Cocaine’s heart-damaging effects likely immediate
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California researchers have found no link between cocaine use and hardening of the arteries in a study of more than 3,000 adults. The findings suggest that the drug’s heart-damaging effects likely occur immediately after use, and do not result from any long-term effects, Dr. Mark Pletcher of the University of California at San Francisco, the study’s lead author, told Reuters Health.
Cocaine use is known to boost heart rate and blood pressure, and has been firmly linked to heart attacks and sudden death, Pletcher and his colleagues write in the American Heart Journal.
But it’s not clear whether using the drug regularly may cause additional harm to the heart and blood vessels, they add. “It has been shown to trigger heart attacks in the short term but there’s been a lot of speculation about how it may also cause atherosclerosis when used chronically,” the researcher said in an interview.
To investigate, Pletcher and his team looked at whether there was any connection between arterial calcium deposits as measured by a scanning technique called computed tomography and reported drug use among 3,038 patients participating in the Coronary Artery Risk Development in Young Adults study. Such calcium deposits are a well-established marker for atherosclerosis, the stiffening of the arteries that increases the risk of heart attack and other cardiovascular problems.
Study participants ranged in age from 35 to 45. Fifty-five percent were female, and 45 percent were black. Thirty-five percent reported having used cocaine in the past.
While cocaine use was linked to coronary calcification on the first analysis of the information, after the researchers adjusted for smoking, male sex, and alcohol use and other factors associated with both cocaine use and atherosclerosis, there was no significant link.
The researchers conclude: “It is likely that previously observed associations between cocaine use and coronary heart disease are explained by the well-documented acute effects of cocaine.”
SOURCE: American Heart Journal, November 2005.
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