Cocaine in Acute Myocardial Infarction

Lippi, Giuseppe; Plebani, Mario; Cervellin, Gianfranco

doi:10.1016/s0065-2423(10)51003-5

Cited by 18 publications

(10 citation statements)

References 54 publications

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“…Drug-induced MI is gaining importance with increased use of recreational drugs. Recreational drugs well known to induce MI include cocaine,3 amphetamines and ecstasy. Their effects on the cardiovascular system are predominantly related to stimulation of the sympathetic nervous system; thus they are known to cause MI secondary to CAS.…”

Section: Discussionmentioning

confidence: 99%

Myocardial infarction following cannabis induced coronary vasospasm

Gunawardena¹,

Rajapakse

Herath

et al. 2014

BMJ Case Reports

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SUMMARYSmoking cannabis is a rare cause of myocardial infarction. We report a 29-year-old man who presented with acute coronary syndrome following consumption of a type of cannabis with the street name 'Kerala Ganja'. KG is smuggled into Sri Lanka from India; it is grown in the south Indian state of Kerala and is much more potent than the local ganja (marijuana). The patient developed dynamic ST-segment elevations in different leads in sequential ECGs, corresponding to different coronary artery territories. Coronary angiogram did not demonstrate evidence of occlusive atherosclerotic disease, but showed slow flow down the left anterior descending artery, which improved with administration of intracoronary nitrates. The patient's cardiac biomarkers were significantly elevated. A diagnosis was made of vasospasm causing myocardial infarction, most likely to have been triggered by cannabis consumption. We highlight the importance of considering this possible aetiology, particularly in patients with ACS with a susceptible social profile. BACKGROUND

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Section: Discussionmentioning

confidence: 99%

Myocardial infarction following cannabis induced coronary vasospasm

Gunawardena¹,

Rajapakse

Herath

et al. 2014

BMJ Case Reports

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“…In addition, cocaine also blocks the fast Na ? channels in membranes, reducing the phase 0 of the action-potential, thereby inducing a local anesthetic effect [56,57].…”

Section: Pharmacological Basis Of Cocaine Effectsmentioning

confidence: 99%

Pathophysiological mechanisms of catecholamine and cocaine-mediated cardiotoxicity

Liaudet¹,

Calderari²,

Pacher³

2014

Heart Fail Rev

132

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Overactivation of the sympatho-adrenergic system is an essential mechanism providing short-term adaptation to the stressful conditions of critical illnesses. In the same way, the administration of exogenous catecholamines is mandatory to support the failing circulation in acutely ill patients. In contrast to these short-term benefits, prolonged adrenergic stress is detrimental to the cardiovascular system by initiating a series of adverse effects triggering significant cardiotoxicity, whose pathophysiological mechanisms are complex and only partially elucidated. In addition to the development of myocardial oxygen supply/demand imbalance induced by the sustained activation of adrenergic receptors, catecholamines can damage cardiomyocytes by fostering mitochondrial dysfunction, via two main mechanisms. The first one is calcium overload, consecutive to β-adrenergic receptor-mediated activation of protein kinase A and subsequent phosphorylation of multiple Ca(2+)-cycling proteins. The second one is oxidative stress, primarily related to the transformation of catecholamines into "aminochromes," which undergo redox cycling in mitochondria to generate copious amounts of oxygen-derived free radicals. In turn, calcium overload and oxidative stress promote mitochondrial permeability transition and cardiomyocyte cell death, both via the apoptotic and necrotic pathways. Comparable mechanisms of myocardial toxicity, including marked oxidative stress and mitochondrial dysfunction, have been reported with the use of cocaine, a common recreational drug with potent sympathomimetic activity. The aim of the current review is to present in detail the pathophysiological processes underlying the development of catecholamine and cocaine-induced cardiomyopathy, as such conditions may be frequently encountered in the clinical practice of cardiologists and ICU specialists.

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“…Among patients with SLE, disease activity and duration may be more important contributors to IHD than modifiable risk factors . Cocaine induces vasospasm and can cause premature IHD death, unrelated to modifiable risk factors . Premature‐onset IHD related to human immunodeficiency virus (HIV) may theoretically be unresponsive to favorable risk‐factor trends, such as improvement in US lipid levels between 1998 and 2010 …”

Section: Introductionmentioning

confidence: 99%

Diabetes and Ischemic Heart Disease Death in People Age 25–54: A Multiple‐Cause‐of‐Death Analysis Based on Over 400 000 Deaths From 1990 to 2008 in New York City

Quiñones

Lobach

Maduro

et al. 2015

Clinical Cardiology

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Background: Over the past decade, ischemic heart disease (IHD) mortality trends have been less favorable among adults age 25-54 than age ≥55 years. Hypothesis: Disorders associated with IHD such as diabetes, chronic inflammatory and infectious diseases, and cocaine use are important contributors to premature IHD mortality. Methods: Multiple-cause-of-death analysis was performed using the New York City (NYC) Vital Statistics database. Frequencies of selected contributing causes on death records with IHD as the underlying cause for decedents age ≥25 were assessed (n = 418,151; 1990-2008). Concurrent Telephone risk-factor surveys (NYC Community Health Survey, Centers for Disease Control Behavioral Risk Factor Survey in New York State) were analyzed. Results: In sum, a prespecified contributing cause was identified on 13.6% of death certificates for IHD decedents age 25-54. Diabetes was reported more frequently for younger IHD decedents (15% of females and 10% of males age 25-54 vs 6% of both sexes age ≥ 55). In contrast, concurrent diabetes prevalence in New York State was 3.4% for those age 25-54 and 13.6% for those age >55 (P < 0.0001). Systemic lupus erythematosus, human immunodeficiency virus, and cocaine were also more likely to contribute to IHD death among younger than older people. Conclusions: Diabetes may be a potent risk factor for IHD death in young people, particularly young women, in whom it was reported on IHD death records at a rate 5× higher than local prevalence. The high frequency of reporting of studied contributing causes in younger IHD decedents may provide a focus for further IHD mortality-reduction efforts in younger adults. IntroductionIn the United States, about 405,000 deaths in 2008 were attributed to ischemic heart disease (IHD), 1 a 70% decrease from the peak rate in 1968. This trend has not been consistent across groups. From 1999 to 2010, IHD mortality did not significantly change in young women, whereas young men experienced a small decrease and larger declines were observed among older women and men. 1 Over a similar period, the decline in IHD mortality was slower for Americans age < 55 years than older individuals. 2 Although the IHD mortality rate is much lower among younger than

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Cocaine in Acute Myocardial Infarction

Cited by 18 publications

References 54 publications

Myocardial infarction following cannabis induced coronary vasospasm

Myocardial infarction following cannabis induced coronary vasospasm

Pathophysiological mechanisms of catecholamine and cocaine-mediated cardiotoxicity

Diabetes and Ischemic Heart Disease Death in People Age 25–54: A Multiple‐Cause‐of‐Death Analysis Based on Over 400 000 Deaths From 1990 to 2008 in New York City

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