Stimulants What kind of heart damage is typical of amphetamines?

[elitewalrusxx]

I'm having trouble finding exactly what kind of damage is common besides congenital heart disease in long term users. I have definitely had my heart altered by it in some way but the doctors say I am 100% healthy.

My Symptoms:

• A forceful but not necessarily faster heart rate. I can't ignore it when I lie on my side and if I'm up and walking around I can feel it beating forcefully; Even through my winter coat. I remember trying to feel my heartbeat earlier in 2017 and I had to lay in bed on top of my hand just to feel even the slightest beating.

• An increased but still technically healthy blood pressure. Before this began, I took my blood pressure and it was in the healthy range. Now when I take my blood pressure the bottom number is usually in the healthy range (below 80) but the top number (systolic) is consistently higher than 120.

• I can feel the veins in my neck throbbing just by gently putting my hand to it after the most moderate physical activity such as climbing the stairs.

• I can very easily feel pulses across my body, such as when I put my hand into a fist and I can feel a pulse in my palm or if I rest my arm on something.

• On three different nights I noticed my heart would beat extra forcefully every few seconds or so in an irregular fashion. It was always gone when I awoke in the morning.

What the Doctors Said:
I four EKG's an EKG stress test and and echo cardiogram done over the course of two months. I also wore a two electrode heartbeat monitor for four days. When I met with the cardiologist she told my that I had a heart murmur which is very common and probably existed before my heart started acting up. She said that my heart was very healthy as a young fit persons heart should be (I'm majoring in computer science I hardly move) and she was surprised to see that the heart monitor showed zero extra beats, something that even a healthy person would likely experience a few times over the course of four days. She predicts that the irregular heart beats that I had experienced on those three nights were the result of extra beats in the upper chamber of the heart. She said unless I lose consciousness or have a racing heartbeat that wont relent, I shouldn't come back. During all of this I was too ashamed to admit that drugs were involved. I'm tired of everyone saying it is just anxiety. I know something changed.

How it Happened:
A while ago I had a huge supply of amphetamine and I very foolishly abused it for a few months. I was taking anywhere from taking 10-40mg doses once a day and sometimes twice. One night I made the horrible decision to take Xanax so I could sleep and I blacked out. The next morning I woke up to find the amphetamine on my desk almost gone. There was probably at least 200mg in there. I had to deal with two days of psychosis; solid object waving in the wind, breathing walls, specks that looked like bugs in my periphery, people walking around at night, auditory hallucinations, and a rat creature in my closet that was really just a rolled up blanket when i would get close enough to see it. This was all fascinating as I didn't have any paranoia and I knew none of it was real. I just went to school and work normally, the week went by in what felt like just a few days and I fully recovered without anyone even knowing. A month or so after this happened I noticed when I would take the amphetamine my heart would beat forcefully in my chest. After this happened a few times I quit my daily habit but my heart problems continued. I went to the walk in clinic and he told me to go to the er. I have very little interest in using drugs after all this but I still really want to explore the use of psychedelics. I've tripped twice since and the anxiety of having heart problems haunts me. I can no longer enjoy it.

 

[Hodor]

I've tripped twice since and the anxiety of having heart problems haunts me.

That seems to be your main issue: You're obsessing too much about your blood pressure. It is no wonder your BP is increased whenever you measure it if measuring it makes you that much more nervous than before.

40 mg of amphetamine (as in Adderall?) is a perfectly normal therapeutic amount. Even 2x40 mg could still be considered "therapeutic" for certain patients.
Sure, >200mg is "a bit" much, but as you said the effects subsided after two days. There are plenty of people who regularly take that kind of dose when partying without having their hearts explode - I am obviously not saying that abusing amps like that is a good idea and risk-free, just that it is unlikely for a healthy person to do significant damage to their heart in a single stim binge.

 

[BurritoJimmy]

During the four day period you wore the monitor did you experience one of the episodes that is bothering you? If so then the monitor caught whatever you experienced and it was a normal rhythym otherwise the Dr. would have pointed it out.

It's not uncommon to develop panic disorder after amphetamine use which is what you seem to have. I have it too and swore something was wrong with me other than that for a couple of years. You can expect it to worsen if you continue to use amphetamine. Psychedelics are a wild card but it is likely to worsen with these too. Your best bet is to lay off alcohol and drugs, except prescriptions to treat your anxiety if you decide to go that route.

