Withdrawal states causing cardiomyopathy

• Introduction
  • Withdrawal states can have a wide range of cardiovascular and neurological signs and symptoms
  • While neurological findings such as agitation, seizures, or lethargy are often the predominant focus in management, cardiovascular changes can have significant implications on a patient’s clinical course
  • Cardiomyopathies, specifically stress-induced cardiomyopathy, can accompany withdrawal states from multiple agents
• Pathophysiology
  • Stress Induced Cardiomyopathy à Takotsubo Cardiomyopathy (TTC)
    
  • Transient LV dysfunction due to akinesia of midapical segments without primary coronary vessel pathology
    
  • Catecholamine toxicity leading to vasospasm of distal coronary arteries
    
  • Supraphysiologic levels of epi change function of myocyte beta receptors
    
  • Intracardiac gradient secondary to basal hypercontractility with LVOT obstruction causing           apical ischemia/wall stress

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• Offending Agents
  • EtOH Withdrawal
    •   Most common etiology of withdrawal induced cardiomyopathy
    •  Chronic EtOH use alters neurotransmitter and receptor biology
    •  Increasing insensitivity to GABA (tolerance) with a secondary increasing of the number of glutamate receptors to allow normal state of arousal in the setting of increased inhibitory  tone.
    • Sudden withdrawal of EtOH decreases inhibitory tone resulting in unopposed excitatory signaling from glutamate pathways
    • Peripherally presents as tremulousness and autonomic/sympathetic hyperactivity
  • Benzodiazepine withdrawal
    • TTC seen in few case reports following acute benzodiazepine withdrawal
    • Presumed similar mechanism to EtOH
  • Opioid withdrawal
    • Case reports after long acting opioid methadone
    • Sympathetic surge resulting in echocardiographic findings of TTC
  • Methamphetamine and cocaine cardiomyopathy
    • Seen during acute intoxication rather than withdrawal period
    • Adrenergic surge can cause TTC or can exacerbate underlying vascular disease
• Evaluation & Treatment
  • Patient may present with chest pain, shortness of breath, or other findings suggestive of LV failure
  • EKG can show nonspecific findings or anterior ST elevations with minor enzyme elevations
    • If there is concern for ACS PCI if available
    • If no critical coronary disease, ventriculogram may show characteristic shape
  • Echocardiogram with hyperactive basal segments and akinetic apex
  • Supportive Care
    • Ionotropic support if needed
    • Anticoagulation
    • Fluid balance management
    • Benzodiazepines, alpha-2 agents as tolerated
  • Symptoms often resolve spontaneously in 1-4 weeks 

 
 
References:
Stout BJ, Hoshide R, Vincent DS. Takotsubo Cardiomyopathy in the Setting of Acute Alcohol Withdrawal. Hawai’i Journal of Medicine & Public Health. 2012;71(7):193-194.
 
Peng TJ, Patchett ND, Bernard SA. Takotsubo Cardiomyopathy and Catatonia in the Setting of Benzodiazepine Withdrawal. Case Reports in Cardiology. 2016;2016:8153487. doi:10.1155/2016/8153487.
 
Spadotto V, Zorzi A, ElMaghawry M, Meggiolaro M, Pittoni GM. Heart failure due to “stress cardiomyopathy”: a severe manifestation of the opioid withdrawal syndrome. European Heart Journal Acute Cardiovascular Care. 2013;2(1):84-87. doi:10.1177/2048872612474923.

Authored by: Russell Trigonis, MD