• N&PD Moderators: Skorpio | thegreenhand

Beta Blocker (Bisoprolol) + Cocaine

oneoneeight

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Jan 23, 2016
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I realize there's been many topics about this, but I'm wondering what is it like in my particular case. I'm 28yo on 80mg Telmisartan & 2.5mg Bisoprolol a day due to high blood pressure and anxiety (since 10 years). I do a gram of coke every second weekend, especially mostly enjoying it with few beers (5-6), sitting on the couch. Am I putting my life in danger because of combining these medicines with coke & alcohol? Since I'm not doing more than 1 gram of coke a session (usually even less) and I'm only taking 2.5mg a day of beta blocker, is the risk still high and I'm still in a big risk of getting a heart attack?

I really enjoy sniffing and if coke is really dangerous in that combination, would changing to amphethamine be any less damaging?
 
Why are you prescribed beta blockers? I would have thought that in itself is a big alarm bell about you using cocaine, which is extremely cardiotoxic
 
Combining propranolol and stimulants can be extremely dangerous -- propranolol does not block the indirect alpha1 effects of cocaine, resulting in potential BP increase.

Second problem is that drinking alcohol with cocaine results in transesterification to cocaethylene, which is considerably more cardiotoxic then cocaine.
 
Why are you prescribed beta blockers?
High blood pressure caused partially by anxiety, also irregular heartbeat (extra beats every now and then)

So even with small amounts I'm taking (of both coke and beta blocker) and considering I'm only 28, am I still at the high risk of a heart attack doing coke and drinking alcohol? Would amphetamine be any safer?
 
Combining propranolol and stimulants can be extremely dangerous -- propranolol does not block the indirect alpha1 effects of cocaine, resulting in potential BP increase.

Second problem is that drinking alcohol with cocaine results in transesterification to cocaethylene, which is considerably more cardiotoxic then cocaine.

It's actually bisoprolol, not propranolol. You say it can be extremely dangerous, what are the chances it actually will be?

Also, even if I'm doing it and I'm feeling totally fine, does my heart still get damaged every time more and more?
 
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Cocaine multiplies the risk for sudden cardiovascular death in otherwise healthy adults. The risk is much greater when cocaine is taken with alcohol (cocaethylene supposedly increases the risk of sudden death 25-fold). Cocaine use is even more risky for someone with underlying cardiovascular illness. But no one is really going to be able to predict exactly how dangerous it is for you. I guess the question is how much risk are you willing to tolerate?

http://www.ncbi.nlm.nih.gov/pubmed/25041688
[url]http://www.ncbi.nlm.nih.gov/pubmed/22981213

[/URL]
 
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If anyone could add any input to this I would appreciate it...

30 or 40 years ago, propranolol was a mainstay in the treatment of cocaine toxicity. Then in the early 80's it was shown that patients given beta blockers while also suffering from cocaine toxicity had elevations in BP and that vasospasm may be worsened. Rather quickly, beta blockers fell out of favor for patients with MI or acute coronary syndrome associated with cocaine abuse and to this day, it is extremely unlikely any emergency or cardiac physician would treat such patients with beta blockers. However, the past decade or so has shown a reignition of the debate on the benefits of beta blockers for patients with acute cardiac issues due to cocaine use.

Much of the data supporting the theory of beta blockade results in unopposed alpha stimulation comes from small cases reports or animal studies not randomized studies making the veracity of the theory dubious. Further more, it has been shown that vasospasm may not be the cause of MI in cocaine toxicity, rather thrombosis formation due to cocaine's ability to cause platelet aggregation, increase vascular permeability and other factors. So if vasospasm is not the culprit and in all other ACS patients, beta blockers are recommended, it is a disservice to the cocaine abusing patients to withold them in treatment.

There are also conditions such as severe trauma, heart failure, and subarachnoid hemmorage that cause overstimulation of catecholamines in which beta blockers are widely used due to decreases in mortality and cardiac necrosis associated with beta stimulation. Utilizing beta blockers in these cases would lead to the same unopposed alpha stimulation theorized in cocaine toxic persons receiving beta blockers and as I said, there is no deleterious effects, rather beneficial results. So while you still probably would not get beta blockers if you go to the ER with chest pain after using cocaine, this is more from history rather than actual data showing the negative consequences.

Your situation is different as you are using bisoprolol for chronic management of hypertension, not an acute syndrome. I am unaware of any data saying combining cocaine with a beta blocker for high blood pressure, positive or negative. There are a few small reports of physicians utilizing carvedilol with great success in cocaine addicts with chronic heart failure, though. While not the same thing and carvedilol differs from most beta blockers as it also is an alpha blocker, it shows there may not be risks in administering beta blockers in those with long term CV disease who also use cocaine. And if the vasospasm due to alpha stimulation theory is actually correct, carvedilol may be ideal as its dual mechanism protects from both overstimulation of alpha and beta receptors.
 
^

Without refuting your larger point, I will mention that vasospasm and thrombosis are two very strongly connected phenomena.

Coronary artery vasospasm causes increases heart rates with decreased ejection fractions, increasing pulmonary arterial pressure, reductions in the integrity of peripheral circulation, issues with vasovagal response and cerebral vasoregulation and.........

...Tends to be a precursor to thrombotic events. In fact, there has been a shift in the focus of medical research regarding long-term endothelial damage. Arterial plaques point to damaged endothelium--but site-specific endothelial damage often predates and predicts the formation of arterial plaque. Additionally, spastic arteries causes the release of site-specific inflammatory mediators--thrombogenic substances


Now this doesn't invalidate your larger claim that beta blockers may not be quite as strongly countraindicated with cocaine use as previously suspected--and may even be beneficial/life-saving when administered under medical supervision. However, it must be strongly noted the the connection between vasospasm and cardiovascular events--including but not limited to thrombosis--is not the least bit tenuous.
 
Yes of course but for quite some time it was theorized that vasospasm and the resulting vasoconstriction and ischemia was the primary, if not only cause of ACS or infarction in cocaine users and thrombis formation had little to do with the relatively young, risk factor-free patients who often showed no sign of CAD. Think Prinzmetal's angina rather than typical atherosclerosis.
 
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