Bachi Keren, Mani Venkatesh, Jeyachandran Devi, Fayad Zahi A, Goldstein Rita Z, Alia-Klein Nelly
Brain Imaging Center (BIC), Psychiatry and Neuroscience, Icahn School of Medicine at Mount Sinai, One Gustave L. Levy Place, New York, NY 10029, USA.
Translational Molecular Imaging Institute (TMII), Icahn School of Medicine at Mount Sinai, One Gustave L. Levy Place, New York, NY 10029, USA.
Atherosclerosis. 2017 Jul;262:154-162. doi: 10.1016/j.atherosclerosis.2017.03.019. Epub 2017 Mar 14.
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.
可卡因是一种强效血管收缩剂，可引发包括细胞因子升高在内的免疫反应。长期使用可卡因与可能由血管病变介导的脑功能损害有关。尽管快克可卡因的流行已有所下降，但其血管方面的后果在那段时期患有可卡因使用障碍且现已步入老年的人群中日益明显。矛盾的是，在预防措施可能产生作用的时期，这一人群至多只能接受心理社会治疗。我们回顾了记录可卡因诱发血管毒性的主要尸检和体外研究。使用PubMed和Academic Search Complete数据库及相关检索词进行检索。研究结果包括可卡因诱发血管收缩、内皮功能障碍和加速动脉粥样硬化的主要机制，重点阐述了可卡因的急性、慢性及继发效应。可卡因急性和慢性血管效应的潜在病因是多因素的，包括高血压、内环境稳态受损、血小板功能异常、血栓形成、血栓栓塞以及血流改变。文中还讨论了通过多模态成像早期检测可卡因成瘾者血管疾病的方法。治疗可能与具有传统风险因素患者的治疗指征相似，少数情况除外，如加强支持治疗、使用苯二氮䓬类药物和酚妥拉明进行镇静，以及避免使用β受体阻滞剂。鉴于可卡因诱发的血管毒性，再加上吸烟和酒精合并使用的影响，以及与快克一代人群老龄化的相互作用，识别可卡因成瘾中血管损伤的症状前标志物并采用预防性治疗以减少无症状疾病进展，已成为一项公共卫生要务。
