ORIGINAL CONTRIBUTION chest pain, cocaine; cocaine, chest pain

Cocaine-Associated Chest Pain Study objectives: To describe the clinical and ECG features of cocaine abusers evaluated in the emergency department and admitted to the medical coronary care unit with chest pain consistent with myocardial ischemia. Design: A four-month retrospective review of all cocaine abusers who presented to the ED with chest pain and a diagnosis of possible myocardial infarction. Setting: Urban county hospital. Type of participants: Forty-eight adult cocaine abusers admitted with chest pain. Measurements and m a i n results: Patients included 34 m e n and 14 women with a mean age of 29 +- 7.3 years. The average duration of cocaine abuse in 28 patients for whom it was reported was 5 +- 4.8 years. Chest pain occurred within one hour of cocaine abuse in I3 admissions (27%), more than one hour after abuse in 13 admissions (27%), and it was not recorded in 23 admissions (47%). Initial ECGs were evaluated in all patients and revealed significant repolarization abnormalities consisting of abnormal ST segment elevations in 18 (37%) and T-wave inversions in 20 (41%) that often persisted on subsequent ECGs. Three patients sustained acute myocardial infarctions. Conclusions: Our findings confirm a small but significant incidence of myocardial infarction in cocaine abusers presenting to the ED with chest pain. The chronicity of cocaine abuse, the persistence of ECG abnormalities, and the variable temporal relationship of chest pain to cocaine abuse suggest possible chronic myocardial changes as etiologies of ischemia. [Zimmerman JL, Dellinger RP,, Majid PA: Cocaine-associated chest pain. Ann Emerg Med June 1991;20:611-615.]

Janice L Zimmerman, MD* R Phillip Dellinger, MD* Pirzada A Majid, MBBS1Houston, Texas From Critical Care/Emergency Medicine* and the Cardiology Section,t Department of Medicine, Baylor College of Medicine, Houston, Texas. Received for publication January 25, 1990. Revision received December 14, 1990. Accepted for publication January 17, 1991. Address for reprints: Janice L Zimmerman, MD, Ben Taub General Hospital, 1502 Taub Loop, Houston, Texas 77030.

INTRODUCTION The spectrum of acute toxicity associated with cocaine abuse continues to expand. The increase in popularity of cocaine abuse due to the availability of "crack" exacerbates this problem. Seizures, intracerebral hemorrhage, cerebrovascular infarction, cardiac dysrhythmias, acute pulmonary edema, abruptio placentae, and rhabdomyolysis have been described after cocaine use. 1-6 A well-documented consequence of cocaine abuse is the development of acute myocardial infarction. 7-1z However, little attention has beeri focused on.the more frequent occurrence of cocaine-associated chest pain without myocardial necrosis. During a period of high cocaine availability and abuse in the Houston, Texas, metropolitan area (January through May 1988), we evaluated a large number of patients admitted with cocaine-related chest pain. We present a detailed description of the clinical and ECG features of cocaine abusers who presented to the emergency department with chest pain and were admitted to the medical coronary care unit. MATERIALS A N D METHODS The records of all patients admitted from the Ben Taub General Hospital ED to the medical coronary care unit with chest pain and a diagnosis of a possible myocardial infarction were reviewed retrospectively for a fourmonth period. Admissions of patients identified as cocaine abusers were

