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Prinzmetal's variant angina

Prinzmetal's angina, also known as variant angina or angina inversa, is a syndrome typically consisting of angina (cardiac chest pain) at rest that occurs in cycles. more...

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It is caused by vasospasm, a narrowing of the coronary arteries caused by contraction of the smooth muscle tissue in the vessel walls rather than by atherosclerosis (buildup of fatty plaque and hardening of the arteries). It was first described in 1959 by the American cardiologist Dr. Myron Prinzmetal (1908-1987).


Symptoms typically occur at rest, rather than on exertion. 2/3 of patients have concurrent atherosclerosis of a major coronary artery, but this is often mild or not in proportion to the degree of symptoms.

It is associated with specific ECG changes (elevation rather than depression of the ST segment)


Patients who develop cardiac chest pain are generally treated empirically as an "acute coronary syndrome", and are generally tested for cardiac enzymes such as creatine kinase isoenzymes or troponin I or T. These may show a degree of positivity, as coronary spasm too can cause myocardial damage. Echocardiography or thallium scintigraphy is often performed.

The gold standard is coronary angiography with injection of provocative agents into the coronary artery. Rarely, an active spasm can be documented angiographically (e.g. if the patient receives an angiogram with intent of performing a primary coronary intervention with angioplasty). Depending on the local protocol, provocation testing may involve substances such as ergonovine, methylergonovine or acetylcholine. Exaggerated spasm is diagnostic of Prinzmetal angina.


Prinzmetal angina typically responds to the same treatments as other forms of angina, although nitrates and calcium channel blockers are relatively more effective.


  • Prinzmetal M, Kennamer R, Merliss R. A variant form of angina pectoris. Am J Med 1959;27:375-88. PMID 14434946.


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The cocaine-abused heart - Cardiology Casebook
From American Journal of Critical Care, 11/1/03 by Kathryn Buchanan Keller

A 34-year-old African American man came to the emergency department (ED) complaining of chest pressure and shortness of breath, 2 hours in duration. He admitted to smoking cocaine for the first time 2 days ago and inhaling 1 g at a party 1 hour before the onset of symptoms. The patient had been in good health, did not smoke cigarettes or drink alcoholic beverages, and ran 5 miles daily. There was no family history of heart disease. On physical examination, he was agitated, blood pressure 180/100 mm Hg, heart rate 130/min and regular; there was an [S.sub.4], [S.sub.1], and [S.sub.2], no murmurs were heard. Findings on chest radiographs were normal, and the electrocardiogram (ECG) revealed cove-plane Y waves in [V.sub.2]-[V.sub.6] (Figure 1). The level of the first set of cardiac enzymes (the troponins) was elevated. The patient was admitted to the telemetry unit for further evaluation and monitoring.



1. Most illicit drug-related deaths are due to which of the following?

a. heroin

b. cocaine

c. amphetamines

d. [gamma]-hydroxybutyrate (GHB)

2. Deleterious cardiovascular(CV) effects of cocaine are mediated through which of the following?

a. [alpha]-adrenergic stimulation

b. [beta]-adrenergic stimulation

c. coronary thrombosis

d. tachyarrhythmias

e. all of the above

3. Among cocaine users presenting to the ED, the most frequent symptom(s) is/are which of the following?

a. palpitations

b. shortness of breath

c. chest pain

d. agitation

e. seizures

4. Most useful in the early diagnosis of cocaine-induced myocardial infarction (MI) is/are which of the following?

a. history and physical examination

b. ECG

c. cardiac enzymes

d. echocardiography

e. coronary angiography

f. all of the above

5. Which of the following drugs is/are contraindicated in cocaine-induced MI?

a. [beta]-blockers

b. thrombolytics

c. aspirin

d. nitroglycerin

e. lidocaine

f. thrombolytics


1. b. cocaine

Data from the Drug Abuse Warning Network implicate cocaine as the most frequent cause of illicit drug-related deaths and visits to the ED in the United States. (1) These alarming statistics are not only due to the toxicity of cocaine, but also to its popularity, as evidenced by a steady increase in the number of users since the early 1980s. Since the late 1990s approximately 25 million Americans have used cocaine at least once, 3.7 million have used it in the previous year, and 1.5 million are current users? (1,2) The typical patient is a man in his thirties who is nonwhite and a cigarette smoker. (1,3) Cocaine may be administered by smoking (free-base), nasal insufflation, or intravenous injection. Smoking (ie, "crack" cocaine) is the most common method of administration and the most potent form of use. The free-base form is called "crack" because it makes a popping sound when heated. Cocaine is rapidly absorbed through the respiratory tract within seconds to minutes of administration. Cardiac events can follow administration by any of the routes.

