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.

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 .

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 .

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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.

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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.

Fig. 2. Cocaine-induced major pathophysiological load to the cardiovasculature, cerebrovasculature, and arteries.

• Cocaine crosses the blood–brain-barrier perhaps better than other psychoactive chemicals and may even induce its breakdown 17,18.
• 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.
• 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 .
• Findings consist of the major mechanisms of cocaine-induced vasoconstriction, endothelial dysfunction, and accelerated atherosclerosis, emphasizing acute, chronic, and secondary effects of cocaine.
• 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.

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 acute and chronic effects of cocaine on cardiovascular health pmc 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.

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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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. ).

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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).

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.

Phenomenology contributing to vascular damage

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 .

• 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.
• 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.
• It is the opposite of chronic.
• 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.
• These mechanisms underlie inadequate myocardial oxygen equilibrium, which may lead to ischemia and manifest as angina or infarction 2,13.
• 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 .

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

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.

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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 that characterizes atherosclerosis in the carotid arteries in asymptomatic cocaine users is scarce.

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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 . 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.