20:6 June 1991

Annals of Emergency Medicine

611/33

CHEST PAIN Zimmerman, Dellinger & Majid

FIGURE l. ECGs of patients with cocair~e-associated chest paJn. A top: A d m i s s i o n ECG of a 45-year-old man. Bottom: Discharge EGG two days later w i t h persistent abnormalities in the precordia] leads. B top: Admission ECG of a 25-year-old man. Bottom; Discharge ECG two days later with changed but persistent abnormalities in the precordial leads. analyzed. Cocaine abuse was considered to be present based on a voluntary history of such abuse or a urine drug screen positive for benzoylecgonine (the usual cocaine metabolite measured in urine). The standard urine benzoylecgonine analysis was used. 13 It is policy for our housestaff to question patients presenting with chest pain concerning history of cocaine abuse. C r i t e r i a for a d m i t t i n g c o c a i n e abusers with chest pain to rule out myocardial infarction include any of the following: sustained or persistent chest pain, chest pain with known risk factors for coronary artery disease, or chest pain with EGG changes suggestive of ischemia. Young cocaine abusers with no risk factors for coronary artery disease who have brief chest pain temporally related to cocaine abuse and normal ECGs are not routinely admitted. Standard protocol for patients admitted to rule out myocardial infarction at our hospital includes cardiac enzymes every eight hours for 24 hours, daily ECGs, and repeat EGGs with recurrent or increased chest pain as well as with new findings consistent with a potential change in cardiovascular status. Clinical characteristics at time of presentation as well as EGGs, chest radiographs, and cardiac e n z y m e s were specifically analyzed. EGGs were retrospectively and blindly interpreted by one of the authors who is a cardiologist. Sinus tachycardia was defined as a heart rate of more than 100, and sinus bradycardia was defined as a heart rate of less than 60. Significant ST segment elevation and depression were defined as elevation and depression of more than 1 m m in the limb leads or more than 2 m m in the precordial leads. Hyperacute T waves were defined as those more than t0 m m in the precordial leads. Statistical analysis of QT intervals corrected for heart rate (QTcs) was 34/612

I

A

II

V2

III

V3

V4

IIIIIIIII""'II

i .

~.---,--. . . . • r.

I.~:-; =~z .:= ::i' -I ; :

rI~ .i ,:il l'. ... . .

t

. . . . . . :,:':::::'

7~!:.I::

• : :

.

.

.

.

.

.

.

.

.

, ~ ' . ' :

I. . . . . i , . . , . . I - - - ] . ' ! ~ : "~ ~

'" :-~:-- :::i ~ : ~ . : ~ : 1

~I;

;

,

" !:

done using the two-tailed t test. Criteria for diagnosis of acute myocardial infarction were clinical presentation compatible with myocardial ischemia, ECG compatible with acute myocardial infarction, and increase in cardiac enzymes (creatinine phosphokinase [CPK]-MB of more than 10% total CPK and more than or equal to 20). RESULTS The records of 49 admissions (48 patients) were eligible for study. Mean patient age was 29 + 7.3 years (range, 17 to 51 years). There were 34 men and 14 women. Thirty-eight patients were black, six were Caucasian, and four were Hispanic. No patient had diabetes mellitus, previous myocardial infarction, or a significant family history of coronary artery disease. Three patients reported a history of hypertension, but they were not receiving antihypertensive medication. One patient had hypertension requiring therapy. One had Wolff-Parkinson-White syndrome but was not on medication. A third patient suffered minimal blunt .trauma Annals

.

.!

i.JE ::

::i~ ~ i ':

~ .,!; ~i,:" ~!I-~-!~.... li:._~ .... ~ ! i = ~ ~...... .

;'~;t{ "'i{':qt't I~: i ~ i i t t ~ t !qi{i

-: .: . . . . . . . . . .

.::~ : i : :: =?.1-: ~

.

~ii~$-~-~:I: -:~:_~.:::~iii-~!i:

,., ....... ---,-.:,. ................... - :. . . .

II

of Emergency

Medicine

-i

;~

:~':::-:~-:. : :.'.!

i

i

.

