Coronary Plaque Progression and Regression in Asymptomatic African American Chronic Cocaine Users With Obstructive Coronary Stenoses: A Preliminary Study

Abstract

Objective 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 coronary plaque regression in cocaine users. Methods Fifteen African American chronic cocaine users with previously coronary CT 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 (pre-intervention), CCTA was performed at the intervention baseline and post-intervention. Plaque analyses were performed to determine (1) the trajectory of plaque changes in the absence of intervention by comparing the pre-intervention to the intervention baseline studies, and (2) the trajectory of plaque changes associated with the intervention by comparing the intervention baseline to the post-intervention studies, and (3) whether reduced cocaine use was independently associated with changes in coronary plaque burden. Results During the 12-month cash-based incentive intervention period, cocaine use in participants was lower. The medians of noncalcified plaque indices were 37.8(IQR:29.3–44.0),43.1(IQR:38.3–49.0), and 38.7(IQR:31.2–46.8) mm2 at pre-intervention, intervention baseline and post-intervention, respectively. Multivariable generalized estimating equation analysis showed that (1) both total plaque and noncalcified plaque indices at pre-intervention were significantly lowered as compared with intervention baseline levels, (2) both total plaque and noncalcified plaque indices after intervention were significantly lowered as compared with intervention baseline levels, and (3) reduced cocaine use was independently associated with lower total plaque volume index (P<0.0001) and noncalcified plaque volume index (P=0.010). Conclusions Our findings suggest that continued cocaine use may be associated with noncalcified plaque progression while reduced cocaine use may be associated with noncalcified plaque regression. Larger studies are needed to confirm these findings.

Cocaine use modifies the association between antiretroviral therapy and endothelial dysfunction among adults with HIV infection

“…Although existing studies have indicated the adverse impact of cocaine use on endothelial function, the molecular mechanisms that underlie the intervening effects of cocaine use on NNRTIs and their associated endothelial dysfunction need a further investigation. Our prior research has detected the association of cocaine use with endothelial damage measured as elevated ET‐1 concentrations and observed noncalcified plaque regression at 12‐month follow‐up in cocaine users who reduced their cocaine use . In human aortic endothelial cells, long‐term exposure to cocaine suppressed NO production and endothelial NO‐synthase expression .…”

“…In human aortic endothelial cells, long‐term exposure to cocaine suppressed NO production and endothelial NO‐synthase expression . Cocaine use may also increase the concentrations of inflammation biomarkers, such as C‐reactive protein (CRP) and serum amyloid A . Systematic inflammation levels in HIV‐infected people may be reduced by ART regiments including NNRTIs but remain higher than those in HIV‐negative counterparts .…”

Unintentional drug overdose deaths involving cocaine among middle-aged and older adults in New York City

“…Recent data show high rates of premature heart disease and stroke deaths among Black males in New York City ages 18 to 65 with high rates in several neighborhoods in the Bronx (NYCDOHMH, 2017c). Given cocaine's association with myocardial injury and vascular events, including coronary plaque progression (Sandfort et al, 2017), it is not surprising to find high rates of cocaine involved overdoses in populations with high rates of underlying cardiovascular and cerebrovascular disease. However, this study cannot delineate the role of underlying cardiovascular diseases among the decedents of this study, especially in the setting of other substances present on toxicology.…”

Cocaine use may induce telomere shortening in individuals with HIV infection

“…Taken together, these studies consistently suggest that (1) although ART substantially reduces HIV/AIDS-related mortality, long-term exposure to ART may be associated with comorbidities, including subclinical atherosclerosis, myocardial and hepatic steatosis, and telomere shortening, and (2) these ART-associated comorbidities could potentially be reduced or minimized in cocaine users with HIV infection if cocaine abstinence or even reduced use could be achieved. Although cocaine is highly addictive, we have demonstrated that cocaine abstinence or reduced use can be achieved with the use of a cash-based incentive intervention, and that cocaine abstinence or reduced use lowers a marker of endothelial dysfunction and is associated with coronary plaque regression (Lai, et al, 2015; Sandfort, et al, 2017). Despite the absence of FDA-approved medications for cocaine dependence, several candidate medications have demonstrated promising results in clinical trials (Kampman, 2009; Kampman, et al, 2015; Nuijten, et al, 2016).…”