 

[Scrofula]

.	Cardiotoxicity stemming from catecholamine excess is observed in both cocaine and MA users. Although the cardiac effects are more profound for MA users because this drug results in even greater elevation of catecholamines than cocaine, the incidence of fatalities following myocardial infarction has been less frequent until the recent increase in inhaling (smoking) or injecting MA.
.	Stimulants, especially cocaine, have been linked to virtually every form of heart disease, including different forms of arrhythmias, coronary vasospasm, myocardial ischemia, myocardial infarction, and cardiomyopathy. Case reports of fatalities from myocardial infarction and tachyarrhythmias document their occurrence at all dose levels and routes of administration in otherwise healthy young adults without the usual coronary risk factors, but preexisting coronary artery disease can exacerbate the response and increase the likelihood of sudden death, as can hyperthermia and agitation. Tachycardia, hypertension, ruptured blood vessels, arrhythmias, and arteriosclerotic lesions typically precede myocardial ischemia and infarction. With prompt medical intervention, patients generally survive stimulant-induced cardiomyopathy with heart failure.
From a helpful National Library of Medicine Book Chapter from TIP-33 Medical aspects of Stimulant Use Disorders​ https://www.ncbi.nlm.nih.gov/books/NBK64323/

 

[CFC]

There's also a rather bulky summary I wrote here OP:

The dominant cardiovascular concern for meth/amp and other stimulant users is more typically the chronic harms - ones that build slowly over time like cardiomyopathies, valvular damage, aortic dilatation and so on. These can increase the risk of premature death, potentially taking years or even decades off a person's normal lifespan, despite not being obviously and directly related to morbidity at the time of death - and so inconveniently not registering in any coroner's report (assuming one's even written - which is rarely the case).

Despite that, and the consequent inadequacy of information we have to hand, even a tip-of-the-iceberg analysis suggests meth use is present in at least 5% of all patients presenting to the ER with heart failure [https://www.ncbi.nlm.nih.gov/pubmed/18940295] and 40% of patients under the age of 45 admitted to hospital with cardiomyopathy [https://www.ncbi.nlm.nih.gov/pubmed/17275458]. Acute coronary syndrome (ie unstable angina and acute myocardial infarction) was diagnosed in 25% of US emergency department patients presenting with chest pain following meth use [https://www.ncbi.nlm.nih.gov/pubmed/12745036]

A selection of reports and studies discussing heart attacks (MI) resulting from meth/amp abuse can be found here:

https://www.ncbi.nlm.nih.gov/pubmed/15011896
https://www.ncbi.nlm.nih.gov/pubmed/12745036
https://www.ncbi.nlm.nih.gov/pubmed/10978660
https://www.ncbi.nlm.nih.gov/pubmed/10097363
https://www.ncbi.nlm.nih.gov/pubmed/17565561

Acute aortic dissection, another well-known complication of meth use, can be read about here:

https://www.ncbi.nlm.nih.gov/pubmed/9987866
https://www.ncbi.nlm.nih.gov/pubmed/10097363
https://www.ncbi.nlm.nih.gov/pubmed/7815027

Meth/amp is also strongly associated with cardiac arrhythmias and sudden cardiac death. You can read more about these cases here:

https://www.ncbi.nlm.nih.gov/pubmed/10344175
https://www.ncbi.nlm.nih.gov/pubmed/7588189
https://www.ncbi.nlm.nih.gov/pubmed/6482074
https://www.ncbi.nlm.nih.gov/pubmed/2979169
https://www.ncbi.nlm.nih.gov/pubmed/7840041
https://www.ncbi.nlm.nih.gov/pubmed/2293467
https://www.ncbi.nlm.nih.gov/pubmed/12877759
https://www.ncbi.nlm.nih.gov/pubmed/6519024

As for the more chronic pathologies, they also include underlying processes and mechanisms that lead to many of the acute outcomes listed above. So for example aortic dissection typically involves prolonged and repeated exposure to elevated BP and heart rate, leading to aortic dilatation, which slowly expands and weakens for years before the aorta finally ruptures in an acute episode. And prolonged tachycardia and catecholamine exposure can modify the behaviour of the heart's pacemaker and its elecrophysiological behaviour (affecting pulse conductivity, for example), leading to atrial fibrillation, which can then lead to clots, thrombus and ultimately MI, sudden death and so on.

However the classic chronic issues are coronary artery disease (CAD) and cardiomyopathy. Minimal to severe CAD is found in around 1-in-5 (20%) of meth users compared to 1-in-20 of the normal population, and occurs at a significantly younger age [https://www.ncbi.nlm.nih.gov/pubmed/17565561].

But as quoted in that paper: "cardiac pathology takes time to develop [and] there may be a long ?incubation? period prior to methamphetamine-related death." As already suggested, this implies many of the harms inevitably go unrecorded or get blamed on traditional causes like ageing, poor genetics, a lack of exercise and unhealthy Western diets.

