Sandfort Veit, Bluemke David A, Vargas Jose, Brinker Jeffrey A, Gerstenblith Gary, Kickler Thomas, Zheng Gang, Li Ji, Chen Shaoguang, Lai Hong, Fishman Elliot K, Lai Shenghan
Department of Radiology and Imaging Sciences (VS, DAB, JV), National Institutes of Health Clinical, Center, Bethesda; Department of Radiology (DAB, HL, EKF, SL), Johns Hopkins School of Medicine, Baltimore, MD; MedStar Health Research Institute (JV), Georgetown University Hospital, Washington, DC; Department of Medicine (JAB, GG, SL); and Department of Pathology (TK, GZ, JL, SC, SL), Johns Hopkins School of Medicine, Baltimore, MD.
J Addict Med. 2017 Mar/Apr;11(2):126-137. doi: 10.1097/ADM.0000000000000282.
Although rapid progression of coronary atherosclerosis was observed in chronic cocaine users, it is unknown whether reduced cocaine use retards the progression of atherosclerosis. We investigated whether reduced cocaine use over a 12-month period was associated with coronary plaque regression in cocaine users.
Fifteen African American chronic cocaine users with previously coronary computed tomography angiography (CCTA)-confirmed >50% coronary stenosis in Baltimore, Maryland, were enrolled in a study to investigate whether reduced cocaine use is associated with changes in coronary plaque burden over a 12-month period of cash-based incentive intervention, which was implemented to systematically reinforce cocaine abstinence. In addition to previous CCTA (preintervention), CCTA was performed at the intervention baseline and at postintervention. Plaque analyses were performed to determine the trajectory of plaque changes in the absence of intervention by comparing the preintervention with the intervention baseline studies; the trajectory of plaque changes associated with the intervention by comparing the intervention baseline with the postintervention studies; and (3) whether reduced cocaine use was independently associated with changes in coronary plaque burden.
During the 12-month cash-based incentive intervention period, cocaine use in participants was lower. The medians of noncalcified plaque indices were 37.8 (interquartile range [IQR] 29.3-44.0), 43.1 (IQR 38.3-49.0), and 38.7 (IQR 31.2-46.8) mm at preintervention, intervention baseline, and postintervention, respectively. Multivariable generalized estimating equation analysis showed that both total plaque and noncalcified plaque indices at preintervention were significantly lowered as compared with intervention baseline levels; both total plaque and noncalcified plaque indices after intervention were significantly lowered as compared with intervention baseline levels; and reduced cocaine use was independently associated with lower total plaque volume index (P < 0.0001) and noncalcified plaque volume index (P = 0.010).
Our findings suggest that continued cocaine use may be associated with noncalcified plaque progression, whereas reduced cocaine use may be associated with noncalcified plaque regression. Larger studies are needed to confirm these findings.
尽管在慢性可卡因使用者中观察到冠状动脉粥样硬化进展迅速，但减少可卡因使用是否会延缓动脉粥样硬化进展尚不清楚。我们调查了在12个月期间减少可卡因使用是否与可卡因使用者的冠状动脉斑块消退有关。
15名非裔美国慢性可卡因使用者，他们之前在马里兰州巴尔的摩经冠状动脉计算机断层扫描血管造影（CCTA）证实冠状动脉狭窄>50%，被纳入一项研究，以调查在为期12个月的现金激励干预期间减少可卡因使用是否与冠状动脉斑块负担变化有关，该干预旨在系统强化可卡因戒断。除了之前的CCTA（干预前），在干预基线和干预后均进行了CCTA。通过比较干预前与干预基线研究来确定无干预情况下斑块变化的轨迹；通过比较干预基线与干预后研究来确定与干预相关的斑块变化轨迹；以及（3）减少可卡因使用是否与冠状动脉斑块负担变化独立相关。
在为期12个月的现金激励干预期间，参与者的可卡因使用量较低。非钙化斑块指数的中位数在干预前、干预基线和干预后分别为37.8（四分位间距[IQR]29.3 - 44.0）、43.1（IQR 38.3 - 49.0）和38.7（IQR 31.2 - 46.8）mm。多变量广义估计方程分析显示，与干预基线水平相比，干预前的总斑块和非钙化斑块指数均显著降低；与干预基线水平相比，干预后的总斑块和非钙化斑块指数均显著降低；减少可卡因使用与较低的总斑块体积指数（P<0.0001）和非钙化斑块体积指数（P = 0.010）独立相关。
我们的研究结果表明，持续使用可卡因可能与非钙化斑块进展有关，而减少可卡因使用可能与非钙化斑块消退有关。需要更大规模的研究来证实这些发现。
