https://erowid.org/plant...ms/mushrooms_death.shtml
Incident: Anonymous Female, 2012 #
In 2012, a 24-year-old female died following a cardiac arrest 2-3 hours after consuming magic mushrooms. She had received a heart transplant 10 years prior.
Lim TH, Wasywich CA, Roygrok PN. "Letter to the Editor: A fatal case of 'magic mushroom' ingestion in a heart transplant recipient". Internal Medicine Journal. Nov 19, 2012 (online).1268-9.
Autopsy confirmed a healthy cardiac allograft (no allograft vasculopathy). Plasma toxicology revealed a psilocin level of 30 mg/L (consistent with magic mushroom toxicity) and a tetrahydrocannabinol level of 4 mg/L. No alcohol or other common drugs of abuse were detected. [...] Only two deaths have been previously reported directly attributable to magic mushroom ingestion ... We postulate that in this case excessive sympathetic stimulation of the transplanted heart as a result of Psilocybe mushroom toxicity led to fatal ventricular arrythmias."

Single oral doses of 10–20 mg psilocybin produced an average peak plasma psilocin concentration of 8.2 ng/ml between 1 and 2 h after administration
https://www.sciencedirec...ics/chemistry/psilocybin

https://www.health.harva...th-what-you-need-to-know
One of the few things scientists know for sure about marijuana and cardiovascular health is that people with established heart disease who are under stress develop chest pain more quickly if they have been smoking marijuana than they would have otherwise. This is because of complex effects cannabinoids have on the cardiovascular system, including raising resting heart rate, dilating blood vessels, and making the heart pump harder. Research suggests that the risk of heart attack is several times higher in the hour after smoking marijuana than it would be normally. While this does not pose a significant threat to people who have minimal cardiovascular risk, it should be a red flag for anyone with a history of heart disease. Although the evidence is weaker, there are also links to a higher risk of atrial fibrillation or ischemic stroke immediately following marijuana use.

Incident: Anonymous Female, 1996 #
One death (commented on by Lim, Wasywich, and Roygrok) was reportedly the result of "neurological sequelae (somnolence and convulsions) 6-8 h after ingestion of an unknown quantity of magic-mushrooms". Post-mortem toxicology revealed very high plasma psilocin concentration (4000 mg/L).
https://erowid.org/plant...ms/mushrooms_death.shtml

Single oral doses o 10–20 mg psilocybin produced an average peak plasma psilocin concentration of 8.2 ng/ml between 1 and 2 h after administration.
https://www.sciencedirec...ics/chemistry/psilocybin

Post-mortem toxicology revealed very high plasma psilocin concentration (4000 mg/L).

4000mg/L is 0.4%

If you ground up fresh mushrooms and replaced your blood with the resulting resulting slurry, you'd be at 0.1% psylocybin concentration.

Something seems fishy...

Thanks for this review. The only concern in my mind is the psychological side (there's a pun in there somewhere).

The cardiovascular effects of an unintentional mushroom overdose were previously described in my report on this forum. These seemed to be of a largely psychological nature, although there has been some work done studying the phenylethylamine (PEA) content of P. cubensis where it was postulated that PEA might be responsible for the cardiovascular effects sometimes experienced during mushroom trips.

The average blood volume of a female is about 3.5L so the latter case, if the 4000mg/L was correct, would have absorbed 14 grams of psilocybin into her body. Given that the highest measured concentration of psilocybin in a dried mushroom is about 3%, she would have had to have eaten at least 5kg of extremely potent mushrooms - with 100% absorption into the bloodstream - for that figure to be anywhere near possible. This is impossible. The figure is wrong. Unless, perhaps, the physicians involved took a direct sample from her stomach lining???

It really is just way, way off.
Also
With regards to the first case, my first thoughts were exactly that, that the cardiosensitising effects of cannabis use were wholly overlooked. Psilocybin does have some affinity for the 5-HT-2b receptor, which may not have helped.

Claiming that psilocybin was solely responsible for the cardiac arrest in both these cases seems lazy and ill-informed. It still behoves us to be mindful of the manner in which we use these substances.