These concerns about the largely under-reported cardiovascular harms aren't just limited to American researchers either:

In a series of 371 Australian coronial cases of methamphetamine-related deaths, cardiovascular complications were the leading direct cause of death after drug toxicity/overdose, responsible for death in 14% of cases. Fifty-four per cent of the cohort exhibited cardiovascular pathology. Notably, this data from 2008 precedes the current rise in methamphetamine use and purity. From 2011/12 - 2012/13, there was an 88% increase in methamphetamine-related ambulance callouts in metropolitan Melbourne and a 109% increase in rural Victoria. Methamphetamines are now the second most common culprit after opioids for drug-related hospital attendances. Methamphetamine-related mortality has also doubled from 2001 to 2009

[https://www.ncbi.nlm.nih.gov/pubmed/26706652]

In Crystal Methamphetamine‐Associated Cardiomyopathy: Tip of the Iceberg? [https://www.ncbi.nlm.nih.gov/pubmed/14705845], the authors summarise the cardiovascular-related harms quite nicely:

The most common cardiovascular manifestations of amphetamine‐related compounds include chest pain, tachycardia, and hypertension. At higher doses tachyarrhythmias may occur. Amphetamines are also linked with coronary artery disease, myocardial ischemia and infarction, acute pulmonary edema, necrotizing vasculitis, endocarditis, pulmonary hypertension, acute aortic dissection, ischemic stroke, cerebrovascular hemmorhage, acute rhabdomyelosis, and sudden cardiac death.

Autopsy studies have demonstrated the occurrence of cardiomyopathy in patients with methamphetamine‐related deaths. Histological analysis of myocardial tissue from methamphetamine users has shown the presence of contraction band necrosis, which usually is an indicator of catecholamine toxicity and a recognized feature in the hearts of cocaine abusers.

Several experimental studies have shown the development of myocyte atrophy, hypertrophy, contraction bands, patchy cellular infiltration, eosinophilic degeneration, cellular edema, myocytolysis, fibrosis, and vacuolization when animals and cultured myocytes are exposed to methamphetamine. The accompanying ultra structural features include sarcolemmal injury, mitochondrial degeneration, myofibrillar hypercontraction, and loss of myofilaments.

The plausible mechanisms for the development of dilated cardiomyopathy in chronic methamphetamine users include recurrent coronary artery spasm, small vessel disease, or diffuse myocardial toxicity due to repeated stimulation of alpha and beta‐adrenergic receptors in the heart. Thus, the adverse pathogenetic role of adrenergic receptor stimulation in this setting is likely similar to that of cocaine and catecholamine‐induced cardiomyopathy.

Evidence for all those harms/claims can be linked directly through the paper (I had to remove the messy hyperlinks unfortunately).

In Cardiovascular Responses Elicited by the ?Binge? Administration of Methamphetamine [https://www.ncbi.nlm.nih.gov/pubmed/11907169], the authors have begun to investigate the impact of repeated binge dosing of meth on the cardiovascular system, since this more accurately reflects typical usage patterns, noting that:

The binge administration of METH can produce significant cardiac pathology. In rats subjected to this dosing regimen, we observed myocardial foci of predominantly mononuclear inflammatory infiltrates (primarily monocytes/macrophages) with areas of disrupted architecture and occasional myofibril necrosis. Mast cells, normally present in the rat myocardium (Majeed, 1994), were not increased in rats receiving METH.

One potential mechanism suggests that a METH-induced increase in peripheral catecholamines is responsible for the cardiotoxicity (see Jiang and Downing, 1990). It is known that catecholaminergic stimulation can produce myocardial necrosis and infiltration similar to that observed after administering METH. The mechanisms mediating catecholamine-induced cardiac damage may include ischemia due to catecholamine-mediated coronary vasoconstriction, calcium overload, and the production of oxygen free radicals by either the auto-oxidation of catecholamines or their degradation by monoamine oxygenase. Reactive oxygen species may also be produced by catecholamine degradation, mitochondrial dysfunction, leukocyte activation, and/or xanthine oxidization during the reperfusion of ischemic areas.

METH may produce cardiac damage by direct effects on the myocytes. METH is cytotoxic to myocytes in culture systems devoid of catecholamines. METH may also damage cardiac cells by initiating apoptosis. Apoptotic processes occur in several pathological conditions including myocardial ischemia and reperfusion, infarction, and cardiomyopathy.

The binge administration of METH can produce significant changes in cardiovascular and cardiovascular reflex function and result in significant cardiac pathology. During the binge administration of METH, there was an increase in sensitivity to the pressor actions of the drug and decreases in sensitivity to the depressor actions of NP, Iso, and Ach.

I bring this tendency for binging to aggravate the heart's reaction to meth's pressor effect up as it's of direct concern to OP, who's heart is clearly quite sensitive as it is. Which is a very good reason for OP to further ponder the gravity of his/her addiction to meth, and to try even harder to stop. And all without even needing to consider the escalating risks to the brain, other organs, long-term mental health, intensified addiction and so on.

 

[hoffsteader]

My cardiologist told me that drug use never really leads to long term damages. I'd say rare is more like it. I was relieved as an amphetamine user on and off for years that my heart is still in tip top shape according to the doctor.