TABLE l. Initial EGG abnormalities in patients with cocaineassociated chest pain ECG Finding

Sinus tachycardia Sinus bradycardia Hyperacute T waves T-wave inversion ST depression ST elevation

No. of Patients

%

11 5 5 20 3 18

22 10 10 41 6 37

to the chest wall (struck by a fist during an altercation) on the day of admission. Testing for HIV antibody was performed in 14 patients; results were positive in two. No patient met criteria for the diagnosis of AIDS. All had chest radiographs negative for acute pulmonary pathology. The route of cocaine abuse was smoking in 29 patients (59%), IV injection in 16 (32%), smoking and IV injection in three (6%), and unknown in one (2%). The duration of cocaine abuse was reported in 28 patients. Only one reported first-time abuse of 20:6 June 1991

CHEST PAIN Zimmerman, Dellinger & Majid

TABLE 2. Clinical data at time of presentation in three patients with acute myocardial infarction Location of Route of Abuse/ Patient Myocardial Last Abuse (by History) Age/Sex Infarction 28/F

Anteroseptal Smoking/2wk

28/M

Inferior

Smoking/within 12 hr

32/M

Inferior

IV/4 d

Characteristics of Presenting Complaint Chest pain, crushing and substernal Chest pain, pressureiike and radiating to right arm Chest pain, crushing and radiating to left arm

•o •Q

••ooo o0•

0,40

0.35

0.30 0

*P < .001 I

A

D

2

cocaine. Twenty-two of the patients had abused cocaine for more than one year. Mean duration of cocaine abuse was 5 -+ 4.8 years. Urine was tested for the presence of benzoylecgonine in 29 patients and detected in 26. Of the three patients with negative drug screens despite a history of cocaine abuse, two reported their last use four days and two weeks, respectively, before the onset of chest pain. This test is positive within five minutes of smoking or IV abuse of cocaine and positive within 30 minutes after insufflation. It typically remains positive for 24 to 36 hours (longer in some daily highlevel chronic abusers). Last abuse of cocaine was not reported for the third patient. Benzoylecgonine was detected in combination with another drug or alcohol in 16 cases; amphetamines were detected in five patients; and opiates in three. Onset of c h e s t p a i n o c c u r r e d within one hour of cocaine use in 13 patients (27%). Chest pain occurred more than one hour after use of co20:6:June1991

90/59 mm Hg 150/98 mm Hg

105

Sinus; ST depression V3-V6; poor R wave progression Sinus; right bundle branch block

R

None

180/70 rnm Hg

52

67

F

Complete heart block

Sinus; ST segmentelevation, II, Ill, aVF; ST segmentdepression V2-V6

R

None

Initial ECG

sociated chest pain.

0.50

0

Complication

Initial Initial Blood Pressure Pulse

FIGURE 2. Comparison of Q T c on a d m i s s i o n ECG (A) and discharge ECG (D) in patients with cocaine-as-

0.55

0.45

First-Time (F) or Recurrent (R) Symptoms

caine in 13 patients (27%). Three patients described chest pain occurring more than 24 hours after their last use of cocaine. Information regarding onset of chest pain after cocaine use was unavailable for 23 admissions. A component of the chest pain was typical for myocardial ischemia in all patients including character (pressurelike) and location (retrosternal). Chest pain usually occurred only at rest. Sixteen patients (33%) described an additional pleuritic component to their chest pain. The chest pain was recurrent in 23 patients {47%) and o c c u r r e d for the first t i m e in 19 (39%). This information was not reported for seven patients. Initial blood pressure measurements in the ED revealed only two patients with a diastolic blood pressure of more than 100 m m Hg. An initial heart rate exceeding 100 was recorded in 17 admissions {35%). ECGs at presentation were available for all patients. These findings are described (Table 1). Only eight patients (16%)had normal ECGs. Sinus tachycardia as the only ECG abnormality was present in 10% of patients. Repolarization abnormalities on initial ECG were present in 16 patients (32.7%) and consisted of upward-coved ST segment elevation and T-wave abnormalities. Follow-up ECGs during hospitalization were available for 31 patients. A significant finding was the persistence of repolarization abnormalities (ten of 11 patients with follow-up ECGs) (Figure 1). Transient ST segment elevations were not seen in any Annals of Emergency Medicine

