In the International Registry of Acute Aortic Dissection (IRAD), cocaine use was reported in 1.8% of all cases[6]. Acute type A aortic dissection occurs at a population-based incidence ranging from 2.1 to 16.3 per 100.000 persons[7,8]. The European Union had about 513.5 million inhabitants in 2019. Thus, the number of acute aortic dissections is between 10,784 and 83,701 cases per year. Based on these figures, it could be estimated that aortic dissection occurs in 194-1,507 cocaine users per year. The overall mortality for acute aortic dissection is described by 27.4%[9].
There are various known pathophysiological consequences of cocaine consumption that could increase the risk of aortic dissection. Cocaine stimulates the autonomic nervous system by restraining catecholamine reuptake and expanding affectability of adrenergic nerve endings to norepinephrine[10,11]. The autonomic nervous system reacts to cocaine in a similar way as to stress, with an increased heart rate and increased blood pressure[12,13]. Cocaine and the effects from alpha agonists show a synergy in terms of vasoconstriction[14]. Cocaine is also suspected to cause endothelial dysfunction and have a prothrombotic effect[15,16]. The elastic properties of the aorta have been demonstrated to alter in cases of chronic cocaine abuse, showing a decrease in aortic strain and distensibility, as well as a higher aortic stiffness index[17]. In addition, the relationship between acute aortic dissection and cocaine use may be modified by other factors such as demographics, lifestyle, or co-use of other drugs. Male gender, smoking, and use of alcohol are the most frequent accompanying risk factors[18]. To what extent the risk of acute aortic dissection increases for cocaine users is currently unknown.
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In addition to cocaine use itself, factors such as lifestyle, health behavior, and smoking may play a significant role in the causal relationship to aortic dissections. In all published case series, the proportion of smokers was between 61% and 100%. In our study, history of nicotine abuse was prevalent in 84% of cases. Previous studies also found an increased prevalence of cocaine-related aortic dissection among young, hypertensive, male patients who smoke[23]. The prevalence of cocaine use among cases of aortic dissection in the IRAD was 1.8%. The real number may be even higher due to patients not providing truthful information about their drug consumption. A self-reporting method may have introduced a significant bias. The use of urine toxicology screening might help identifying patients who really used cocaine within the past two to four days before the onset of symptoms and those with detectable cocaine metabolites. But nevertheless, drug screening comes with an ethical issue: the willingness of the patients to go through such work-ups that might produce undesired proofs against themselves (e.g., in criminal cases). According to current state of knowledge, it remains unknown how much the risk for an aortic dissection actually increases by cocaine use. We also do not know whether there is a possible relationship between dose and risk.
Because concurrent cocaine use is a relatively rare feature among all aortic dissection cases, patients could be misdiagnosed due to cardiovascular genesis being more likely associated to cocaine use[4]. In the history-taking setting of a patient with acute chest pain in the emergency room, the use of drugs should be included in the differential diagnostic considerations and the diagnosis of acute aortic dissection should be considered[8,24,25].
1. Adkins MS, Gaines WE, Anderson WA, Laub GW, Fernandez J, McGrath LB. Chronic type A aortic dissection: an unusual complication of cocaine inhalation. Ann Thorac Surg. 1993;56(4):977-9. doi:10.1016/0003-4975(93)90372-o.
8. Dabbagh A, Arabnia MK, Foroughi M, Shahzamani M, Rahmian H. The use of intraoperative transesophageal echocardiography in thoracic aortic dissection due to chronic cocaine abuse. Anesth Pain Med. 2016;7(1):e35254. doi:10.5812/aapm.35254.
12. Dobrilovic N, Stockwell PH, Singh AK. Valve-sparing aortic root replacement after cocaine-induced acute ascending aortic dissection. J Card Surg. 2011;26(2):207-10. doi:10.1111/j.1540-8191.2010.01191.x.
26. Palmiere C, Burkhardt S, Staub C, Hallenbarter M, Paolo Pizzolato G, Dettmeyer R, et al. Thoracic aortic dissection associated with cocaine abuse. Forensic Sci Int. 2004;141(2-3):137-42. doi:10.1016/j.forsciint.2003.12.018.
29. Riaz K, Forker AD, Garg M, McCullough PA. Atypical presentation of cocaine-induced type A aortic dissection: a diagnosis made by transesophageal echocardiography. J Investig Med. 2002;50(2):140-2. doi:10.2310/6650.2002.31309.
Advocates for the defund movement like Phillip McHarris and Thenjiwe McHarris argue that shifting funding to social services that can improve things such as mental health, addiction, and homelessness is a better use of taxpayer money. This approach further enhances the push to decriminalize and destigmatize people with mental health conditions and addiction problems. Ever since the overcriminalization of people addicted to crack cocaine in the 1990s, some scholars, practitioners, and policymakers have said that this shift is long overdue.
Abstract:Currently, there are no approved pharmacotherapies for addiction to cocaine and other psychostimulant drugs. Several studies have proposed that cannabidiol (CBD) could be a promising treatment for substance use disorders. In the present work, the authors describe the scarce preclinical and human research about the actions of CBD on the effects of stimulant drugs, mainly cocaine and methamphetamine (METH). Additionally, the possible mechanisms underlying the therapeutic potential of CBD on stimulant use disorders are reviewed. CBD has reversed toxicity and seizures induced by cocaine, behavioural sensitization induced by amphetamines, motivation to self-administer cocaine and METH, context- and stress-induced reinstatement of cocaine and priming-induced reinstatement of METH seeking behaviours. CBD also potentiated the extinction of cocaine- and amphetamine-induced conditioned place preference (CPP), impaired the reconsolidation of cocaine CPP and prevented priming-induced reinstatement of METH CPP. Observational studies suggest that CBD may reduce problems related with crack-cocaine addiction, such as withdrawal symptoms, craving, impulsivity and paranoia (Fischer et al., 2015). The potential mechanisms involved in the protective effects of CBD on addiction to psychostimulant drugs include the prevention of drug-induced neuroadaptations (neurotransmitter and intracellular signalling pathways changes), the erasure of aberrant drug-memories, the reversion of cognitive deficits induced by psychostimulant drugs and the alleviation of mental disorders comorbid with psychostimulant abuse. Further, preclinical studies and future clinical trials are necessary to fully evaluate the potential of CBD as an intervention for cocaine and methamphetamine addictive disorders.Keywords: cannabidiol; cocaine; methamphetamine; mice; rat; reinstatement; reward; self-administration; conditioned place preference; addiction 2ff7e9595c
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