2. a. [alpha]-adrenergic stimulation

b. [beta]-adrenergic stimulation

Both [alpha]- and [beta]-adrenergic receptor sites are activated by increased catecholamine levels. Cocaine blocks the presynaptie reuptake of norepinephrine, thereby increasing the amount of this catecholamine at the postsynaptic receptor site of the postganglionic neuron. The increase in catecholamine levels leads to peripheral [alpha]-adrenergic receptor activation, which causes vasoconstriction and hypertension. This vasoconstrictive effect is somewhat counterbalanced by peripheral [beta]-adrenergic receptor activation, which is also a result of increased catecholamines. Therefore, the therapeutic use of [beta]-antagonists ([beta]-blockers, eg, propranolol) in cocaine-induced coronary ischemia may cause unopposed peripheral [alpha]-receptor activation, inducing coronary vasoconstriction and initiating or enhancing existing hypertension (3) (Figure 2).

Cocaine stimulates the [beta]-receptors in the myocardium, which increase the heart rate and contractility, thereby increasing oxygen demand. The [alpha]-adrenergic stimulation can lead to coronary vasoconstriction. (1,3) Cocaine increases production of endothelin, a powerful vasoconstrictor, and decreases production of nitric oxide, a powerful vasodilator. Following cocaine-induced angina, significant reductions in the diameters of the left anterior descending and circumflex coronary arteries have been observed during angiography. The vasoconstrictive effects of cocaine are more pronounced in areas with preexisting stenosis; however, many cocaine induced MIs have no angiographic evidence of coronary artery disease. (4) Nevertheless, it should be noted that the probabilities of coronary artery occlusion and resulting infarction are enhanced when coronary plaques have preexisted. Cocaine enhances platelet aggregation as a result of increased levels of platelet agonists thromboxane [A.sub.2] and adrenaline. (5) In addition, cocaine enhances clot formation by elevating levels of plasminogen activator inhibitor. Chronic use is associated with intimal hyperplasia, accelerated atherosclerosis, and endothelial dysfunction, which also contribute to a prothrombotic environment. (6)

Cocaine can directly affect myocardial muscle by causing acute deterioration of left ventricular systolic and diastolic function and may also alter calcium ([Ca.sup.2+]) handling by myocytes. (7) Pathophysiological effects of cocaine are also found in the conduction system, namely, inhibition of the fast sodium channel, which prolongs QRS and QT intervals. These changes may result in cardiac arrhythmias, such as torsade de pointes, atrial fibrillation, supraventricular tachycardia (SVT), and ventricular tachycardia (VT). (8)

3. c. chest pain

Most cocaine-related visits to the ED, which account for more than 64000 ED evaluations per year, are due to chest pain. More than 50% of those patients are ultimately admitted to the hospital at an estimated cost of $85 million a year. These numbers may even underestimate the true incidence of cocaine-induced ED visits, because most EDs do not routinely perform toxicology screening as part of a chest pain evaluation and many patients will not admit their illicit drug use. (9,10) Many of these patients are admitted for the purpose of ruling out myocardial ischemia, which may appear odd because the vast majority of these patients are quite young. However, since the early 1980s, numerous cases of MIs occurring in young patients with and without coronary artery disease have been reported. These cases can be attributed to the epidemic of obesity in America's young population, which is most likely responsible for the steady increase in the incidence of coronary artery disease in this age group. As a consequence, an increasing number of cocaine-induced MIs are being seen in patients in their twenties and thirties. Approximately 6% of patients with cocaine-induced chest pain are found to have an MI. (11-13) Furthermore, it is estimated that cocaine use accounts for 25% of all MIs in patients between 18 to 45 years old. (14) Thus, in a young patient with an MI, it is important to determine if cocaine had been used recently, because this would alter standard therapeutic interventions. The ischemic events are not related to the amount of cocaine used and the risk for MI is highest within the first hour of cocaine use and declines rapidly with time. (7) It is important to keep in mind that there are many other potential CV complications associated with cocaine use, including myocarditis, acute aortic dissection, endocarditis, arrhythmias, and sudden death. (1,2)

4. c. cardiac enzymes

In cocaine-induced vasospastic coronary ischemia, the history and physical examination are important in determining the presence of risk factors for coronary events and are helpful in the differential diagnosis. Elevated levels of cardiac enzymes (troponins) and serial ECGs, however, are needed to diagnose MIs. The interpretation of the initial ECG can be challenging. Approximately 70% to 90% of patients with cocaine-induced chest pain show ECG evidence of ST elevation, at times with T-wave inversion. Forty-three percent of the patients met the criteria for thrombolysis from the Thrombolysis in Myocardial Infarction Trial (TIMI); however, in most cases the ST-segment elevation was due to the high prevalence of the early repolarization changes that can be seen in young black men. (15) Healthy black men frequently exhibit early repolarization changes that mimic the ST elevations in an acute anterior wall MI or in acute pericarditis. (15,16) Accelerated ventricular repolarization is the mechanism responsible for the characteristic ECG pattern and is a normal variant (Figures 3 and 4).

