Unstable angina / non ST elevation myocardial infarction drug and substance abusers


 * Associate Editor-In-Chief: Smita Kohli, M.D.

Overview of Drug and Substance Abusers with UA / NSTEMI
Cocaine and methamphetamine are common drugs associated with MI.

Cocaine
Cocaine usage can produce myocardial ischemia leading to UA/NSTEMI.

Mechanism of action:
 * Cocaine blocks the presynaptic reuptake of neurotransmitters such as norepinephrine and dopamine, which produces excess concentrations at the postsynaptic receptors that lead to sympathetic activation with consequent vasoconstriction, an acute rise in arterial pressure, tachycardia, and a predisposition to ventricular arrhythmias and seizures.
 * There may also be a direct contractile effect on vascular smooth muscle.


 * Cocaine usage can also predispose to coronary thrombosis as a consequence of coronary spasm.
 * Moreover, cocaine increases the response of platelets to arachidonic acid, thus increasing thromboxane A2 production and platelet aggregation and thus predisposing to cocaine related arterial thrombosis.
 * Cocaine also causes sinus tachycardia, as well as an increase in blood pressure and myocardial contractility, thereby increasing myocardial oxygen demand. These increases can precipitate myocardial ischemia and UA/NSTEMI in both the presence and absence of obstructive coronary atherosclerosis and coronary spasm.

Clinical presentation:

Typical patient with cocaine related chest pain, unstable angina or MI is:
 * Young (usually less than 40 yrs),
 * Male gender,
 * Cigarette smoker,
 * Has symptom onset minutes or even several hours after cocaine use.

It can occur with all routes of administration and with small or large doses.

Treatment:
 * Treatment includes nitroglycerin and calcium channel blockers.
 * If patients have STEMI and show no response to sublingual NTG and calcium channel blockers, immediate coronary angiography should be performed, if possible.
 * PCI has been successfully performed in these patients but can problematic in subjects with cocaine-related MI since those in whom stents are deployed are at substantial risk of subsequent in-stent thrombosis unless double-antiplatelet therapy (ASA and clopidogrel) is ingested regularly and predictably for several months afterward, and those who partake in substance abuse often are unreliable in adhering to such a regimen.
 * Beta blockers should not be used in patients with cocaine induced MI as it can augment cocaine induced coronary arterial vasoconstriction.
 * In order to control sinus tachycardia and hypertension (after initial NTG and calcium channel blockers), labetalol, an alpha blocker and beta blocker, has been advocated, because it has been shown not to induce coronary artery vasoconstriction.

Methamphetamine
Rapid increase in methamphetamine abuse has also led to increase incidence of patients presenting with methamphetamine induced myocardial ischemia. However, there is not sufficient evidence base for the management of this condition. On the basis of similarities in pathophysiology seen in few case report series, current treatment recommendation is similar to that of cocaine induced MI.

==ACC / AHA Guidelines (DO NOT EDIT) == {{cquote|

Class I
1. Administration of sublingual or intravenous NTG and intravenous or oral calcium antagonists is recommended for patients with ST segment elevation or depression that accompanies ischemic chest discomfort after cocaine use. (Level of Evidence: C)

2. Immediate coronary angiography, if possible, should be performed in patients with ischemic chest discomfort after cocaine use whose ST segments remain elevated after NTG and calcium antagonists; PCI is recommended if occlusive thrombus is detected. (Level of Evidence: C)

3. Fibrinolytic therapy is useful in patients with ischemic chest discomfort after cocaine use if ST segments remain elevated despite NTG and calcium antagonists, if there are no contraindications, and if coronary angiography is not possible. (Level of Evidence: C)

Class IIa
1. Administration of NTG or oral calcium channel blockers can be beneficial for patients with normal ECGs or minimal ST segment deviation suggestive of ischemia after cocaine use. (Level of Evidence: C)

2.Coronary angiography, if available, is probably recommended for patients with ischemic chest discomfort after cocaine use with ST-segment depression or isolated T wave changes not known to be previously present and who are unresponsive to NTG and calcium antagonists. (Level of Evidence: C)

3. Management of UA / NSTEMI patients with methamphetamine use similar to that of patients with cocaine use is reasonable. (Level of Evidence: C)

Class IIb
1. Administration of combined alpha and beta blocking agents (e.g., labetalol) may be reasonable for patients after cocaine use with hypertension (systolic blood pressure >150 mm Hg) or those with sinus tachycardia (pulse >100 bpm) provided that the patient has received a vasodilator, such as NTG or a calcium antagonist, within close temporal proximity (i.e., within the previous hour). (Level of Evidence: C)

Class III
1.Coronary angiography is not recommended in patients with chest pain after cocaine use without ST segment or T wave changes and with a negative stress test and cardiac biomarkers. (Level of Evidence: C)}}