patient. QT¢ interval was measured serially. Although the QT c interval at baseline was in the upper limits of normal with a mean of 0.45 seconds (range, 0.33 to 0.53 seconds), there nevertheless was a significant decrease (P < .001) in the QT¢ intervals of the 31 patients who had serial ECGs available for study (Figure 2). T h r e e p a t i e n t s (6%) had a c u t e myocardial infarctions: a 28-year-old man with an inferior wall myocardial infarction, a 28-year-old woman with an anteroseptal myocardial infarction, and a 32-year-old man with an inferior wall myocardial infarction (Table 2). Initial ECG revealed evidence of acute transmural infarction in all three patients. Cardiac catheterization was performed in the 32year-old patient with an inferior wall myocardial infarction and revealed less than 50% stenosis of the right coronary artery with posterobasilar akinesis and a preserved left ventricular ejection fraction of 55%. Four of the patients who were ruled out for myocardial infarction subsequently had normal cardiac catheterizations. 14 DISCUSSION This was a retrospective analysis of hospitalized cocaine abusers with chest pain consistent with myocardial ischemia. By the nature of that design, all patients with cocaine-related myocardial disease evaluated in the ED during this period may not be represented. The presence of cocaine abuse was made from either patient history or urine screening. Because urine screens for benzoylecgonine are not routinely done on all patients seen in the ED with chest pain, it is likely that some cocaine abusers with chest pain were not identified as such and possible (although less 613/35

CHEST PAIN Zimmerman, Dellinger & Majid

likely) that s o m e admitted cocaine abusers w i t h chest pain were not identified. One w o u l d expect the most-ill patients to have a greater likelihood of admission and the cohort to represent those w i t h the greatest likelihood of myocardial disease.

Published reports of cardiovascular complications after cocaine abuse have centered on the occurrence of myocardial infarction, w h i c h was first described in 1982.8 Myocardial infarction has been associated with all routes of cocaine abuse. Although cardiac catheterization has revealed both normal and abnormal coronary arteries, many patients fail to demonstrate evidence of coronary atherosclerosis. 7,9,11 Myocardial infarction in our group of patients was uncommon when compared with the number of patients a d m i t t e d with ischemic chest pain. The 6% incidence of myocardial infarction in our study population is low compared with the usual rate of 18% among all medical coronary care unit admissions (personal communication, Peter Puleo, MD, March 1991). However, myocardial infarction in young adults with few or no underlying risk factors for coronary artery disease is a major concern. Previous literature reflects a rule-in myocardial infarction rate of 4% in those 25 to 39 years old. is The opportunity to evaluate a large population of young cocaine abusers presenting with chest pain is of significant clinical interest. Most of the patients were young, chronic abusers of cocaine whose ischemialike chest pain presents a problem for the emergency physician. The IV and inhaled routes of abuse in our patient population reflect the current practice of using routes of abuse that provide rapid and high blood levels of cocaine. The additional pleuritic component of the chest pain in approximately one third of the patients is without explanation. The pathophysiologic mechanisms responsible for myocardial ischemia after cocaine use are poorly understood. Cocaine inhibits the reuptake of norepinephrine at adrenergic nerve endings and potentiates the effects of circulating catecholamines on target organs. 16 As a result of sympathetic stimulation, the heart and peripheral vasculature are subjected to a hemodynamic burden that can adversely affect myocardial oxygen supply and 36/614

