Cocaine-induced epicardial coronary artery thrombosis resulting in extensive myocardial injury assessed by cardiac magnetic resonance imaging

Robaei, Daniel; Grieve, Stuart M.; Nelson, Greg C.; Bhindi, Ravinay; Figtree, Gemma A.

doi:10.1093/eurheartj/ehq229

Cited by 9 publications

(6 citation statements)

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“…A previous publication in a casual cocaine user has demonstrated multiple spots of midmyocardial LGE taken as potential evidence of cocaine-induced vasoconstriction of coronary arterioles [ 41 ]. Furthermore, myocardial infarction can occur as a result of coronary thrombus in patients with otherwise normal coronary arteries [ 42 ]. Therefore, some of the midmyocardial areas of LGE found might well account for coronary vasospasm or small areas of thrombus occlusion, bearing in mind that this pattern is also observed in a number of cardiomyopathies.…”

Section: Discussionmentioning

confidence: 99%

Long term effects of cocaine on the heart assessed by cardiovascular magnetic resonance at 3T

Maceira

Ripoll

Cosı́n-Sales

et al. 2014

Journal of Cardiovascular Magnetic Resonance

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BackgroundCocaine is an addictive, sympathomimetic drug with potentially lethal effects. The prevalence and features of cocaine cardiotoxicity are not well known. We aimed to assess these effects using a comprehensive cardiovascular magnetic resonance (CMR) protocol in a large group of asymptomatic cocaine users.MethodsConsecutive (n = 94, 81 males, 36.6 ±7 years), non-selected, cocaine abusers were recruited and had a medical history, examination, ECG, blood test and CMR. The CMR study included measurement of left and right ventricular (LV, RV) dimensions and ejection fraction (EF), sequences for detection of myocardial oedema and late gadolinium enhancement (LGE). Images were compared to a cohort of healthy controls.ResultsYears of regular cocaine use were 13.9 ± 9. When compared to the age-matched healthy cohort, the cocaine abusers had increased LV end-systolic volume, LV mass index and RV end-systolic volume, with decreased LVEF and RVEF. No subject had myocardial oedema, but 30% had myocardial LGE indicating myocardial damage.ConclusionsCMR detected cardiovascular disease in 71% of this cohort of consecutive asymptomatic cocaine abusers and mean duration of abuse was related to probability of LV systolic dysfunction.

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Section: Discussionmentioning

confidence: 99%

Long term effects of cocaine on the heart assessed by cardiovascular magnetic resonance at 3T

Maceira

Ripoll

Cosı́n-Sales

et al. 2014

Journal of Cardiovascular Magnetic Resonance

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“…This sub-group of users have previously been observed to start using cocaine on a “social-recreational” basis; and do “not expect to become dependent on a drug that is believed to be relatively harmless”, and “have an image of themselves as invincible” [27]. Significantly, it was from a similar group that we witnessed a spate of individuals presenting with large MIs [9]. One of the difficulties with recruiting via the community and not via formal drug rehabilitation centres is the reluctance of those who do not identify as having a formal clinical addiction to volunteer for medical research.…”

Section: Discussionmentioning

confidence: 79%

“…These acute effects are attributed to a number of mechanisms including cocaine's powerful sympathomimetic properties [5], coronary artery vasoconstriction by direct vessel smooth muscle activation [6], the inhibition of endogenous nitric oxide production and the release of potent vasoconstrictors such as endothelin-1 [7]. Cocaine also has an acute effect on arterial thrombosis through a number of mechanisms acting on platelets [8], [9].…”

Section: Introductionmentioning

confidence: 99%

Regular Cocaine Use Is Associated with Increased Systolic Blood Pressure, Aortic Stiffness and Left Ventricular Mass in Young Otherwise Healthy Individuals