In cocaine-induced angina, the measurement of cardiac enzymes is more specific than the ECG findings in the diagnosis of acute MI, and the cardiac troponins are the most specific and sensitive of all the indicators of myocardial damage. (3,13,17) Echocardiography can be useful in selective cases to confirm the presence of new regional wall abnormalities.

5. a. [beta]-blockers

[beta]-Blockers have been proven to reduce mortality in acute myocardial ischemia and infarction due to atherosclerosis. There are 2 exceptions when [beta]-blockers are contraindicated in ischemia: one when ischemia is due to cocaine and the other in Prinzmetal's angina. Cocaine stimulates both [alpha]- and [beta]- peripheral receptors; as a result, [beta]-blockade in cocaine-induced angina would leave [alpha]-activity unopposed, which would enhance coronary vasoconstriction, systemic hypertension, and heart rate. (8,10) Similarly, coronary vasospasm is the primary abnormality in Prinzmetal's angina and not an increase in oxygen demand in the setting of narrowed atherosclerotic coronary arteries and thus, therapy with [beta]-blockers would intensify coronary vasospasm. For these reasons, [beta]-blockers are contraindicated in vasospastic angina, which is the pathophysiological state in the 2 clinical conditions just mentioned. (9)

Thrombolytics must be used with caution, because a confirmed diagnosis of an acute MI due to a thrombotic occlusion is infrequent and may be elusive in cocaine-induced acute coronary events. Early serial repolarization changes on ECG (cove-plane T waves) and elevated cardiac troponin levels will confirm a diagnosis of myocardial necrosis, usually the result of a thrombotic occlusion. Percutaneous coronary intervention is preferable when coronary occlusions are due to intense vasospasm, a pathophysiological state in which thrombolytics are not indicated. (8) In fact, to date, no studies have shown any benefits in the use of thrombolytics in this patient population. Statistically the hospital mortality of cocaine-induced MI is very low and may even approach zero. (17)

Aspirin reduces clotting activity and is recommended to prevent the formation of thrombi. Nitroglycerin, a vasodilator, relieves chest pain, reverses cocaine-induced coronary artery vasospasm, and is the drug of choice in the management of these patients. The calming effects of benzodiazepines are useful for severe agitation by reducing the heart rate and thus myocardial oxygen consumption. In addition, seizures may be prevented by increasing the seizure threshold. (8,9,11) With continued severe chest pain after the administration of nitroglycerin, benzodiazepine and aspirin, the use of an [alpha]-adrenergic antagonist such as phentolamine can be useful in reversing coronary artery vasoconstriction. (8) Cocaine may cause wide-complex SVT because of its property as a sodium-channel blocker; VT may occur as a result of myocardial ischemia. Intravenous lidocaine is indicated for the treatment of VT and sodium bicarbonate for wide-complex SVT. (8,18,19)


Recreational use of cocaine dates back to the lncas in South America 5000 years ago. Cocaine is derived from the leaves of Erythroxylon coca, a shrub native to South America. In the late 1800s, Sigmund Freud popularized the drug in Europe. He used cocaine to treat depression, asthma, cachexia, and for overcoming morphine addiction. Also in this period cocaine rapidly gained acceptance in surgical procedures as a local anesthetic and vasoconstrictor. Cocaine reached the United States in the early 1900s, and its popularity led President Taft to declare it public enemy number one in 1910. Cocaine became popular again in the 1980s.

Currently cocaine use is responsible for more ED visits then any of the other illicit drugs. Because most cocaine users are young, they are at a lower risk for coronary artery atherosclerotic disease. An estimated 25 million people between the ages of 26 and 34 years have used cocaine at least once, 20% were women and 30% men. Habitual users of cocaine are estimated to number 1.5 million. (1,2)

Most cocaine-induced chest pains do not progress to MI, and in fact many originate in the chest wall. The chest pains due to cocaine, however, are induced by myocardial ischemia, a result of vasospasm and not a thrombotic occlusion of a coronary artery that has a ruptured atheromatous plaque. ECG findings can be misleading in the diagnosis because the early repolarization syndrome, a normal variant, is a frequent finding in young African American men. Measurement of cardiac troponin levels is the most reliable diagnostic test. Percutaneous coronary intervention and angioplasty, rather than thrombolysis, is the treatment of choice because intense coronary vasospasm is the primary pathophysiology in cocaine-induced MI.


