One of the most common emergency presentations occurring after cocaine use is chest pain (Baumann et al., 2000; Brody, Slovis & Wrenn, 1990), although cardiac profiles show wide variability. In one study (Baumann et al., 2000), patients with cocaine-associated chest pain described their pain as pressure (63%); it was usually located substernally (48%) or in the left anterior chest (37%).The most common associated symptoms were shortness of breath (74%), light-headedness (69%), nausea (67%) and palpitations (65%). Although 56% of these patients were given a diagnosis of possible ischaemia and 88% of patients were hospitalised in a monitored setting, only one sustained a myocardial infarction (4%). After review of the hospital records, none of the patients experienced any cardiac complications, including arrhythmias, hypotension, or congestive heart failure (Baumann et al., 2000).

Most patients experience onset of symptoms within 24 hours of drug use, although cocaine withdrawal may also result in myocardial ischaemia (Hollander, 1995a). Although most of the literature examining cardiovascular toxicity and psychostimulants focuses on cocaine use, myocardial ischaemia may also occur after amphetamine use (Costa et al., 2001). Other possible presentations related to psychostimulant use may include hypertensive crisis, acute myocardial infarction and ventricular arrhythmias (Baumann et al., 2000; Dowling et al., 1987).


The typical patient with cocaine-associated myocardial infarction is a young tobacco-smoking man with a history of repetitive cocaine use but few other cardiac risk factors. The following variables cannot reliably predict or rule out acute myocardial infarction in subjects with cocaine-associated chest pain: demographic characteristics, drug use history, location, or duration or quality of chest pain (Hollander, 1995a). As there may be no clinical differences between those who experience myocardial infarctions and those who do not, it is important to test all patients with cocaine-related chest pain for possible myocardial infarction (Hollander, Hoffman, Gennis, Fairweather et al., 1994).

Diagnosis of heart attack in cocaine users with chest pain is difficult but may be assessed with ECGs, measurements of creatinine kinase and cardiac troponin I (Hollander, 1995b). Interpreting the ECGs of patients with cocaine-associated chest pain is difficult. ECGs are abnormal in 56% to 84% of patients with cocaine-associated chest pain and as many as 43% of cocaine-using patients without infarction meet the standard electrocardiographic criteria for the use of thrombolytic agents. J-point and ST-segment elevation due to early repolarisation or left ventricular hypertrophy often makes the identification of ischaemia more difficult in these patients (Hollander, 1995a).
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Increased concentrations of creatine kinase and creatine kinase MB (the cardiac component of creatine kinase) may occur even in the absence of unequivocal electrocardiographic evidence of myocardial infarction. A pattern of continuously rising enzyme concentrations is more likely to occur in patients with myocardial infarction; initial elevations that rapidly decline indicate infarction less commonly (Hollander, 1995a). The immunoassay for cardiac troponin I has no detectable cross-reactivity with human skeletal-muscle troponin I, making it a more specific test than that for creatine kinase MB in assessing myocardial injury when concomitant skeletal-muscle injury exists. Use of the immunoassay for cardiac troponin I may therefore enhance the accuracy of a diagnosis of myocardial infarction in patients with cocaine-associated ischaemia (Hollander, 1995a).

Those patients experiencing recurrent symptoms, increased levels of markers of myocardial necrosis, or dysrhythmias should be monitored more thoroughly and for longer periods (Weber, Shofer, Larkin, Kalaria & Hollander, 2003).

Most serious complications of cocaine-associated myocardial infarction occur before or soon after hospital presentation (Hollander et al., 1995). Consequently, monitored patients with cocaine-associated chest pain who do not have evidence of ischaemia or cardiovascular complications over a 9 to 12 hour period in chest pain observation units have a very low risk of death or myocardial infarction during the 30 days after discharge (Weber et al., 2003). Hollander and colleagues report that all patients with cardiovascular complications were identified within 12 hours after presentation by observing ischaemia or infarction on an initial electrocardiogram, or by elevated creatine kinase MB (Hollander et al., 1995).

No single explanations of the causes of myocardial ischaemia can explain all cases. Explanations include increased myocardial oxygen consumption (Summers et al., 2001) and coronary artery vasoconstriction, intracoronary thrombosis and accelerated atherosclerosis (Benzaquen, Cohen & Eisenberg, 2001). Signs of occlusive disease or significant risk factors (other than smoking) are rarely present.

There is much less information available about amphetamine-related chest pain. Cocaine-associated chest pain has a variety of additional aetiological mechanisms (see above) that are not known for amphetamines.


The pharmacologic treatment of patients with cocaine-related ischaemic chest pain differs in several important ways from that of patients with the usual type of myocardial ischaemia. Treatment recommendations based on the pathophysiology of cocaine-associated myocardial ischaemia must take into account the toxic effects of cocaine on the CNS and other vital organs. For example, aspirin must be avoided in patients at risk for subarachnoid haemorrhage. If treatment strategies could be altered by the knowledge of recent cocaine use, rapid bedside toxicological assays for the drug or its metabolites may be useful, since the patient's own reporting is not entirely reliable (Hollander, 1995a). The appropriate management of amphetamine-related chest pain is unknown although some of the principles of the management of cocaine-associated chest pain are likely to be valid.