et al. 2014

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BackgroundThe cardiovascular impact of cocaine use in otherwise healthy individuals who consider themselves ‘social’ users is not well established.Methods/ResultsTwenty regular cocaine users and 20 control subjects were recruited by word-of-mouth. Cardiovascular magnetic resonance was performed to assess cardiac and vascular structure and function. Cocaine users had higher systolic blood pressure compared to non-users (134±11 vs 126±11 mmHg, p = 0.036), a finding independent of age, body surface area, smoking and alcohol consumption. Cocaine use was associated with increased arterial stiffness - reflected by reduced aortic compliance (1.3±0.2 vs 1.7±0.5 cm2×10−2.mmHg−1, p = 0.004), decreased distensibility (3.8±0.9 vs 5.1±1.4 mmHg−1.10−3, p = 0.001), increased stiffness index (2.6±0.6 vs 2.1±0.6, p = 0.005), and higher pulse wave velocity (5.1±0.6 vs 4.4±0.6 m.s−1, p = 0.001). This change in aortic stiffness was independent of vessel wall thickness. Left ventricular mass was 18% higher in cocaine users (124±25 vs 105±16 g, p = 0.01), a finding that was independent of body surface area, and left atrial diameter was larger in the user group than controls (3.8±0.6 vs 3.5±0.3 cm, p = 0.04). The increased left ventricular mass, systolic blood pressure and vascular stiffness measures were all associated with duration and/or frequency of cocaine use. No late gadolinium enhancement or segmental wall motion abnormalities were seen in any of the subjects.ConclusionsCompared with the non-user control cohort, cocaine users had increased aortic stiffness and systolic blood pressure, associated with greater left ventricular mass. These measures are all well known risk factors for premature cardiovascular events, highlighting the dangers of cocaine use, even in a ‘social’ setting, and have important public health implications.

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“…[20][21][22] Cocaine activates circulating platelets by increasing expression of platelet factor 4, thromboglobulin B, and P-selectin. 23,24 Elevated levels of C-reactive protein, von Willebrand factor, and fibrinogen also affect coagulation, with no compensatory increase in fibrinolytic activity.…”

Section: Prothrombotic Effectsmentioning

confidence: 99%

Rethinking Cocaine-Associated Chest Pain and Acute Coronary Syndromes

Finkel

Marhefka

2011

Mayo Clinic Proceedings

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Every year more than 500,000 patients present to the emergency department with cocaine-associated complications, most commonly chest pain. Many of these patients undergo extensive work-up and treatment. Much of the evidence regarding cocaine's cardiovascular effects, as well as the current management of cocaine-associated chest pain and acute coronary syndromes, is anecdotally derived and based on studies written more than 2 decades ago that involved only a few patients. Newer studies have brought into question many of the commonly held theories and practices regarding the etiology, diagnosis, and treatment of this common clinical scenario. However, there continues to be a paucity of prospective, randomized trials addressing this topic as it relates to clinical outcomes. We searched PubMed for Englishlanguage articles from 1960 to 2011 using the keywords cocaine, chest pain, coronary arteries, myocardial infarction, emergency department, cardiac biomarkers, electrocardiogram, coronary computed tomography, observation unit, β-blockers, benzodiazepines, nitroglycerin, calcium channel blockers, phentolamine, and cardiomyopathy; including various combinations of these terms. We reviewed the abstracts to confirm relevance, and then full articles were extracted. References from extracted articles were also reviewed for relevant articles. In this review, we critically evaluate the limited historical evidence underlying the current teachings on cocaine's cardiovascular effects and management of cocaine-associated chest pain. We aim to update the reader on more recent, albeit small, studies on the emergency department evaluation and clinical and pharmacologic management of cocaine-associated chest pain. Finally, we summarize recent guidelines and review an algorithm based on the current best evidence. Proc. 2011;86(12):1198-1207 ACS = acute coronary syndrome; AHA = American Heart Association; CCB = calcium channel blockers; CCP = cocaine-associated chest pain; DBP = diastolic blood pressure; ECG = electrocardiography; ED = emergency department; HR = heart rate; MAP = mean arterial pressure; MI = myocardial infarction; PCI = percutaneous coronary intervention; SBP = systolic blood pressure; STEMI = ST-segment elevation myocardial infarction; TIMI = Thrombolysis in Myocardial Infarction E very year millions of Americans abuse cocaine, many of whom present to the emergency department (ED) with cocaine-related complications, most commonly chest pain. Unfortunately, much of the current thinking on cocaine and its cardiovascular effects is either anecdotally derived or based on small studies conducted more than 2 decades ago. Recently, newer studies have brought into question many of the commonly held theories and practices regarding the etiology, diagnosis, and management of cocaine-associated chest pain (CCP) and suspected myocardial ischemia. Mayo ClinWe searched PubMed for English-language articles from 1960 to 2011 using the keywords cocaine, chest pain, coronary arteries, myocardial infarction, emergency department, card...

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Cocaine-induced epicardial coronary artery thrombosis resulting in extensive myocardial injury assessed by cardiac magnetic resonance imaging

Cited by 9 publications

References 0 publications

Long term effects of cocaine on the heart assessed by cardiovascular magnetic resonance at 3T

Long term effects of cocaine on the heart assessed by cardiovascular magnetic resonance at 3T

Regular Cocaine Use Is Associated with Increased Systolic Blood Pressure, Aortic Stiffness and Left Ventricular Mass in Young Otherwise Healthy Individuals

Rethinking Cocaine-Associated Chest Pain and Acute Coronary Syndromes

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