Vascular disease in cocaine addiction


      • Cocaine induces immune responses including cytokine elevations. Chronic cocaine use is associated with functional brain impairments potentially mediated by vascular pathology. Paradoxically, during the period when prevention efforts could make a difference, this population receives psychosocial treatment at best.
      • We review major findings of cocaine-induced vasoconstriction, endothelial dysfunction, and accelerated atherosclerosis, emphasizing acute, chronic, and secondary effects of cocaine.
      • Given the known vascular toxicity cocaine induces further compounded by smoking and alcohol comorbidity and interacting with the progressing age of the crack generation, there is a public health imperative to identify pre-symptomatic markers of vascular impairments in cocaine addiction.


      Cocaine, a powerful vasoconstrictor, induces immune responses including cytokine elevations. Chronic cocaine use is associated with functional brain impairments potentially mediated by vascular pathology. Although the Crack-Cocaine epidemic has declined, its vascular consequences are increasingly becoming evident among individuals with cocaine use disorder of that period, now aging. Paradoxically, during the period when prevention efforts could make a difference, this population receives psychosocial treatment at best.
      We review major postmortem and in vitro studies documenting cocaine-induced vascular toxicity. PubMed and Academic Search Complete were used with relevant terms.
      Findings consist of the major mechanisms of cocaine-induced vasoconstriction, endothelial dysfunction, and accelerated atherosclerosis, emphasizing acute, chronic, and secondary effects of cocaine. The etiology underlying cocaine's acute and chronic vascular effects is multifactorial, spanning hypertension, impaired homeostasis and platelet function, thrombosis, thromboembolism, and alterations in blood flow. Early detection of vascular disease in cocaine addiction by multimodality imaging is discussed. Treatment may be similar to indications in patients with traditional risk-factors, with few exceptions such as enhanced supportive care and use of benzodiazepines and phentolamine for sedation, and avoiding β-blockers.
      Given the vascular toxicity cocaine induces, further compounded by smoking and alcohol comorbidity, and interacting with aging of the crack generation, there is a public health imperative to identify pre-symptomatic markers of vascular impairments in cocaine addiction and employ preventive treatment to reduce silent disease progression.



      CUD (cocaine use disorder), MRI (magnetic resonance imaging), PET (positron emission tomography), CT (computed tomography), CBF (cerebral blood flow), 18F-FDG (18F-fluorodeoxyglucose)
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      Linked Article

      • Reply to: “β-blocker treatment of vascular disease in cocaine addiction”
        AtherosclerosisVol. 264
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          In his Letter to the Editor, John R. Richards suggested that our statements regarding the use of β-blockers [1] are “incorrect and should be discussed further and amended to reflect modern-day evidence”. Richards and colleagues (2016) performed an extensive systematic review on the pharmacologic treatment of cocaine cardiovascular toxicity and determined β-blockers were safe and effective, especially for concomitant cocaine-induced hypertension and tachycardia [2].
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      • β-blocker treatment of vascular disease in cocaine addiction
        AtherosclerosisVol. 264
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          I appreciated the article by Bachi and colleagues regarding vascular disease in cocaine addiction [1]. However, their statements regarding the use of β-blockers are incorrect and should be discussed further and amended to reflect modern-day evidence. In the abstract, the authors write “Treatment for cocaine-induced acute vascular events may be similar to indications in patients with traditional risk-factors, with few exceptions. For example, enhanced supportive care and use of benzodiazepines and phentolamine for sedation, and avoiding β-blockers, which can lead to severe hypertension and coronary vasoconstriction resulting from the interaction of β-blockers with cocaine.” with an outdated supporting reference [2].
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