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.

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.

Nearby words

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.

• Ischemia is suggested as the main mechanism of acute damage responsible for various clinical presentations .
• But rarer and more serious ones include acute gallstone disease, pancreatitis and serious allergic reactions.
• 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.

The Words of the Week – Nov. 28

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. 1. Cocaine’s acute and chronic toxicity mechanisms.

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 .

• 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.
• We review major postmortem and in vitro studies documenting cocaine-induced vascular toxicity.
• 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 .
• As evident from this review, there is ample data on cocaine-induced endothelial dysfunction, vasoconstriction, and accelerated atherosclerosis.
• Prevention of cocaine-induced systemic complications could be considered as part of a harm reduction strategy.

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.

Can you solve 4 words at once?

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 .

Popular in Wordplay

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.

Other Word Forms

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.

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.

HOW TO USE THE DICTIONARY

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

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 .

Related Words

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

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.

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 acute and chronic effects of cocaine on cardiovascular health pmc elicits autophagy involving nitric oxide and glyceraldehyde-3-phosphate dehydrogenase signaling cascade .