Download
cocaine induced chest pain focus on acute coronary syndromes n.
Skip this Video
Loading SlideShow in 5 Seconds..
Cocaine-induced chest pain Focus on Acute coronary syndromes PowerPoint Presentation
Download Presentation
Cocaine-induced chest pain Focus on Acute coronary syndromes

Cocaine-induced chest pain Focus on Acute coronary syndromes

203 Views Download Presentation
Download Presentation

Cocaine-induced chest pain Focus on Acute coronary syndromes

- - - - - - - - - - - - - - - - - - - - - - - - - - - E N D - - - - - - - - - - - - - - - - - - - - - - - - - - -
Presentation Transcript

  1. Cocaine-inducedchest painFocus on Acute coronary syndromes Daniel Brouillard, R3 McGill Emergency Medicine December 12 2001

  2. Objectives • What is the prevalence of ACS/AMI in cocaine users? • What is the role of the EKG in the diagnosis of ACS in this particular patient population? • What is the most beneficial approach to management based on the current litterature? • What is the role of reperfusion therapy in these patients?

  3. Plan • Cocaine 2) Cocaine associated-C/P 3) Cocaine-related myocardial ischemia

  4. Cocaine • Erythroxylon coca • Benzoylmethylecgonine (cocaine) • Primarly grown in South America • Hydrochloride salt • « free base »

  5. History • 3000 B.C. Coca leaves are chewed in South America, believed to be a gift from God. • 1400’s Coca plantations operated by Incas. • 1662 First indepedent mention of coca in the English litterature: « A legend of Coca » by Abraham Coley. • 1850 Coca tinctures used in throat surgery. • 1855 Cocaine is first extracted from coca leaves. • 1870 Vin Mariani is for sale in Europe, in contains 6mg of cocaine per ounce of wine.

  6. History (continued) • 1884 Sigmund Freud publishes « On Coca » in witch he recommends the use of cocaine in the treatment of various conditions. • 1886 Introduction of Coca-Cola: contains cocaine syrup. • 1895 First cases of associated deaths reported in the Lancet. • 1912 5000 cocaine related fatalities per year • 1914 Harrison’s Narcotics Act • 1970’s -80’s Days of Glory • Mid-80’s Freebase cocaine( crack)

  7. . Presentation and pharmacology

  8. Onset and duration of action

  9. Effects 1) Sodium channel blocking properties (Quinidine-Like) 2) Systemically, blocks the re-uptake of amines in the synapse.

  10. Excretion • Metabolised by liver and plasma esterase • Ecgonyl methyl ester (30-50%) • Benzylecgonine (40%) • Detection possible in urine - Free cocaine : 6h - Benzylecgonine : up to 72 h.

  11. Cocaethylene • 2 substances often consummed together • Product of combination of cocaine and ET-OH in the liver. • Dose related myocardial depression in dogs. • Longer half life • Could account for delayed presentation.

  12. Part II

  13. Cocaine and people • 30 million American at least one time users • 5 million current users • 160,000 visits per year in the USA • Statistiques Canada 1994: close to 2% of Canadian population are current users

  14. Prevalence-Questions • In cocaine users who present to the ED, how many will have a major complaint of C/P ? • How many of these patients have ACS ? • How many of these patients have AMI ?

  15. Hollander and al. Annals of emergency medicine 1994 • Prevalence of cocaine use in patients older then 18 y presenting with C/P • 359 patients • Anonymous urine collection on everybody • Found 20 % prevalence in urban area • Prevalence of 7% at the rural sites • 28% of positives denied use when questioned

  16. Rich, Annals of EM, June 1991« Cocaine related Symptoms in patients presenting to the ED » • 146 patients • Retrospective chart review • Overall prevalence 16% for C/P (23 patients) • Total of 3 patients admitted • Stronger association with nasal route (11/23)

  17. Brody, Am. Journal of medicine, 1990« Cocaine-related medical problems » • 233 patients • Retrospective chart review • 40% prevalence of C/P • Most had acute complaints(3 h<) • Overall mortality 1%

  18. Cocaine related complaints

  19. Differential diagnosis • Cardiomyopathy • Myocarditis • Pulmonary embolus or thrombus • Pneumonia • Endocarditis • Aotic dissection • Pneumothorax, pneumopericardium, pneumomediastinum • ACS

  20. Differential diagnosis(2) • Most articles discuss the prevalence of AMI/ACS. • Case reports • Most C/P will, in the end, have a benign diagnosis.

  21. Prevalence studies-Cocaine MI

  22. Problems • Subjected to reporting bias • All studies done on inpatients. • No studies use Troponin. • Small amount of long term follow-up. • Population difficult to follow as outpatient

  23. AMI vs ACS • All studies essentially look at incidence of MI. Questions: • Acute event in a otherwise normal coronary? • Prevalence of actual CAD ? • Prevalence of Acute Coronary Syndromes? • Reversible ischemia?