Hollander (Hollander, 1995a; Hollander, 1995b) recommends a stepped approach to the treatment of patients with cocaine-associated myocardial ischaemia. He suggests that after treatment with oxygen and the establishment of intravenous access, benzodiazepines, aspirin and nitroglycerine should be administered. Patients who continue to have severe chest pain after such an intervention may be treated with either low-dose phentolamine, or verapamil as second-line therapy. If evidence of continued myocardial infarction persists after medical management, the strategy is then to establish reperfusion with either primary angioplasty or thrombolytic therapy. When possible, the patient's current ECG should be compared with earlier ones. If the ST-segment elevations are unchanged from prior electrocardiograms, diagnostic cardiac catheterisation may be indicated and reperfusion, if necessary, can be accomplished with primary angioplasty. If the ST-segment elevations are new, it is reasonable to give the patient thrombolytic agents, in the absence of the traditional contraindications.

Hypertension is often transient and as such may not require pharmacological intervention unless severe. Hypertension requiring treatment often responds to sedation with IV benzodiazepines. Benzodiazepines are recommended for patients with cocaine-associated myocardial ischaemia who are anxious, have tachycardia, or are hypertensive (Albertson et al., 2001; Hollander, 1995a), as they reduce blood pressure and heart rate, thereby decreasing myocardial oxygen demand in addition to their anxiolytic effects. Hypertension not responding to benzodiazepines is best managed with IV nitroprusside, titrated slowly to response.

A small, randomised controlled trial examined the efficacy of diazepam, nitroglycerine or both in the treatment of acute cocaine-induced cardiovascular effects. (Baumann et al., 2000) reported that both medications, alone or in combination, led to a reduction of chest pain and improvements in cardiac performance. The small sample size (N=40) limited detection of any differential benefit of one treatment regimen above the others.
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Aspirin should be administered to prevent the formation of thrombi. This recommendation is based on theoretical considerations, the drug's good safety profile and the extensive investigation of aspirin in patients with ischaemic heart disease unrelated to cocaine, although there are no clinical data on the use of aspirin in patients with cocaine-associated myocardial ischaemia (Hollander, 1995a).

Nitroglycerine limits the size of acute myocardial infarction and reduces infarct-related complications in patients with myocardial ischaemia unrelated to cocaine. Sublingual nitroglycerine, in a dose sufficient to reduce the mean arterial pressure by 10% to 15%, reverses cocaine-induced coronary-artery vasoconstriction and relieves symptomatic chest pain. Therefore, nitroglycerine is recommended as a primary therapy for cocaine-associated myocardial ischaemia (Hollander, 1995a).

Alpha-adrenoceptors are critical for many haemodynamic responses to cocaine. Phentolamine, an alpha-adrenergic antagonist, reversed the increase in arterial pressure and heart rate and the decrease in coronary vessel diameter produced by cocaine (Lange, Cigarroa, Yancy, Willard et al., 1989). The use of a low dose (1 mg) may avoid the hypotensive effects of the drug while maintaining the anti-ischaemic effects (Hollander, 1995a).

There are a number of reports suggesting that calcium channel antagonists, such as verapamil, may be able to prevent some of the pathological effects of cocaine on the heart (discussed by Hollander, 1995a; Knuepfer, 2003), but they may only be effective when administered prior to cocaine ingestion, limiting their usefulness as treatments for cocaine toxicity.

Beta-blockers, one of the mainstays of treatment of acute myocardial ischaemia unrelated to cocaine use, should be avoided in patients who have recently used psychostimulants (Hollander, 1995a). Research on this issue is conflicting (Knuepfer, 2003), as is clinical opinion (Blaho, Merigian & Winbery, 1996; Derlet & Horowitz, 1996; Rajput & Sunnergren, 1996). However, these drugs enhance stimulant-induced vasoconstriction and increase blood pressure (Albertson et al., 2001; Lange et al., 1990) and may exacerbate adverse effects (Sand, Brody, Wrenn & Slovis, 1991). Some authors suggest that their use in combination with a vasodilator such as nitroglycerin or nitroprusside may reduce such risks (Lester et al., 2000).

Some authors have cautioned against the use of thrombolytic therapy in cocaine-associated acute myocardial infarction (Hollander, 1995a). Concerns raised include potentially fatal complications of thrombolytic agents (Bush, 1988), the low mortality of patients in this group and the possibility of misdiagnosis because of the high incidence of J point elevation in this population. Hypertension is a relative contraindication in both cocaine-associated and traditional S-T elevation acute myocardial infarction. One study argues that the risk-benefit analysis favours use of thrombolysis for S-T elevation acute myocardial infarction with or without associated cocaine use (Boniface & Feldman, 2000). They suggest that standard treatment of aspirin, nitrates and opiate analgesics followed by reperfusion (thrombolytic therapy) for non-responders should also be appropriate for those with suspected use of cocaine or other amphetamine derivatives.

It has been recommended that strategies for substance-abuse treatment should be incorporated into management, since there is an increased likelihood of non-fatal myocardial infarction in patients who continue to use cocaine (Weber et al., 2003).