Cocaethyleen, lekkerder en verslavender dan cocaine zelf?

The pathogenesis of cocaine-related myocardial ischemia and infarction is most likely multifactorial and can include increased oxygen demand (1), vasoconstriction of the coronary arteries that can be marked (2), and enhanced platelet aggregation and thrombus formation.(3)
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(1)
Cocaine directly induces and causes an increase in the three major determinants of myocardial oxygen demand: the heart rate, systemic arterial pressure, and left ventricular contractility.
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(2)
Cocaine-induced vasoconstriction of the coronary arteries is mostly a result of stimulation of coronary arterial alpha-adrenergic receptors.
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Cocaine also causes increased endothelial production of endothelin (a potent vasoconstrictor) and decreased production of nitric oxide (a potent vasodilator), all of which may promote vasoconstriction.
Aside from the effects of cell mediators on vasospasm, various neurotransmitters in the form of catecholamines also contribute to the cardiac toxicity of cocaine.
Vasoconstriction is caused by preventing the reuptake of catecholamines in the CNS and stimulating the release of norepinephrine from adrenergic nerve terminals. Norepinephrine (or noradrenaline) increases myocardial oxygen demand and coronary artery spasm. The spasm decreases the size of vessels leading to myocardial infarction.
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Onset of chest pain symptoms can occur several hours after cocaine use when blood concentration of the drug is very low or even undetectable. This is a slightly different mechanism than the aforementioned action of the coronary vessels. The delayed onset of chest pain is due to cocaine’s metabolites (benzoylecgonine and ecgonine methyl ester)
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(3)
Aside from vasoconstriction, cocaine may induce thrombus formation via enhanced platelet activation, aggregability, and increasing plasminogen-activator inhibitor.

The cardiovascular toxicity of amphetamines results mostly from the increased release of catecholamines and 5-HT into the synaptic cleft and the blood stream. Amphetamines act as highly potent releasers of monoamines in the CNS. Although the cardiovascular system is mainly regulated by the autonomic system, the CNS pathways can easily interfere with cardiac homeostasis.
Importantly, the NA pathways of the brain play a crucial role in the regulation of cardiovascular functions.
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In addition, recent evidence points to the involvement of secondary mechanisms in the development of amphetamine-induced cardiotoxic effects, including metabolic bioactivation and hyperthermia.
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AMPH was shown to induce an increase in TH activity, which further increases the catecholamine availability, and thus, the stimulation of adrenoceptors in the CNS. This adrenoceptors-stimulation indirectly triggers alterations in the cardiovascular function. On the other hand, the direct action on heart receptors or the direct action of the molecules on the myocardial tissue can cause stress cardiomyopathy, myocardial infarction, and tachycardia, among other cardiovascular disorders
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There are several papers reporting AMPH toxicity toward the cardiovascular system in a drug abuse scenario. AMPH causes myocardial infarction, and coronary spasm, among other cardiovascular effects.
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In summary, amphetamines are without doubt cardiotoxicants, as reported by several cellular and animal studies, but especially by human studies and case reports. The most obvious mechanism to their cardiac toxicity is their ability to activate the catecholaminergic system in the CNS and in the peripheral organs. This catecholaminergic activation can cause direct lesion on the heart or heart coronary system. In fact, several studies proved that also the direct action of amphetamines and/or their metabolites can trigger cardiotoxicity and that this direct cardiotoxic potential cannot be neglected in future studies.