  24. People with chest painUsers vs non-users • American Survey 1995-1996 • 4639 chest pain visits • In the general population( ages 25-40) • 5.6% of C/P in ED will be ACS • 2.5% prevalence of AMI Burt, Am. Jour. Of Emerg. Med, October 1999

  25. Epidemiology • High proportion is male ( 70-80%) • Mostly African-American • Median age : 35 yo • Cardiac risk similar vs control • High concommitant use of cigarettes • More likely to be admitted to ICU/CCU • Cost of 83 millions $$$$$$

  26. Dangers of body-packing

  27. Third Nationnal Health and Nutrition survey 10 085 patients aged 18-45 yo 731 infrequent users 532 frequent users ( about 5% of population) 46 non fatal MI’s HNADES III ’88-’94 Results: 1) OR 6.9 for frequent users. CI95% 1.3 to 58 2) OR 0.1 infrequent users. CI95% 0.002 to 0.8 *More smokers, HTN Frequent vs non-frequent users

  28. Time to presentation Mittleman and al., Circulation 99 • 3946 MI patients • 38 admitted to cocaine use • 9 within 1h of MI • 1within 2h of MI • 1 within 3h of MI • RR 23.7 in the first hour

  29. Prevalence of ACS • Feldman, Annals of emergency med. 1999 -241 patients over 2 years. - High risk (69) went directly to CCU. - Moderate and low risk had tehcnicium99 sestamibi done in the following 90 min. - 6 MI’s (6/218= 2.5%) or 8.7% of CCU patients - Stress studies on 70 patients: 6 reversible ischemia (6/67= 8.6%) at follow-up. - No recurrence at 30 days

  30. CAD vs Non-CAD events ? • Review articles : 31 to 67% have CAD. • Hollander , Meta-analysis, 1997 - 66 patients with cocaine-associated MI - Angio-proven CAD in 41% of patients - Presence of other risk factors NOT associated with greater incidence of CAD.

  31. Complications/ short term • Reported in the prospective studies: 5-10% • One study designed to look at complications: - Hoffman, Archives of internal med, 1995 - Retrospective study of 130 patients with MI. - 36% had complications - 90% within 12 h of presentation - 48% on arrival to the ED

  32. Complications

  33. Mortality • Feldman 2000 : 0% • Weber 2000: 0% • Hoffman 1995: 0% • Hollander 1994: 0% -No study reports death following arrival to the hospital.

  34. In summary • Up to 40% of cocaine-related complaints • Young population • Smokers • Delayed presentation • Frequent users are more at risk • Most complications occur within 12h • Very low mortality

  35. In summary(2) • 6% prevalence of AMI in most studies. • Prevalence of ACS is not known • Maybe close to 9-10% • 30 to 67% of these patients have CAD

  36. PART III

  37. Animal testing

  38. Part III Cocaine- related ACS • Pathophysiology • Diagnosis • Treatment • Conclusion

  39. Pathophysiology 1) Increased workload on the heart • Sympathomimetic state • Increased afterload • Increased myocardial O2 needs. Impact: Rise in BP of 20/10mmHg Rise in HR of 30 beats/min Equivalent to mild exercise at recretionnal doses. ( 2 mg/kg).

  40. Pathophysiology(2) • Coronary vasoconstriction • Most human studies use doses 2mg/kg 1-4 • Effect starts at 3-5 min Decrease in diameter of 4% to 29% • Effect is worse on diseased arteries. 5 • Presence of temporal variations • 1)Lange and al., N Engl J Med 1989;321:1557-62.2 )Flores ED, Am Coll Cardiol 1990;16:74-9.3)Molnerto DJ, N Engl J Med 1994;330:454-9. 4)Majid MJ, Clin Cardiol 1992;15:253-8.5)Daniel WC, Am J Cardiol 1996;78:288-91

  41. Pathophysiology(3) • Thrombosis and platelet aggregation. - Cocaine associated to thrombus in coronary arteries in some of the AMI cases. - Angiographic and pathologic evidence.1-4 - Mecanism is believed to be expression of thrombogenic substances in-situ 1)Simpson RW, Arch Pathol Lab Med 1986;110:479-84. 2)Cooke CT, Pathology 1988;20:242, 305-6 3)Patel GQ, Circulation 1988;78(II Suppl):II436 4)Steinberg RG,Arch Pathol Lab Med 1989;113:521-4

  42. Pathophysiology (4) • Accelerated intracoronary atherosclerosis - Wilson and al, J Emerg Med 1998;16:631-4. - Review of previous series and 2 new cases. #1 Significant LAD lesion over 10 months #2 Significant 3 vessel disease over 16 months - Rapid progression in chronic abusers. - Recurrence of ACS with continuous use.

  43. Pathophysiology

  44. Evaluation • History and physical examination. • EKG • Cardiac enzymes

  45. History and physical exam • Unable to differentiate between the various causes on the basis of the clinical evaluation. - Localisation - Quality - Associated symptoms - Pleuritic component * 28% of patients with MI had a pleuritic component. *Hofffman, Academic emergency med, 1994

  46. EKG • Primary determinent to thrombolysis in AMI. • Sensitivity: 54-89% ( 95% CI ) • Specificity: 67-96% Do these findings apply to cocaine-induced chest pain?

  47. EKG (2) • Gitter and al., Annals of int. Medicine, 1991 - Serie of 101 patients with cocaine-C/P - 43% met TIMI criteria for reperfusion. - NO AMI found • Tokarski, Ann. of emerg. Med, 1990 - Serie of 42 patients - All normal EKG’s - 19% of patients had CK-MB elevation

  48. EKG (3) • Pitfalls : - High prevalence of repolarisation abnormalities in young population. (BER). - Presence of repolarisation abnormalities in cocaine users without C/P. - Higher incidence of left ventricular hypertrophy in cocaine users.