And not to hammer you, copperwindow, but I disagree that cocaine is extremely toxic to the heart. Yes, it can trigger ventricular arrhythmias at no predictable dose, and if it does that to you, you’re dead, barring extremely rapid EMS response and a big dose of luck. But it is a neurotransmitter analog, and as such, it exerts its effects by combining with a receptor on cell membranes, which endogenous molecules are intended to trigger. That’s not toxic. Then it disappears completely once it has been cleared from the bloodstream, likely leaving no permanent effects behind. So I cannot agree with you that it is a toxin.
There is only one literature-supported area of heart damage I can think of for cocaine, and this is based on ten-year-old research. Wonderful study in Texas (where else could they do this stuff?) where they put a bunch of volunteers on exercycles, got them cathed and wired up to test their coronary arteries, and then gave them cocaine up their noses. (I wonder did they pay the volunteers, or did the volunteers pay them.) The stated purpose of the research was to find out if cocaine up the nose in nasal surgery endangered the heart. The unstated purpose seemed to me to be to fiind out if recreational cocaine use endangered the heart.
Interesting finding. Cocaine, while it functions as an analog neurotransmitter, is a paradoxical inotrope. (Paging Qadgop the Mercotan - QtM, are you in the house?) This means that it makes your heart beat harder, but narrows your coronary arteries while it does so. Note, Copperwindow, that this does not cause permanent damage to the heart, even if it’s temporarily trying. Not a toxin by my definition (think snake venom).
The interesting thing was this. Usually, we think of a dangerous arterial narrowing as one that’s over 75%, although with plaque fissuring, we have learned that even a 35% coronary artery stenosis (narrowed spot) can lead to a heart attack in unlucky people. However, in these volunteers, even a 10% stenosis caused a much more significant temporary narrowing of the coronary artery while under the influence of cocaine. (The temporary narrowing is due to muscle cells in the outer coat of the artery constricting to narrow it down, because the muscle cells are responding to the fake neurotransmitter in their membranes, which is how cocaine exerts its paradoxical inotrope effects. The heart cells also respond by contracting harder than normal. That’s how it makes your coronaries narrower and your heart work harder. But that’s a completely temporary effect, not like deposits of atherosclerosis.)
The researchers theorized that maybe the cells that line cornary arteries, the endothelial cells (paging KarlGauss, are you in the house), normally secrete a substance which counters the effects of the fake neurotransmitter cocaine, but that when they are stretched across even a small atherosclerotic plaque, they can’t.
That was speculation on their part to explain their observed data, and I never followed up the article to see if they went on to prove that.
Still, even coronary artery narrowing, if it does not bring on a thrombosis on the stenosis, is a completely temporary effect on the heart, and does not qualify for what I would call toxic.
By the way, I am not a cocaine user (have never been), and I see people who die from it monthly if not weekly.
Sorry for the string of posts - interesting topic, and I seem to be the only one up this early on a Saturday morning.