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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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
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.
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.
Prevention of cocaine-induced systemic complications could be considered as part of a harm reduction strategy. The PET with 18F-FDG can quantify vessel-wall inflammation in atherosclerotic plaques 101,102 and three dimensional black-blood dynamic contrast-enhanced MRI can characterize carotid wall morphology (plaque microvessels, composition and burden). Therefore, the ability to identify plaques before luminal stenosis develops is fundamental for early disease detection .
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- Heart mechanisms adapted from Ref. ; figure based on following references 2,5,6,10,13,15–19,23–44.
- Preventing acute events in pre-symptomatic individuals must include special consideration.
- Furthermore, Ca2+ increases could also underlie the reported enhanced hemodynamic and field potential responses to sensory stimulation after acute cocaine administration 67,69.
- The information provided herein should not be used during any medical emergency or for the diagnosis or treatment of any medical condition.
Atherosclerosis of the carotid arteries is of particular relevance to CUD because these arteries supply blood to the brain regions that acute and chronic effects of cocaine on cardiovascular health pmc 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.
Fig. 1. Cocaine’s acute and chronic toxicity mechanisms.
Notably, traditional cardiac biomarkers, such as myeloperoxidase and c-reactive protein are not useful as biomarkers for CUD , since imaging evidence reveal that the relationships between myocardial fat and body mass index in CUD is different than non-drug users . First, in terms of risk detection, studies with CUD document that Framingham risk scores label the majority of CUD as low risk, underestimating the indications for preventive action. Preventing acute events in pre-symptomatic individuals must include special consideration.
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 .
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- Notably, traditional cardiac biomarkers, such as myeloperoxidase and c-reactive protein are not useful as biomarkers for CUD , since imaging evidence reveal that the relationships between myocardial fat and body mass index in CUD is different than non-drug users .
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- Advanced atherosclerosis of intracranial vessels is noted as the cause of cocaine-induced stroke in numerous studies 4,29.
- Critical adds to acute implications of imminent change, of attendant suspense, and of decisiveness in the outcome.
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 .
Fig. 2. Cocaine-induced major pathophysiological load to the cardiovasculature, cerebrovasculature, and arteries.
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.
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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.
Add acute to one of your lists below, or create a new one. To add acute to a word list please sign up or log in. Critical adds to acute implications of imminent change, of attendant suspense, and of decisiveness in the outcome.
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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 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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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.
These effects, as well as others (e.g., myocardial edema), may show a cocaine dose-related response . In the heart, the significant interaction of cocaine with norepinephrine transporters 26,27 can lead to left ventricular dysfunction by effect of dilation, reduction of ejection phase and reduced contractility . Furthermore, Ca2+ increases could also underlie the reported enhanced hemodynamic and field potential responses to sensory stimulation after acute cocaine administration 67,69.
All content on this website, including dictionary, thesaurus, literature, geography, and other reference data is for informational purposes only. It follows a trend of homelessness among the youngest care leavers which campaigners say is growing more acute. „The flu season has now started in Wales, and acute respiratory infections are common in children, particularly at this time of year,” he added. Origin of acute1
