4.00 DOB, 4.00 MDA, 4.00 Aleph-2, 4.00 2C-B-fly,
4.00 2C-B, 4.00 TMA, 4.00 psilocin, 4.00 TMA-2, 4.00 2C-E,
4.00 2C-T-2, 4.00 4C-T-2, 4.00 MEM, 4.00 DOM, 3.97
mescaline, 3.93 6-F-DMT, 3.91 5-MeO-DIPT, 3.91 DMT, 3.88
DPT, 3.70 DOET, 3.64 MDMA, 3.48 DIPT, 3.32 5-MeO-MIPT,
3.13 DOI, 3.11 LSD, 3.01 lisuride, 2.72 cis-2a, 2.17 SS-2c, 1.81
RR-2b, 0.69 5-MeO-DMT; 0.00 salvinorin A;

Lisuride, which is an agonist at two related serotonin receptors (5-HT 2 A and 5-HT 2 C )
but is not a 5-HT 2 B agonist, was not associated with valve disease.

Clearly, practitioners should avoid prescribing drugs that are potent 5-HT 2 B –receptor agonists — a growing list of medications that now includes ergot derivatives (ergotamine, methysergide, and dihydroergotamine [..] and amphetamine derivatives [..] MDMA)

Cardiac fibrosis
Recreational drugs which also act at 5-HT2B receptors

Several serotonergic recreational drugs, including the empathogens MDA and MDMA ("Ecstasy",[16] and some hallucinogens such as DOI[17] and bromo-dragonfly,[18] have all been shown to act as 5-HT2B agonists in vitro, but how significant this may be as a risk factor associated with their recreational use is unclear. The piperazine derivative mCPP (a major metabolite of Trazodone) is a 5-HT2B agonist in animal models, but actually behaves as a 5-HT2B antagonist in humans.[19][20][21] One study of human users of "ecstasy" found that they did have heart valve changes suggestive of early cardiac fibrosis, which were not present in non-ecstasy using controls,[22] suggesting that ecstasy use certainly has the potential to cause this kind of heart damage. On the other hand there is no statistical evidence as yet to suggest significant increases in rates of cardiac valvopathies in current or former MDMA users, and it is most likely that as with other 5-HT2B agonists, development of heart valve damage will be highly dependent on the frequency and duration of use and the total cumulative exposure over time, and only a small proportion of the heaviest users are likely to face a substantial risk of heart damage.

The chemist Alexander Shulgin first popularized MDMA and MDA, and he invented DOI and many other recreational drugs that are also 5HT-2B receptor agonists. In 2008 Shulgin underwent surgery to replace a defective aortic heart valve. It is unknown whether or not Shulgin's lifelong use of psychedelic drugs caused the failure of his heart valve.

I actually emailed the PI on this paper awhile back with a few questions and did not get a response...

My name is XXXXXXX, I'm a medicinal chemist that has a side interest in the work you recently published. I was wondering if you happened to have the relative affinity profiles for serotonin, dopamine, and norepinephrine, and anandamide to match the panel of psychedelics you screened? What I'm thinking is it might be very useful to look at how the binding profile of these compounds differs from their natural neurotransmitters.

BTW I consider your paper ground breaking. It's been common knowledge for far to long that psychedelics elicit their response solely at the 5HT1a and 5HT2a receptors. I'm sure you must be aware of Dr Shulgins work. It would be awesome to take a study like your across the complete panel of known neurotransmitter receptors as well as all the compounds from Shulgins books TIHKAL and PIHKAL.

Sincerely
XXXXX