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Cocaine induced myocardial ischemia

Cocaine induced myocardial ischemia. Sean Caine Grand Rounds Emergency Medicine October 16, 2008. Objectives. Epidemiology Pharmacology Review Pathophysiology of CIMI Diagnosis Disposition Management Summary. Epidemiology. In Alberta. 12.3% report use of cocaine/crack in lifetime 2

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Cocaine induced myocardial ischemia

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  1. Cocaine induced myocardial ischemia Sean Caine Grand Rounds Emergency Medicine October 16, 2008

  2. Objectives • Epidemiology • Pharmacology Review • Pathophysiology of CIMI • Diagnosis • Disposition • Management • Summary

  3. Epidemiology

  4. In Alberta • 12.3% report use of cocaine/crack in lifetime2 • Above the national average of 10.6% • 2.4% of patients report using in past year2 • Steadily trending upward: • 1.3% (1994) • 1.1% (1989) • Average age of 1st use is 23.81

  5. Epidemiology

  6. Cocaine and the ED • Detected in 25% of adults age 15-44 suffering fatal injuries7 • Cocaine is second only to alcohol for acute drug related ED visits • 2% of pts over age 60 tested positive for cocaine at an inner city ED

  7. Rates of ED visits for selected illicit drugs: 2005

  8. Epidemiology • ED visits for cocaine related phenomenon include: Psychiatric Neurologic Cardiac Pulmonary Trauma Addiction-related symtoms/comlaints Infectious Disease Obstetric/Gynecology Genitourinary MSK • Chest pain is the most common presenting complaint of cocaine users in the ED • CP accounts for 20-40% of presenting complaints among cocaine users in the ED4,5

  9. Pharmacology

  10. Cocaine (benzoylmethylecgonine) • Alkaloid from Erythroxylon coca plant • Crystalloid form created by dissolving alkaloid in hydrochloric acid • Crack cocaine is an unpurified free base • “rocks” are obtained from combining cocaine HCl with a base (NaHCO3) and cooking in water • Free Base is an ether extracted purified form of Crack

  11. Cocaine Pharmacology by Route of Administration Modified from Rosen’s Emergency Medicine6 and Levis and Garmel3

  12. Metabolism Ecgonine methylester 30-50% plasma cholinesterase DETECTED IN URINE TOX SCREEN Cocaine (Benzoylmethylecgonine) 40% Benzoylecgonine Non-enzymatic hydolysis • Minor metabolites: • Norcocaine • Ecgonine

  13. Na fast channel moderate blocked 5HT and DA: Inhibits reuptake Vagal nuclei: Direct stimulation (brief) NE and E: Increased presynaptic release Reuptake inhibition Mechanism of Action

  14. Sympathomimetic toxidrome Hypertension Tachycardia Mydriasis Diaphoresis Hyperthermia CNS excitation/aggitation

  15. Cocaine Induced Myocardial Ischemia

  16. Case… 26 yo male. Works in Fort McMurray. Back in Calgary for the weekend. Reports new onset CP after using cocaine.

  17. Noncardiac Pneumothorax Pneumomediastinum Pneumopericardium   Aortic dissection    Pulmonary infarction    Infection   MSK Asthma Pneumonitis  Cardiac chest pain    Endocarditis Pericarditis Ischemia/infarction During acute intoxication   After acute intoxication DDx of chest pain

  18. Cocaine Induced Myocardial Ischemia • 25% of non-fatal MIs btwn age 18-45 are attributable to frequent cocaine use9 • Cocaine-associated CP has a 57% admission rate10 • 5.7% of pts presenting with cocaine-associated CP will have a MI documented by elevated cadiac enzymes11 • Large clinical trials have demonstrated that only 31-67% of cocaine associated MI have atherosclerotic CAD12,13 • Risk of AMI is same for all routes of administration15

  19. MI can occur with minutes to days following cocaine use Risk of MI is highest within 1 hours Risk of MI after cocaine use Mittleman, Mintzer, Maclure. Circulation. 199914

  20. Pathophysiology of cocaine associated myocardial ischemia

  21. mediated by α-adrenergic receptor stimulation and impaired endothelial dysfunction Human studies show decreases of 8-12% of left coronary artery diameter with doses smaller than typical recreational use17 33%-46% decreases in LAD artery diameter has been demonstrated in animal studies16 This effect further potentiated by presence of cigarette smoking and pre-existing CAD15 Vasoconstriction can be prolonged with co-ingestion of ethanol due to formation of cocaethylene Coronary vasoconstriction and spasm

  22. Increased myocardial oxygen demand • Cardiac workload is increased due to increased HR and systemic arterial pressures • Negative inotropy also demonstrated in human in vitro studies BOTTOM LINE = the heart is beating FASTER and LESS EFFICIENTLY against GREATER RESISTANCE

  23. In vitro studies have demonstrated: ↑ platelet activation ↑platelet aggregation ↑thromboxane production Endothelial dysfunction Increased fibrin deposition Thrombogenesis

  24. Noted commonly among cocaine users undergoing angiography 34% of cocaine users vs 7.6% of control pts Coronary Aneurysms Angiogram of a 49 yo male with history of cocaine use. Arrows show a right coronary artery aneurysm. New York Times May 10, 2005

  25. Chronic use… • Spont ischemic episodes during withdrawal • Accelerated atherosclerosis • Left ventricular hypertrophy • Systolic dysfunction • Dilated cardiomyopathy

  26. Jones and Weir. Med Clin N AM. 200515

  27. Diagnosis

  28. 26 yo male. New onset CP 2 hours after snorting a line. Investigations?