Supported in part by a grant from the Applebaum Foundation, in loving memory of Joseph Applebaum.


(1.) Lange RA, Hillis LD. Cardiovascular complications of cocaine use. N Engl J Med. 2001;345:351-358.

(2.) Kloner RA, Rezkalla SH. Cocaine and the heart. N Engl J Med. 2003;348(6):487-488.

(3.) Erwin MB, Deliargyris EN. Cocaine-associated chest pain. Am J Med Sci. 2002;324:37-44.

(4.) Minor RL, Brook DS, Brown DD, et al. Cocaine-induced myocardial infarction in patients with normal coronary arteries. Ann Intern Med 1991;115:797-806.

(5.) Kugelmass AD, Oda A. Monahan K, et al. Activation of human platelets by cocaine. Circulation. 1993;88:876-883.

(6.) Kolodgie FD, Virmani R, Cornhill JF, et al. Increase in atherosclerosis and adventitial mast cells in cocaine abusers; an alternative mechanism of cocaine-associated coronary vasospasm and thrombosis. J Am Coll Cardiol. 1991;117:1553-1560.

(7.) Mittleman MA, Mintzer D, Maclure M, et al. Triggering of myocardial infarction by cocaine. Circulation. 1999;99:2737-2741.

(8.) Hahn IH, Hoffman RS. Cocaine use and acute myocardial infarction. Emerg Med Clin North Am. 2001;19:493-500.

(9.) Hollander JE. The management of cocaine-associated myocardial ischemia. N Engl J Med 1995;333:1267-1272.

(10.) Hoffman RS, Hallander JE. Evaluation of patients with chest pain after cocaine use. Crit Care Clin. 1997;13:809-828.

(11.) Hollander JE, Hoffman RS, Gennis P, et al. Prospective multicenter evaluation of cocaine-associated chest pain. Acad Emerg Med. 1994;1:330-339.

(12.)Walker NJ, Sites FD, Shofer FS. et al. Characteristics and outcomes of young adults who present to the emergency department with chest pare. Acad Emerg Med. 2001;324:1239-1246.

(13.) Weber JE, Shofer FS. Larkin GL, et al. Validation of a brief observation period of patients with cocaine-associated chest pain. N Engl J Med. 2003;348:510-517.

(14.) Qureshi AI, Suri FK, Guterman LR, et al. Cocaine use and the likelihood of nonfatal myocardial infarction and stroke: data from the third national health and nutrition examination survey. Circulation. 2001;103:502-506.

(15.) Gitter MJ, Goldsmith SR. Dunbar DN. et al. Cocaine and chest pain: clinical features and outcome of patients hospitalized to rule out myocardial infarction. Ann Intern Med. 1991;115:277-282.

(16.) Spodick DH. Pericardial diseases. In: Braunwald E, Zipes D, Libby P, eds. Heart Disease, 6th ed. Philadelphia, Pa: WB Saunders Co; 2001:1823-1876.

(17.) Hollander JE, Hoffman RS, Burstein J, et al. Cocaine-associated myocardial infarction: mortality and complications. Arch Intern Med. 1995; 155:1081-1085.

(18.) Valladares BK. Lemberg L. The Miami vices in the CCU. Part I. Cardiac manifestations of cocaine use. Heart Lung. 1987;16:456-458.

(19.) Henowitz NL. How toxic is cocaine? Ciba Found Symp. 1993;166:125-130.


Ascher EK, Stauffer JCE, Gaasch WH. Coronary artery spasm, cardiac arrest, transient electrocardiographic Q waves and stunned myocardium in cocaine-associated acute myocardial infarction. J Am Coll Cardiol. 1988;61:939-941.

Kushman SO. Storrow AB, Liu T, et al. Cocaine-associated chest pain in a chest pain center, Am J Cardiol. 2000:85:394-396.

Nallamothu BK, Saint S, Kolias TJ, et al. Of nicks and time. N Engl J Med. 2001;345:359-363.

Weber JE, Chudnofsky CR. Boczar M, et al. Cocaine-associated chest pain: how common is myocardial infarction? Acad Emerg Med 2000;7:873-877.

Kathryn Buchanan Keller, RN, PhD, and Louis Lemberg, MD. From the Division of Cardiology, Department of Medicine, University of Miami School of Medicine, Miami, Fla (LL) and Florida Atlantic University Christine E. Lynn College of Nursing, Boca Raton, Fla (KBK).

COPYRIGHT 2003 American Association of Critical-Care Nurses
COPYRIGHT 2004 Gale Group

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