demand. Cocaine produces dose-dependent positive chronotropic and inotropic effects that can increase cardiac work and demand for oxygen.17,18 Increased myocardial oxygen demand may be the sole mechanism responsible for chest pain in patients with underlying coronary artery disease. It is possible, but unlikely, that our patients had underlying fixed coronary artery disease, because 80% were less than 35 years old with no known risk factors for coronary artery disease. Further support for this premise is the absence of significant coronary artery disease on coronary angiography in four of the patients who did not suffer a myocardial infarction. 14 It is also possible that an acute rise in the pressure-rate product m a y induce subendocardial ischemia, particularly in patients with left ventricular hypertrophy in the absence of coronary artery disease. In our patient population, only two patients demonstrated diastolic blood pressures exceeding 100 m m Hg at the time of presentation, and tachycardia was present in approximately one third of patients. The effect of cocaine on the coronary circulation has been the subject of several e x p e r i m e n t a l studies. Some investigators have s h o w n a dose-related increase in coronary vascular resistance with cocaine on the basis of its recognized vasoconstrictor properties. 19 These effects may be further p o t e n t i a t e d by circulating norepinephrine causing c~-adrenergicmediated coronary vasoconstriction. The increase in coronary vascular resistance in the presence of tachycardia and hypertension could account for ischemic symptoms in the absence of coronary artery disease. Cocaine might induce focal spasm of epicardial coronary arteries, resultting in ischemia or infarction. However, focal coronary artery spasm has yet to be demonstrated at angiography, either spontaneously or after ergonovine provocation in the absence of underlying coronary artery disease.7,11,1~,2° The clinical course of our patients was not consistent with intermittent coronary arterial spasm as the basis for chest pain. Chest pain resulting from coronary arterial spasm typically produces transient ST segment elevations that rapidly normalize after resolution of spasm. A significant number of our patients Annals of Emergency Medicine

had evidence of abnormal ST segment elevation on the ECG that persisted and was more suggestive of mild epicardial injury. A n o t h e r m e c h a n i s m causing ischemic chest pain may be thrombus formation resulting from activation of platelets. Irl vitro studies of platelet function have shown that cocaine enhances platelet responsiveness to arachidonic acid in terms of both thromboxane B2 production and the aggregating response. 2~ Catecholamines may compound these effects by independently increasing platelet aggregability. 22 A platelet thrombus hypothesis is supported by some case reports of cocaine-related acute myocardial infarction.11,12,23, 24 One report described nonatherosclerotic intimal proliferation of smooth muscle cells involving epicardial and intramural coronary arteries in addition to acute coronary obstruction from platelet thrombosis. 23 The intimal smooth muscle proliferation could be the result of stimulation by plateletderived smooth muscle growth factor. 2s Clearly, further studies are needed to delineate factors responsible for acute ischemic syndromes related to cocaine use. In particular, the temporal relationship of cocaine abuse to the onset of chest pain was highly variable in our population of chronic abusers and may implicate a chronic abnormality predisposing to myocardial ischemia. We previously reported the presence of thickening of small intramyocardial arteries in seven of 11 chronic cocaine abusers, a6 This abnormality may either be a risk factor for spontaneous ischemia or lower the threshold for ischemia during increased myocardial oxygen demand. It is possible that once thickening of small intramyocardial arteries exists, any stimulus for increased myocardial o x y g e n d e m a n d (ie, cocaine abuse, exertion) m i g h t lead to ischemic chest pain. This theory is supported by our data gathered from a population of young, chronic cocaine abusers with chest pain, some of whom had not abused cocaine immediately preceding chest pain. In contrast to a report that found no ECG evidence of ischemia in patients presenting to the ED with cocaine-related chest pain, ECG abnormalities were common in our patient population. 27 This may be explained b y our experimental design, which 20:6 June 1991

