Cardiovascular Complications of Cocaine Abuse

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Cardiovascular Complications of Cocaine Abuse

• Payal Nanda
• Scotty Gadlin
• Ken Arney
• (aka Night Floaticians)

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Introduction

• Cocaine is the 2nd most commonly used illicit
  drug in the U.S.
• In 2005, there were 450,000 cocaine-related ED
  visits with 40 due to chest pain.
• Even casual use of cocaine is associated with
  cardiovascular toxicity.
• Cocaine use is associated with acute more often
  than chronic cardiovascular illness.
• Cocaine users can present with ACS, arrhythmias,
  myocarditis, aortic dissection and rupture, and
  hypertensive emergency.
• Therefore, identifying cocaine exposure is an
  important part of cardiovascular history-taking.

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Cardiovascular Effects of Cocaine

• The major cardiovascular effects of cocaine are
  caused by inhibition of norepinephrine/dopamine
  reuptake into the synaptic cleft by sympathetic
  neurons.
• This inhibition results in potentiation of the
  response to sympathetic stimulation of innervated
  organs, causing a powerful sympathomimetic
  response.
• Also enhances the release of catecholamines from
  central and peripheral stores.
• Cocaine also promotes thrombus formation via
  activation of platelets and stimulation of
  platelet aggregability.

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Cardiovascular Conditions Associated with Cocaine
Use

• Myocardial ischemia/infarction
• Cardiomyopathy
• Myocarditis
• Arrhythmias
• Stroke
• Aortic dissection
• Coronary artery aneurysms

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Myocardial Ischemia

• Most common complication associated with all
  routes of cocaine intake
• Three proposed mechanisms
• Increased myocardial oxygen demand
• Resulting from sympathomimetic actions of cocaine
  that increase myocardial inotropy, heart rate,
  and BP in dose-dependent manner
• Exacerbated by underlying CAD (e.g. fixed
  stenoses)
• Coronary vasoconstriction and spasm ? decreased
  oxygen
• Cocaine constricts coronary vessels via
  stimulation of alpha-adrenergic receptors,
  increased endothelin-1, and decreased NO
• Coronary thrombosis
• Platelet activation/aggregation and premature
  atherosclerosis
• Most patients have no other cardiac risk factors

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Myocardial Infarction

• Incidence of MI in cocaine-related chest pain is
  0.5-5.7
• Increased incidence in younger patients
• NHANES III study 25 of nonfatal MIs were
  between ages of 18-45
• MI is temporally related to cocaine use two
  thirds of cases occur within 3 hours.
• Most MIs occur in absence of high-grade
  atherosclerotic coronary stenoses.
• Complications post-MI include heart failure and
  ventricular/supraventricular arrhythmias,
  typically occurring within first 12 hours (same
  as in non-cocaine induced infarctions).

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Relative Risk of MI Onset After Cocaine Use
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Cardiomyopathy

• Dilated CM is well-documented among cocaine
  users.
• Pathogenesis
• Direct toxic effects on the heart, which lead to
  the destruction of myofibrils, interstitial
  fibrosis, myocardial dilation, and heart failure
• Hyperadrenergic state may produce contraction
  band necrosis in the heart
• Myocarditis and CM may be caused by infectious
  agents in patients who abuse cocaine parenterally
  via direct invasion of myocardium or stimulation
  of an autoimmune reaction
• Abstinence usually leads to complete reversal of
  myocardial dysfunction.

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Arrhythmias

• Hyperadrenergic state can produce or exacerbate
  arrhythmias.
• Cocaine acts like a class I anti-arrhythmic
  agent, producing local anesthetic effects via
  sodium channel blockade in the heart.
• Sinus tachycardia/bradycardia
• Bundle branch block
• Vfib/Vtach/asystole
• Accelerated idioventricular rhythms
• SVTs
• Torsades de pointe
• Brugada pattern on EKG
• Rhythm disturbances are transient and disappear
  when the drug is metabolized.

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Stroke

• Cocaine use significantly increases the risk of
  ischemic stroke via vasospasm from dopamine
  release, thrombus formation, and changes in
  cerebral vasculature (vasculitis).
• Subtle and severe neurologic deficits can occur
• Repetitive ischemic insults can lead to
  intracerebral and subarachnoid hemorrhage

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Diagnosis

• Hx and physical exam
• Young patient with hx of cocaine or polysubstance
  abuse who presents with chest pain, dyspnea,
  palpitations, agitation, or nausea
• Usually no other cardiac risk factors
• Toxicology screen
• EKG STEMI, T-wave changes, arrhythmias, LVH, LAD
• Difficult to interpret in young patients who have
  a relatively high incidence of early
  repolarization changes and left ventricular
  hypertrophy.
• Up to 43 of cocaine abusers without an MI may
  have ST segment elevation 0.1 mV in two or more
  contiguous ECG leads.
• Because of the difficulty in identifying cocaine
  users with chest pain who are at low risk of
  infarction, most are admitted to the hospital.
• Serum markers Troponins and CK-MB most sensitive
  and specific in cocaine-related MI

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Management
There are no well-designed, randomized,
prospective clinical trials to compare treatment
strategies for cocaine-associated myocardial
ischemia
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The Beta-Blocker Controversy

• Beta Blockers for Chest Pain Associated With
  Recent Cocaine Use
• Rangel, et.al. Archives of Internal Medicine
  2010.
• Retrospective study of consecutive patients
  admitted to San Francisco General Hospital
  between 2001-2006.
• Chest pain and urine toxicology positive for
  cocaine
• The primary predictor was receipt of a B-blocker
  in the ED, and the primary outcome was death.
• Treatment of chest pain in the setting of recent
  cocaine use was not dictated by any established
  protocol, and B-blocker use was determined by the
  discretion of the treating physicians.
• 151 patients received B-blockers IV metoprolol
  in 113 (74), oral metoprolol in 17 (11) the
  rest received labetalol, atenolol, or
  propranolol.
• There were no meaningful differences in EKG
  changes, troponin levels, length of stay, use of
  vasopressor agents, intubation, ventricular
  tachycardia/ventricular fibrillation, or death
  between those who did and did not receive a
  B-blocker.
• B-Blockers did not appear to be associated with
  adverse events in patients with chest pain with
  recent cocaine use.
• Over a median follow-up of 972 days, patients
  discharged on a beta-blocker regimen exhibited a
  significant reduction in cardiovascular death.

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Outcomes with Beta-Blockers in Cocaine-Associated
Chest Pain
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Where the Crack At?
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References

• McCord, et.al. Management of Cocaine-Associated
  Chest Pain and Myocardial Infarction A
  Scientific Statement From the American Heart
  Association Acute Cardiac Care Committee of the
  Council Clinical Cardiology. Circulation 2008.
• Rangel, et.al. Beta-blockers for Chest Pain
  Associated with Recent Cocaine Use. Arch Intern
  Med. 2010. 170(10)874-879
• UpToDate