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Sniff of coke breaks the heart: cocaine-induced coronary vasospasm aggravated by therapeutic hypothermia and vasopressors after aborted sudden cardiac death: a case report.

ABSTRACT: Introduction:Coronary vasospasm and sudden cardiac death are a frequently reported complication of cocaine abuse. We present a case with uniquely severe clinical and angiographic presentation. Case presentation:A 39-year-old patient was presented to the cath lab after out-of-hospital cardiac arrest. Coronary angiography revealed focal coronary vasospasm in the proximal LCx, well responsive for intracoronary nitrates. Accordingly, no coronary intervention was performed and the patient was transferred to the cardiac intensive care unit. There, after systematically cooling sudden haemodynamic deterioration and massive ST-elevation was observed. Repeated coronary angiography revealed subocclusive LAD and LCx vasospasm, which again recovered after intracoronary injection of nitric oxide. Discussion:Coronary-spastic effect of cocaine and its potentially dreadful clinical consequences are well-described phenomena. As novelty this case emphasizes that standard of care, including systematic hypothermia and vasopressor administration after out-of-hospital cardiac arrest can potentiate cocaine-induced coronary spasm with dramatic outcomes.

SUBMITTER: Manninger M

PROVIDER: S-EPMC6177107 | biostudies-literature | 2018 Jun

REPOSITORIES: biostudies-literature

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Sniff of coke breaks the heart: cocaine-induced coronary vasospasm aggravated by therapeutic hypothermia and vasopressors after aborted sudden cardiac death: a case report.

Manninger Martin M Perl Sabine S Brussee Helmut H G Toth Gabor G

European heart journal. Case reports 20180417 2

<h4>Introduction</h4>Coronary vasospasm and sudden cardiac death are a frequently reported complication of cocaine abuse. We present a case with uniquely severe clinical and angiographic presentation.<h4>Case presentation</h4>A 39-year-old patient was presented to the cath lab after out-of-hospital cardiac arrest. Coronary angiography revealed focal coronary vasospasm in the proximal LCx, well responsive for intracoronary nitrates. Accordingly, no coronary intervention was performed and the pati ...[more]

PMID: 31020121

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Project description:BackgroundInitial goal-directed resuscitation for hypotensive shock usually includes administration of intravenous fluids, followed by initiation of vasopressors. Despite obvious immediate effects of vasopressors on haemodynamics, their effect on patient-relevant outcomes remains controversial. This review was published originally in 2004 and was updated in 2011 and again in 2016.ObjectivesOur objective was to compare the effect of one vasopressor regimen (vasopressor alone, or in combination) versus another vasopressor regimen on mortality in critically ill participants with shock. We further aimed to investigate effects on other patient-relevant outcomes and to assess the influence of bias on the robustness of our effect estimates.Search methodsWe searched the Cochrane Central Register of Controlled Trials (CENTRAL; 2015 Issue 6), MEDLINE, EMBASE, PASCAL BioMed, CINAHL, BIOSIS and PsycINFO (from inception to June 2015). We performed the original search in November 2003. We also asked experts in the field and searched meta-registries to identify ongoing trials.Selection criteriaRandomized controlled trials (RCTs) comparing various vasopressor regimens for hypotensive shock.Data collection and analysisTwo review authors abstracted data independently. They discussed disagreements between them and resolved differences by consulting with a third review author. We used a random-effects model to combine quantitative data.Main resultsWe identified 28 RCTs (3497 participants) with 1773 mortality outcomes. Six different vasopressors, given alone or in combination, were studied in 12 different comparisons.All 28 studies reported mortality outcomes; 12 studies reported length of stay. Investigators reported other morbidity outcomes in a variable and heterogeneous way. No data were available on quality of life nor on anxiety and depression outcomes. We classified 11 studies as having low risk of bias for the primary outcome of mortality; only four studies fulfilled all trial quality criteria.In summary, researchers reported no differences in total mortality in any comparisons of different vasopressors or combinations in any of the pre-defined analyses (evidence quality ranging from high to very low). More arrhythmias were observed in participants treated with dopamine than in those treated with norepinephrine (high-quality evidence). These findings were consistent among the few large studies and among studies with different levels of within-study bias risk.Authors' conclusionsWe found no evidence of substantial differences in total mortality between several vasopressors. Dopamine increases the risk of arrhythmia compared with norepinephrine and might increase mortality. Otherwise, evidence of any other differences between any of the six vasopressors examined is insufficient. We identified low risk of bias and high-quality evidence for the comparison of norepinephrine versus dopamine and moderate to very low-quality evidence for all other comparisons, mainly because single comparisons occasionally were based on only a few participants. Increasing evidence indicates that the treatment goals most often employed are of limited clinical value. Our findings suggest that major changes in clinical practice are not needed, but that selection of vasopressors could be better individualised and could be based on clinical variables reflecting hypoperfusion.

Dataset Information

Sniff of coke breaks the heart: cocaine-induced coronary vasospasm aggravated by therapeutic hypothermia and vasopressors after aborted sudden cardiac death: a case report.

Publications

Sniff of coke breaks the heart: cocaine-induced coronary vasospasm aggravated by therapeutic hypothermia and vasopressors after aborted sudden cardiac death: a case report.

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