Clinical effects
The adrenergic effects of these drugs are usually mild and can give rise to general sympathetic arousal leading to dilated pupils, tachycardia, hypertension, and hyperreflexia. Although cardiovascular complications are rarely serious, supraventricular tachyarrhythmias and myocardial infarction have been reported.5 Changes in serotonin-induced platelet aggregation and sympathetically induced arterial vasospasm may have been contributory factors leading to the onset of myocardial infarction.
https://www.ncbi.nlm.nih...pmc/articles/PMC1071198/

resence of phenylethylamine in hallucinogenic Psilocybe mushroom: possible role in adverse reactions.
Beck O1, Helander A, Karlson-Stiber C, Stephansson N.
Author information
Abstract
The use of mushrooms containing the hallucinogenic substance psilocybin for intentional intoxication is relatively common. Occasionally, this results in adverse reactions with typical tachycardia that is not evidently caused by psilocybin. This study demonstrates the presence of phenylethylamine in the species Psilocybe semilanceata using gas chromatography-mass spectrometry and shows that the amount of this substance may vary much more than that of psilocybin. The highest amount of phenylethylamine (146 microg/g wet weight) was observed in mushrooms from a case of three young men hospitalized because of adverse reactions. Comparison of the symptoms observed in clinical cases of magic mushroom intoxication with those after intake of pure psilocybin or phenylethylamine suggests that phenylethylamine might have a role in the development of adverse reactions to Psilocybe mushroom intake.
https://www.ncbi.nlm.nih.gov/pubmed/9491968

Phenethylamine is intrinsically a stimulant, although it doesn't last long enough to express this property. In other words, it is rapidly and completely destroyed in the human body. It is only when a number of substituent groups are placed here or there on the molecule that this metabolic fate is avoided and pharmacological activity becomes apparent. https://erowid.org/libra...e/pihkal/pihkal142.shtml

DOSAGE: greater than 1600 mg.

DURATION: unknown.

QUALITATIVE COMMENTS: (with 200, 400, 800 and 1600 mg) No effects.

(with 500 mg) No effects.

(with 800 and 1600 mg) No effects.

(with 25 and 50 mg i.v.) RNo effects.

EXTENSIONS AND COMMENTARY: Here is the chemical that is central to this entire book. This is the structural point of departure for every compound that is discussed here. It is the RPS in PIHKAL. It is without activity in man! Certainly not for the lack of trying, as some of the dosage trials that are tucked away in the literature (as abstracted in the "Qualitative Comments" given above) are pretty heavy duty. Actually, I truly doubt that all of the experimenters used exactly that phrase, "No effects," but it is patently obvious that no effects were found. It happened to be the phrase I had used in my own notes.

This, the simplest of all phenethylamines, has always been the darling of the psychopharmacologists in that it is structurally clean, it is naturally present in various human fluids and tissues, and because of its close chemical relationship to amphetamine and to the neurotransmitters. These facts continuously encourage theories that involve PEA in mental illness. Its levels in urine may be decreased in people diagnosed as being depressed. Its levels may be increased in people diagnosed as being paranoid schizophrenics. Maybe it is also increased in people under extreme stress. The human trials were initially an attempt to provoke some psychological change, and indeed some clinicians have reported intense headaches generated in depressives following PEA administration. But then, others have seen nothing. The studies evolved into searches for metabolic difference that might be of some diagnostic value. And even here, the jury is still out.

Phenethylamine is found throughout nature, in both plants and animals. It is the end product of phenylalanine in the putrefaction of tissue. One of its most popularized occurrences has been as a major component of chocolate, and it has hit the Sunday Supplements as the love-sickness chemical. Those falling out of love are compulsive chocolate eaters, trying to replenish and repair the body's loss of this compound--or so the myth goes. But this amine is voraciously metabolized to the apparently inactive compound phenylacetic acid, and to some tyramine as well. Both of these products are also normal components in the body. And, as a wry side-comment, phenylacetic acid is a major precursor in the illicit synthesis of amphetamine and methamphetamine.

Phenethylamine is intrinsically a stimulant, although it doesn't last long enough to express this property. In other words, it is rapidly and completely destroyed in the human body. It is only when a number of substituent groups are placed here or there on the molecule that this metabolic fate is avoided and pharmacological activity becomes apparent.
https://erowid.org/libra...e/pihkal/pihkal142.shtml

https://www.sciencedirect.com/topics/chemistry/psilocybin

find 4000 on this page and it takes you to another source of the same story, except it's 4000ug not mg, who ever put 4000mg on eurowid must have had a typo