Transcript Cardiovascular Complications of Cocaine Abuse

Cardiovascular Complications
of Cocaine Abuse
Payal Nanda
Scotty Gadlin
Ken Arney
(aka Night Floaticians)
Introduction
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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.
Cardiovascular Effects of Cocaine
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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.
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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.
Cardiovascular Conditions Associated with
Cocaine Use
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Myocardial ischemia/infarction
Cardiomyopathy
Myocarditis
Arrhythmias
Stroke
Aortic dissection
Coronary artery aneurysms
Myocardial Ischemia
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Most common complication; associated with all routes of
cocaine intake
Three proposed mechanisms:
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Increased myocardial oxygen demand
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Resulting from sympathomimetic actions of cocaine that increase
myocardial inotropy, heart rate, and BP in dose-dependent
manner
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Exacerbated by underlying CAD (e.g. fixed stenoses)
Coronary vasoconstriction and spasm  decreased oxygen
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Cocaine constricts coronary vessels via stimulation of alphaadrenergic receptors, increased endothelin-1, and decreased NO
Coronary thrombosis
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Platelet activation/aggregation and premature atherosclerosis
Most patients have no other cardiac risk factors
Myocardial Infarction
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Incidence of MI in cocaine-related chest pain is 0.5-5.7%
Increased incidence in younger patients
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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).
Relative Risk of MI Onset After Cocaine
Use
Cardiomyopathy
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Dilated CM is well-documented among cocaine users.
Pathogenesis:
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Direct toxic effects on the heart, which lead to the destruction of
myofibrils, interstitial fibrosis, myocardial dilation, and heart failure
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Hyperadrenergic state may produce contraction band necrosis in the
heart
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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.
Arrhythmias
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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.
Stroke
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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
Diagnosis
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Hx and physical exam:
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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
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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
Management
There are no well-designed, randomized, prospective clinical trials to compare treatment
strategies for cocaine-associated myocardial ischemia
The Beta-Blocker Controversy
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Beta Blockers for Chest Pain Associated With Recent Cocaine Use
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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.
Outcomes with Beta-Blockers in CocaineAssociated Chest Pain
Where the Crack At?
References
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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
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