Although using cocaine on a regular basis is tied to a high risk of coronary artery disease, stopping or reducing its use can potentially reverse the disease process, according to a new study published in the Journal of Addiction Medicine.
“In the past, there has been excellent work to uncover the consequences of drug use,” said Dr. Shenghan Lai of Johns Hopkins School of Medicine, Baltimore. “However, few studies have revealed what happens after drug use stops. Studies of this kind give people hope for a healthier life after stopping drug use.”
In particular, the findings show that cutting back on cocaine use leads to the regression of unstable, noncalcified coronary plaques — the type most likely to cause a heart attack or stroke.
Since 2000, the research team has been studying the development of coronary atherosclerosis (hardening of the arteries) in more than 700 African-American patients who were regular cocaine users. The researchers took advantage of previous research showing that a cash incentive program helps patients quit using cocaine, or at least use it less often.
According to their findings, regular cocaine users who cut back showed decreased levels of endothelin-1 (ET-1) — an inflammation-promoting protein that plays a key role in the development of coronary artery disease.
For the new study, the researchers wanted to know whether the drop in ET-1 could lead to reductions in cocaine-induced coronary artery disease. To find out, they conducted a follow-up study in 15 patients who had been using cocaine for an average of 20 years and also had atherosclerosis that was causing more than 50 percent blockage of their coronary arteries. Using imaging scans (CT angiography), the researchers measured the amount and types of coronary plaques, before and after reductions in cocaine use.
As previously reported, the incentive program helped participants decrease their use — from using every day before the program to an average of 50 days during one year of follow-up. Levels of ET-1 and other markers of inflammation decreased as well.
Reduced cocaine use was followed by regression of atherosclerotic plaques in the coronary arteries. The reduction was significant not only for total coronary plaques, but also for noncalcified plaques — the first step in the development of coronary atherosclerosis. Noncalcified plaques are considered unstable or “vulnerable.” Compared to calcified plaques that develop later, they are more likely to rupture and cause heart attack or stroke.
The reductions in coronary plaque remained strong even after the researchers adjusted for other cardiovascular risk factors. In particular, coronary artery disease still regressed even though the patients were not taking cholesterol-lowering “statin” drugs.
Cocaine use remains epidemic in the United States — a 2013 report suggested that there are 1.5 million Americans, or about 0.6 percent of the population, who use cocaine.
“This preliminary study demonstrates potentially beneficial effects of cocaine abstinence/reduction on inflammation and coronary plaque phenotype,” said Lai and coauthors in the paper. While it is unclear how reduced cocaine use leads to regression of coronary artery disease, “Inflammation appears to be a significant link.”
“The findings… may have important implications for the prevention of cocaine-induced coronary artery disease,” the researchers conclude. Since many of the participants were also HIV-positive, the study might also be relevant to people with HIV infection, a population that is already at higher risk for coronary artery disease.
Source: Wolters Kluwer Health