CHEST PAIN Zimmerman, Dellinger & Majid

retrospectively s e l e c t e d p a t i e n t s whose chest pain led to admission. The findings typically comprised diffuse upward-coved repolarization abnormalities affecting the precordial leads. These findings were not consistent with the early repolarization changes frequently seen in the black population. These changes persisted in patients with serial ECGs available for study. None of the patients showed transient elevations of ST segments characteristic of coronary vasospasm. We did not treat our patients differently from those with chest pain secondary to coronary artery disease. All patients received nitrates and calcium channel blockers as needed. ~-Adrenergic antagonists were not routinely used because of theoretical concerns regarding elevation of blood pressure from u n o p p o s e d c~-adrenergic peripheral v a s o c o n s t r i c t i o n . Thrombolytic therapy was not used in our patients with acute transmural myocardial infarction because of delayed presentation. However, this therapeutic modality has been used in patients p r e s e n t i n g w i t h acute myocardial infarction after cocaine abuse. 12 Based on our findings, use of typical ST segment elevation as a criterion for institution of thrombolytic therapy may not reliably indicate infarction in this group of patients. Furthermore, an increased incidence of intracerebral hemorrhage after thrombolytic therapy in IV substance abusers may exist. 28 Shortening of the QT c interval during hospitalization is an observation that has been reported previously in cocaine abusers, z9 Prolongation of the QT interval has also been associated with unilateral stellate ganglion stimulation. 8o Cardiac dysrhythmias have been well described after cocaine abuse, and torsade de pointes , a rhythm usually associated with QT prolongation, has been reported in a patient with cocaine intoxication.hal The relationship between changes in the QT interval and the development of dysrhythmias after cocaine abuse is purely speculative and requires further study. Despite a precise delineation of etiology, chest pain compatible w i t h myocardial i s e h e m i a w i t h o u t evidence of infarction m u s t be recognized as one of the m o s t frequent complications resulting from cocaine 20:6:June1991

abuse. T h e n u m b e r of l o n g - t e r m abusers of cocaine in our study population, the persistence of ST and T wave changes, and the variable temporal relationship of chest pain to cocaine abuse suggest the possibility of chronic cardiac effects participating in the production of ischemia. This is further supported by arterial abnormalities on myocardial biopsy in a cohort of this group. The highest-risk population for cocaine use remains the 18- to 25-yearold age group, but there is increasing prevalence in the 26- to 34-year-old age group. 32 This increase in older adults m a y reflect the passage of young adult cocaine abusers to the next cohort. If true, the number of long-term chronic abusers of cocaine can be expected to increase. These patients may be at particular risk for cocaine-related ischemic chest pain, possibly resulting from chronic myocardial vascular changes. CONCLUSION Chest pain typical for myocardial i s c h e m i a w i t h o u t s u b s e q u e n t evidence of infarction was a frequent finding in our population of cocaine abusers admitted to the medical coronary care unit. T h e clinical and ECG characteristics described in this study indicate chronic abuse of cocaine, a variable temporal relationship of chest pain to cocaine abuse, and persistent ECG changes in our patients. The etiology of ischemia in t h e s e p a t i e n t s m a y be r e l a t e d to chronic myocardial changes.

REFERENCES 1. Myers JA, Earnest MP: Generalized seizures and cocaine abuse. Neurology 1984;34:675-676. 2. Wojak JC, Flarnm ES: Intracranial hemorrhage and cocaine use. Stroke 1987;18:712-715. 3. Levine SR, Welch KMA: Cocaine and stroke. Stroke 1988;19:779-783. 4. Chasnoff IF, Burns WJ, Schnoll SH, et al: Cocaine use in pregnancy. N EngI [ Med 1985;313:666-669. 5. Allred RJ, Ewer S: l~atal pulmonary edema following intravenous "freebase" cocaine use. A n n Emerg Med 1981;10:441-442. 6. Roth D, Alarcon FJ, Fernandez JA, et al: Acute rhabdomyolysis associated with cocaine intoxication. N Engi J Med 1988~319:673-677.

