusual complication of fibreoptic bronchoscopy. Thorax 2003 58 733-4. 

Mittleman MA, Mintzer D, Maclure M, Tofler GH, Sherwood JB, Muller JE. Triggering of myocardial infarction by cocaine. Circulation 1999 99 2737 11. 

Qureshi AI, Suri MF, Guterman LR, Hopkins LN. Cocaine use and the likelihood of nonfetal myocardial infarction and stroke data from the Third National Health and Nutrition Examination Survey. Circulation 2001 103 502-6. 

Carley S, Ali B. Towards evidence based emergency medicine best BETs from the Manchester Royal Infirmary. Acute myocardial infarction in cocaine induced chest pain presenting as an emergency. Emerg Med J 2003 20 174-5. 

Inyang VA, Cooper AJ, Hodgkinson DW. Cocaine induced myocardial infarction. J Accid Emerg Med 1999 16(5) 374-5. 

Amin M, Gabelman G, Karpel J, Buttrick P. Acute myocardial infarction and chest pain syndromes after cocaine use. Am J Cardiol 1990 66(20) 1434-7. 

Ross GS, Bell J. Myocardial infarction associated with inappropriate use of topical cocaine as treatment for epis-taxis. Am J Emerg Med 1992 10(3) 219-22. 

Hollander JE, Hoffman RS. Cocaine-induced myocardial infarction an analysis and review of the literature. J Emerg Med 1992 10(2) 169-77. 

---