Volkow et al. were the first to document that CUD had profound decreases in CBF as evidenced by decreased brain uptake of water. Individuals with underlying arteriovenous malformation or aneurysm are at greater risk for such events . Sudden increases in arterial pressure can induce aneurysms (a localized widening of an artery or vein, resulting from weakening of vessel wall), arteriovenous malformations (abnormal connection between arteries and veins, bypassing the capillary system) and hemorrhagic strokes . Abnormalities in the expression of transcription factors in cells and changes of brain neurotransmitter systems have been reported .
- Origin of acute1
- Cocaine, compared to other illicit drugs, poses a particular risk for vascular disease and is most involved in emergency room visits (40.3%), with highest rates for men aged 35–44 years, amounting to a vast social and economic burden .
- Here too, it is helpful to briefly review prevention and treatment recommendations separately for acute vascular events.
- Add acute to one of your lists below, or create a new one.
Review Date 10/9/2024
The information provided herein should not be used during any medical emergency or for the diagnosis or treatment of any medical condition. It is the opposite of chronic. Definition of acute adjective from the Oxford Advanced Learner’s Dictionary
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Thus, cocaine induces microischemia in various types of vessels and arteriolar branches that is exacerbated with repeated use and is likely to be a contributor to its neurotoxic effects . Additional findings point to reduced acute and chronic effects of cocaine on cardiovascular health pmc arterial caliber, focal narrowing in the anterior (and middle cerebral arteries) and posterior cerebral circulation as well as communicating arteries . Carotid artery dissection might also be caused by cocaine mediated apoptosis of vascular cells leading to ischemic stroke, although the mechanism is not fully understood .
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These factors include the life-course and complexity of CUD, comprised of years (often, decades) of concomitant alcohol and/or tobacco and/or other drug use, potentiating vascular toxicity. Thus, atherosclerosis may impact cognitive and behavioral functioning even before arterial narrowing results in a stroke. Cocaine-induced chronic neurotoxicity consists of monoamine re-uptake inhibition, anti-cholinergic activity, and alpha-adrenergic stimulation . Other reports document aortic damage including dilatation , reduced strain, compliance and distensibility 74,80, and increased stiffness index and pulse wave velocity .
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Cocaine’s acute hematological effects on the vessel (Fig. 1, upper box) 10,23,24 center on the loss of the endothelium’s protective functions, a common denominator in the pathogenesis of ischemic vascular disease 35,36. Early detection of vascular disease in cocaine addiction by multimodality imaging is discussed. Furthermore, guidelines of pharmacological management of addictions should consider preventive treatment for vascular damage in cocaine users, and hopefully this will reduce severe impairment and sudden premature mortality in this population. In patients with acute manifestation of cerebrovascular events it is essential to perform a toxicological drug screening also in presence of normal blood pressure and with spontaneous subcortical hemorrhagic stroke and negative anamnesis for drug abuse at admission . Notably, there is no specific pharmacological antidote for cocaine overdose, yet the administration of benzodiazepines can help alleviate some of the stress that is placed on the heart and may greatly reduce the risk of heart attack, stroke or serious heart damage arising from the overdose.
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We present the main mechanisms of acute and chronic cocaine-induced toxicity on vessels, brain and heart (Fig. 1) and the common vascular and systemic effects of cocaine use in humans (Fig. 2). Findings consist of the major mechanisms of cocaine-induced vasoconstriction, endothelial dysfunction, and accelerated atherosclerosis, emphasizing acute, chronic, and secondary effects of cocaine. Furthermore, chronic cocaine-use reduces capillary flows in brain and may be responsible for cerebrovascular small-vessel ischemic disease (e.g. cocaine-induced leukoaraiosis), possibly involving genetic factors 65,66.
- The first line of treatment for cocaine induced sodium channel blockade is alkalization with hypertonic sodium bicarbonate.
- When vessels are stressed, endothelin-1 (a vasoconstrictor protein produced by vascular endothelial cells) is elevated and nitric oxide (a blood vessel dilator) decreases, leading to vasoconstriction 35,36.
- Acute is also frequently used to describe less troublesome matters, such as keenness of perception (“an acute observer” or “an acute sense of smell”), a type of angle (one measuring less than 90 degrees), or the demand for urgent attention (“acute danger”).
- Notably, there is no specific pharmacological antidote for cocaine overdose, yet the administration of benzodiazepines can help alleviate some of the stress that is placed on the heart and may greatly reduce the risk of heart attack, stroke or serious heart damage arising from the overdose.
- Cocaine-induced chronic neurotoxicity consists of monoamine re-uptake inhibition, anti-cholinergic activity, and alpha-adrenergic stimulation .
Phenomenology contributing to vascular damage
Atherosclerosis of the carotid arteries is of particular relevance to CUD because these arteries supply blood to the brain regions that are implicated in the cognitive impairments documented in CUD 39–41. Such an examination in a rat cortical brain identified a 2.9 ± 0.5 min lag time between the peak neuronal and vascular responses to cocaine . Furthermore, vasoconstriction at presynaptic nerve terminals increases the release of calcium from the sarcoplasmic reticulum in cerebral vascular smooth muscle cells 32,33.
