Myeloperoxidase and C-reactive protein in patients with cocaine-associated chest pain

O’Conor, Katie J.; Chang, Anna Marie; Wu, Alan H.B.; Hollander, Judd E.

doi:10.1016/j.ajem.2012.11.026

Cited by 2 publications

(2 citation statements)

References 44 publications

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“…In general, patients experiencing cocaine-associated myocardial infarction are slightly older, less often have a past history of chest pain, and more often have known coronary artery disease, but are otherwise indistinguishable from those with cocaine-associated chest pain without myocardial infarction [10]. Results of ECG are poorly associated with myocardial infarction [10,72], and traditional cardiac biomarkers, such as myeloperoxidase and C-reactive protein, are not useful as biomarkers in the context of cocaine use [73]. In cocaine users, cardiac troponins are the preferred cardiac biomarker for myocardial infarction; specificity is similar with and without cocaine use [10,74].…”

Section: Diagnosismentioning

confidence: 96%

Cardiovascular consequences of cocaine use

Stankowski

Kloner

Rezkalla

2015

Trends in Cardiovascular Medicine

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Section: Diagnosismentioning

confidence: 96%

Cardiovascular consequences of cocaine use

Stankowski

Kloner

Rezkalla

2015

Trends in Cardiovascular Medicine

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“…The use of beta-blockers show mixed results. Notably, traditional cardiac biomarkers, such as myeloperoxidase and c-reactive protein are not useful as biomarkers for CUD [92], since imaging evidence reveal that the relationships between myocardial fat and body mass index in CUD is different than non-drug users [93]. …”

Section: Prevention and Treatmentmentioning

confidence: 99%

Vascular disease in cocaine addiction

et al. 2017

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Cocaine, a powerful vasoconstrictor, induces immune responses including cytokine elevations. Chronic cocaine use is associated with functional brain impairments potentially mediated by vascular pathology. Although the Crack-Cocaine epidemic has declined, its vascular consequences are increasingly becoming evident among individuals with cocaine use disorder of that period, now aging. Paradoxically, during the period when prevention efforts could make a difference, this population receives psychosocial treatment at best. We review major postmortem and in vitro studies documenting cocaine-induced vascular toxicity. PubMed and Academic Search Complete were used with relevant terms. Findings consist of the major mechanisms of cocaine-induced vasoconstriction, endothelial dysfunction, and accelerated atherosclerosis, emphasizing acute, chronic, and secondary effects of cocaine. 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. Early detection of vascular disease in cocaine addiction by multimodality imaging is discussed. 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. Given the vascular toxicity cocaine induces, further compounded by smoking and alcohol comorbidity, and interacting with aging of the crack generation, there is a public health imperative to identify pre-symptomatic markers of vascular impairments in cocaine addiction and employ preventive treatment to reduce silent disease progression.

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Myeloperoxidase and C-reactive protein in patients with cocaine-associated chest pain

Cited by 2 publications

References 44 publications

Cardiovascular consequences of cocaine use

Cardiovascular consequences of cocaine use

Vascular disease in cocaine addiction

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