  29. Diagnostic Challenge Difficulty of diagnosis highlighted by high admission rate (57%)10 cocaine- associated chest despite low rate of MI (6%)11

  30. Diagnostic Challenge • Patient factors • 25% pts will initially deny use of cocaine19 • Delayed presentation • 19% pts present >24hrs after onset of CP11

  31. ECG • Decreased sensitivity to detect MI11 • Sensitivity: 35.7% • NPV: 95.8% • pts with CAMI are as likely to present with normal or nonspecific changes as they are with ischemic changes • Higher ED miss rate. With 15% of pts with MI discharged home • Increased FP due to presence of LVH and BER11 • Specificity: 89.9% • PPV: 17.9%

  32. Cardiac Enzymes • CK & CKMB • Decreased sensitivity due to skeletal muscle injury and rhabdo • Approx 50% of pts with cocaine-associated CP will have elevated CK • CKMB index calculations are distorted in presence of rhabdo • Rising serum enzyme more concerning • Troponin • Troponin I specificity (95%) is comparable to noncocaine using population • Preferred cardiac marker for ischemia/infarct in setting of cocaine associated MI

  33. 26 yo male with cocaine-associated CP. Initial ECG shows BER. Initial troponin is normal. Chest pain continues.

  34. Management • ASA • Benzodiazepines • Decrease central stimulatory effects and aggitation • Decrease myocardial O2 demand • Shown to decrease HR and BP • Nitrates • Decrease cocaine induced vasoconstriction in pts with CAD • Reduced cocaine-associated CP for 45% of pts20

  35. Management • Phentolamine • Nonselective alpha antagonist • Shown to reverse cocaine induced coronary vasocontriction in humans17 • Suggested careful titration 1mg IV q5min • Onset is immediate. • Duration 15-30min • CI: coronary or cerebral arteriosclerosis, phosphodiesterase inhibitors (ie Sildenifil), hypersensitivy

  36. Management • CCB • Less thoroughly evaluated • Small study of 10 human volunteers showed verapamil relieved cocaine-induced vasospasm

  37. Managment • Unfractionated Heparin or LMWH • Not well studied • Reasonable to give if no clear contraindication

  38. Management • PCI for cocaine-induced MI • Preferred intervention • Provides means of diagnosing underlying etiology (ie vasospasm vs. thrombus) • Perception of being more safe than lytics in due to case reports of pts w/ICH and aortic dissection

  39. Management • Thrombolytics • Not well studied • Only if PCI not readily available • Pts at increased risk for aortic dissection and ICH

  40. The β-blocker controversy

  41. β-blockers • ACC/AHA guidelines: “Beta-blockers should not be administered to patients with STEMI precipitated by cocaine because of risk of exacerbating coronary spasm” • RDBPCT showed proponolol increased coronary artery resistance and decreased coronary sinus flow21 • Labetolol unlikely to offer any benefit and potentially harmful • Inceases seizures and death in animal models12 • Did not reverse vasoconstriction in human studies12

  42. Dattilo et al. Annals of Emergency Medicine. 2008; 51(2): 117-125 • Retrospective cohort study of 363 consecutive pts admitted to ICU or telemetry with positive urine tox • Β-blockers given to 60 of 348 admission • Reports lower rate of MI (6% vs 26%) and death (1.7% and 4.5%) among pts given B-blockers

  43. Dattilo et al. Annals of Emergency Medicine. 2008; 51(2): 117-125 • Results have been heavily scrutinized • Unclear when β-blockers were given during admission • Large differences in baseline characteristics btwn cohorts • Greater number of asthmatics among control cohort • Greater proportion of B-blocker cohort were male, had higher Cr, and had hx CHF, CAD • Severe limitations with MI cohort. • Only 55% of β-blocker cohort had troponin measured vs. 96% • 31/33 pts were given B-blocker after an MI • Only 2 given B blocker – both of home had an MI

  44. Management Summary

  45. Disposition

  46. 26 yo male. Cocaine associated CP. Initial ECG was normal. CP resolved after one hour after given nitro spray x 3 and IV lorazepam. Rpt ECG and troponin normal.

  47. Prospective evaluation of 9-12 hour observation of 302 low/intermediate risk pts with cocaine associated CP Cocaine use confirmed by urine tox Discharge criteria: normal troponin, no new ischemic ECG changes CV complications (dysrhythmia, AMI, or recurrent symptoms) All had follow up w/internist or cardiologist within 48hrs

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