Treatment for cocaine-induced acute vascular events may be similar to indications in patients with traditional risk-factors, with few exceptions. Additionally, genetic factors leading to variability in reaction to cocaine can enhance hemodynamic responsiveness, incidence of coronary vasoconstriction, and vascular damage . In addition to cocaine-specific effects, there are secondary harms resulting from synergetic effects between multiple environmental, psychosocial and behavioral factors comprising the addiction phenomenology that could in turn enhance potential vascular damage. Additional in vivo examinations are clearly required to solidify knowledge concerning early vascular disease detection in CUD, especially, the assessment of carotid plaque composition for determining risk profiles and predicting future clinical events in CUD.
Thus, prevention of secondary harms and halting of further disease progression in CUD mandates cessation of cocaine use and cigarette smoking, limitation of alcohol consumption, as well as enhancing healthy life routines (e.g., regular health monitoring, physical activity, sleep, diet, stress management). Finally, and perhaps most importantly, cocaine abstinence or even reduced use promotes reduction in endothelial-1 damage 45,46. Medication to reduce inflammation (e.g., recombinant IL-10, soluble receptor medication such as Etanercept) may be helpful to control cocaine induced inflammatory cascade . The issue is complicated further by the fact that contaminants such as procainamide, quinidine and antihistamines, which are often mixed with the cocaine, may contribute to the effects seen and influence the underlying pathophysiology . Studies in healthy populations reveal association between cognitive deficiencies and atherosclerosis, indicating that there is an inflammatory pathway that reduces the brain’s executive control network efficiency 82–84. Advanced atherosclerosis of intracranial vessels is noted as the cause of cocaine-induced stroke in numerous studies 4,29.
Heart mechanisms adapted from Ref. ; figure based on following references 2,5,6,10,13,15–19,23–44. Despite advances in characterization of addiction, knowledge about the contribution of vascular aging to brain impairments in human CUD is scarce. We review major postmortem and in vitro studies documenting cocaine-induced vascular toxicity. Although the Crack-Cocaine epidemic has declined, its vascular consequences are increasingly becoming evident among individuals with cocaine use disorder of that period, now aging. Www.merriam-webster.com/dictionary/acute. But rarer and more serious ones include acute gallstone disease, pancreatitis and serious allergic reactions.
Cocaine’s chronic effects on the vessel (Fig. 1, upper box) 10,23,24 consist of repeated endothelial damage leading to premature and severe atherosclerosis in various organs 10,19. Sympathomimetic effects generate a rise of heart rate, blood pressure and myocardial contractility, which enhance myocardial oxygen demand, whereas myocardial oxygen supply is decreased by coronary vasoconstriction and enhanced thrombosis. This cascade reduces blood flow following cocaine use and can lead to acute organ damage. Additional mechanisms implicated in cocaine induced vasoconstriction include increases in calcium .
Cerebral vasospasm is pharmacologically induced via cocaine’s potent sympathomimetic properties and an increase of endothelin-132,34. These mechanisms underlie inadequate myocardial oxygen equilibrium, which may lead to ischemia and manifest as angina or infarction 2,13. Cocaine induces acute cardiotoxicity through multiple pathways (Fig. 1, left box). It was recently demonstrated that cocaine elicits autophagy involving nitric oxide and glyceraldehyde-3-phosphate dehydrogenase signaling cascade .
Cardiovascular, cerebrovascular and arterial pathology in cocaine users as imaged by magnetic resonance imaging and positron emission tomography.a Cocaine’s acute and chronic toxicity mechanisms on the vessel, heart, and the central nervous system (CNS), and their interactions. Cocaine, compared to other illicit drugs, poses a particular risk for vascular disease and is most involved in emergency room visits (40.3%), with highest rates for men aged 35–44 years, amounting to a vast social and economic burden . For example, 18F-fluorodeoxyglucose positron emission tomography (18F-FDG-PET) and magnetic resonance imaging (MRI), PET/MR, allow simultaneous investigation and tracking of brain, cardiac and the carotid arteries function and structure in the same individuals.
Vast efforts are geared toward psychosocial rehabilitation of cocaine use disorder (CUD). Treatment may be similar to indications in patients with traditional risk-factors, with few exceptions such as enhanced supportive care and use of benzodiazepines and phentolamine for sedation, and avoiding β-blockers. Paradoxically, during the period when prevention efforts could make a difference, this population receives psychosocial treatment at best. A licensed medical professional should be consulted for diagnosis and treatment of any and all medical conditions.
Stimulation of dopamine cells in the ventral tagmental area increases blood pressure and this effect is antagonized by the dopamine D2 receptor blockers . In addition, cocaine blocks reuptake of catecholamines in the presynaptic neurons in the central and peripheral nervous systems, resulting in increased catecholamines, sympathetic output and stimulation 2,19. At high doses, cocaine is markedly more dangerous than other central nervous system stimulants, including amphetamines , and can cause sudden cardiac death through its effect on sodium channels and local anesthetic actions 13,14,16. Underlying this addiction is CUD’s association with abnormal brain morphology and function involving inefficiencies in circuits that coordinate reward and self-control processes . Furthermore, the phenomenology of CUD consists of repeated drug use leading to tolerance, withdrawal, and compulsive drug-seeking behavior with inability to abstain, despite adverse effects to medical, social and occupational functioning. “Crack-Cocaine” was introduced in the mid-1980s involving a new route of administration, smoking (as opposed to sniffing), which enhances vascular toxicity.