10. Mathias DW: Cocaine-associated myocardial ischemia. A m J Med 1986~81:675-677. 11. Zimmerman FH, Gustafson GM, Kemp HG: Recurrent myocardial infarction associated w i t h cocaine abuse in a young man with normal coronary arteries: Evidence for coronary artery spasm c u l m i n a t i n g in thrombosis. J A m ColI Cardiol 1987;9:964-968. 12. Smith H-WB, Liverman HA, Brody SL, et al: Acute myocardial infarction temporally related to cocaine use. Ann Intern Med 1987~107:13-18. 13. Weiss RID, Gaivin FH: Protracted elimination of cocaine metabolites in long-terra high-dose cocaine abusers. A m J Med 1988;85:879-880. 14. Majid PA, Patel B, Han-Seob K, et ah An angiographic and histologic study of cocaine-induced chest pain. A m J Cardiol 1990~65:812-814. 15. Lee TH, Cook EF, Weisberg M, et al: Acute chest pain in the emergency room: Identification and examination of low-risk patients. Arch Intern Med 1985; 145:65-69. 16. Kalsner S, Nickerson M: Mechanism of cocaine potentiation of responses to amines. Br J Pharmacol 1969;35:428-439. 17. Fischman MW, Schuster CR, Resnekow L, et al: Cardiovascular and subjective effects of intravenous cocaine administration in humans. Arch Gen Psychiatry 1976;33:983-989. 18. Foltin RW, Fisehman MW, Pedroso JJ, et al: Marijuana and cocaine interactions in humans: Cardiovascular consequences. PharmacoI Biochem Behav I987; 28:459 464. 19. Pierre A, Kossowksy W, Chou ST, et al: Coronary and systemic hemodynamics after intravenous injection of cocaine (abstract). Anesthesiology 1985;63:A28. 20. Halle AA, Insel J, McDonald MB, et al: Ergonovine testing in cocaine induced myocardial ischemia {abstract). J A m Coil Cardio] 1989;13:79A. 21. Togna G, Tempests E, Togna AR, et al: Platelet responsiveness and biosynthesis of thromboxane and prostacyclin in response to in vitro cocaine treatment. Haemostasis 1985;15:100-107. 22. Sehnetzer GW: Platelets and thrombogenesis Current concepts. Am Heart J 1972;83:552-564. 23. Simpson RW, Edwards WD: Pathogenesis of cocaine-induced ischemic heart disease. Arch Pathol Lab Med 1986;110:479-484. 24. Hadiimiltiades S, Covalesky V, Manno BV, et al: Coronary arteriographic findings in cocaine abuse-induced myocardial infarction. Cathet Cardiovasc DJagn 1988;14:433~436. 25. Ross R, Glomset ], Kariya B, et al: A platelet-dependent serum factor that stimulates the proliferation of arterial smooth muscle cells in vitro. Proc NatI Acad Sci USA 1974;71:1207-1210. 26. Majid PA, Patel B, Kim HS, et al: An angiographic and histologic study of cocaine-induced chest pain. A m f Cardiol 1990;65:812-814. 27. Derlet RW, Albertson TE: Emergency department presentation of cocaine intoxication. Ann Emerg Med 1989;18:182-186. 28. Bush HS: Cocaine-associated myocardial infarction - A word of caution about thrombolytic therapy. Chest 1988;94:878. 29. Karch SB: Serum catecholamines in cocaine-intoxicated patients with cardiac symptoms (abstract}. Ann Emerg Med 1987;16:481.

7. Isner JM, Estes M, Thompson PD, et al: Acute cardiac events temporally related to cocaine abuse. N Engf ] Med 1986;315:1438-1443.

30. Schwartz PJ, Snebold NG, Brown AM: Effects of nnilateraf cardiac sympathetic denervation on the ventricular fibrillation threshold. A m J Cardiol 1976; 37:1034-1040.

8. Coleman DL, Ross TP, Naughton JL: Myocardial ischemia and infarction related to recreational cocaine use. West ] Med 1982;135:444-446.

31. RolIingher IM, Belzberg AS, Macdonald IL: Cocaineinduced m y o c a r d i a l i n f a r c t i o n . Can M e d Assoc J 1986;136:45-46.

9. Wilkins CE, Mathur VS, Ty RC, et al: Myocardial infarction associated with cocaine abuse. Tex Heart Inst J 1985~12:385-387.

32. Abelson HI, Miller JD: A decade of trends in cocaine use in the household population. Nat1 lust Drug Abuse Res Monogr Ser i985;51:35-49.

Annals of Emergency Medicine

615/37