Other known mechanisms of cardiotoxicity, include cocaine’s blockage of sodium channels and a subsequent increase in calcium flux and a vasoconstrictor response . Ischemia is suggested as the main mechanism of acute damage responsible for various clinical presentations . While smoking crack or sniffing cocaine, there is a vast accumulation of the drug in the heart affecting myocardial tissue directly . Cocaine crosses the blood–brain-barrier perhaps better than other psychoactive chemicals and may even induce its breakdown 17,18.
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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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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
- Cocaine’s acute and chronic toxicity mechanisms on the vessel, heart, and the central nervous system (CNS), and their interactions.
- We review major postmortem and in vitro studies documenting cocaine-induced vascular toxicity.
- Cocaine induces acute cardiotoxicity through multiple pathways (Fig. 1, left box).
- For example, vasoconstriction, a main underlying cause of ischemic strokes, may result from the increased availability of epinephrine, norepinephrine, and serotonin (especially in large and medium-sized brain vessels) in the vasculature due to cocaine blockade of their reuptake 55–57.
- Prevention of cocaine-induced systemic complications could be considered as part of a harm reduction strategy.
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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. There is also evidence that the cardiovascular actions of cocaine are mediated in part by dopamine , via central and peripheral mechanisms . However, the accelerated development of vascular disease remains mostly undetected and asymptomatic presentation of vascular pathology in CUD results in silent disease progression. Cocaine-induced damage to the cardiovascular and cerebrovascular systems is widely reported, and is linked with hypertension, tachycardia, ventricular arrhythmias ,myocardial infarction 3,4, stroke 4,5, resulting in severe functional impairments or sudden mortality 6–10.
Indeed, silent disease progression is particularly pronounced in CUD who remain asymptomatic until they reach the emergency room with acute events 8,24,73. Atherosclerosis, however, develops during prolonged periods of chronic cocaine use and in its early stages usually does not create symptoms or signs. Given the known vascular toxicity cocaine induces 13,23, further compounded by cigarette smoking and alcohol comorbidity 32,73,96 and interacting with the progressing age of the crack generation 97,98, there is a public health imperative to identify presymptomatic markers of vascular impairments in CUD. Chronic treatments for CUD with cardiovascular problems include antiplatelet and antithrombin agents, statins and diuretics. For example, enhanced supportive care and use of benzodiazepines and phentolamine for sedation; and avoiding β-blockers, which can lead to severe hyper-tension and coronary vasoconstriction resulting from the interaction of β-blockers with cocaine (for review see Ref. ).
- Www.merriam-webster.com/dictionary/acute.
- Volkow et al. were the first to document that CUD had profound decreases in CBF as evidenced by decreased brain uptake of water.
- Treatment for cocaine-induced acute vascular events may be similar to indications in patients with traditional risk-factors, with few exceptions.
- 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.
- 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 .
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.
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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 .
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»). It retains this meaning today, but can also refer to the severity of more general matters, such as «acute embarrassment» or «an acute shortage.» For such a short and simple-looking word, acute has a rather bewildering range of meanings.
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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.
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As nitric oxide/glyceraldehyde-3-phosphate dehydrogenase pathway mediates cocaine induced autophagy, glyceraldehyde-3-phosphate dehydrogenase can be tested for use (see clinical trials in Parkinson’s disease 48,94). Here too, it is helpful to briefly review prevention and treatment recommendations separately for acute vascular events. Cocaine use promotes vascular disease, while also influencing the course of disease management, and therapy. The prevailing low socio-economic status, limited awareness of health issues, lack of sleep, and poor nutrition, could further hasten vascular disease 43,44. Literature acute and chronic effects of cocaine on cardiovascular health pmc that characterizes atherosclerosis in the carotid arteries in asymptomatic cocaine users is scarce.
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.
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.
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.
Chest pain 8,13,76 and cerebrovascular events 5,31,63 may occur within minutes to just a few hours from cocaine use. As evident from this review, there is ample data on cocaine-induced endothelial dysfunction, vasoconstriction, and accelerated atherosclerosis. The first line of treatment for cocaine induced sodium channel blockade is alkalization with hypertonic sodium bicarbonate.
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Additionally, inflammation and atherosclerosis are substantial potentially lethal vascular effects of cocaine use that have acute and chronic systemic impact 2,4,10,13,16,23,35,37,38,42,50. Particular attention was given to the imaging studies that measured cocaine-induced changes to the human heart, brain, and arteries (Table 1), since these methods are gaining a central role as markers of inflammatory disease. The etiology underlying cocaine’s acute and chronic vascular effects is multifactorial, spanning hypertension, impaired homeostasis and platelet function, thrombosis, thromboembolism, and alterations in blood flow. Consequently, cocaine use should be included in protocols and guidelines as a risk factor for cardiovascular, cerebrovascular and other vascular and arterial disease. Multimodality imaging studies could promote the identification of CUD with silent pre-symptomatic atherosclerosis in the brain, heart and arteries 100–104. The major cerebrovascular effects of cocaine consist of ischemic and hemorrhagic (including subarachnoid and intracerebral hemorrhages) strokes 5,13,29–32,59–61 (Fig. 2).
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
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