Electrocardiographic Diagnosis of Acute Coronary Occlusion Myocardial Infarction in Ventricular Paced Rhythm Using the Modified Sgarbossa Criteria.

STUDY OBJECTIVE: Ventricular paced rhythm is thought to obscure the electrocardiographic diagnosis of acute coronary occlusion myocardial infarction. Our primary aim was to compare the sensitivity of the modified Sgarbossa criteria (MSC) to that of the original Sgarbossa criteria for the diagnosis of occlusion myocardial infarction in patients with ventricular paced rhythm. METHODS: In this retrospective case-control investigation, we studied adult patients with ventricular paced rhythm and symptoms of acute coronary syndrome who presented in an emergency manner to 16 international cardiac referral centers between January 2008 and January 2018. The occlusion myocardial infarction group was defined angiographically as thrombolysis in myocardial infarction grade 0 to 1 flow or angiographic evidence of coronary thrombosis and peak cardiac troponin I ≥10.0 ng/mL or troponin T ≥1.0 ng/mL. There were 2 control groups: the "non-occlusion myocardial infarction-angio" group consisted of patients who underwent coronary angiography for presumed type I myocardial infarction but did not meet the definition of occlusion myocardial infarction; the "no occlusion myocardial infarction" control group consisted of randomly selected emergency department patients without occlusion myocardial infarction. RESULTS: There were 59 occlusion myocardial infarction, 90 non-occlusion myocardial infarction-angio, and 102 no occlusion myocardial infarction subjects (mean age, 72.0 years; 168 [66.9%] men). For the diagnosis of occlusion myocardial infarction, the MSC were more sensitive than the original Sgarbossa criteria (sensitivity 81% [95% confidence interval [CI] 69 to 90] versus 56% [95% CI 42 to 69]). Adding concordant ST-depression in V4 to V6 to the MSC yielded 86% (95% CI 75 to 94) sensitivity. For the no occlusion myocardial infarction control group of ED patients, additional test characteristics of MSC and original Sgarbossa criteria, respectively, were as follows: specificity 96% (95% CI 90 to 99) versus 97% (95% CI 92 to 99); negative likelihood ratio (LR) 0.19 (95% CI 0.11 to 0.33) versus 0.45 (95% CI 0.34 to 0.65); and positive LR 21 (95% CI 7.9 to 55) versus 19 (95% CI 6.1 to 59). For the non-occlusion myocardial infarction-angio control group, additional test characteristics of MSC and original Sgarbossa criteria, respectively, were as follows: specificity 84% (95% CI 76 to 91) versus 90% (95% CI 82 to 95); negative LR 0.22 (95% CI 0.13 to 0.38) versus 0.49 (95% CI 0.35 to 0.66); and positive LR 5.2 (95% CI 3.2 to 8.6) versus 5.6 (95% CI 2.9 to 11). CONCLUSION: For the diagnosis of occlusion myocardial infarction in the presence of ventricular paced rhythm, the MSC were more sensitive than the original Sgarbossa criteria; specificity was high for both rules. The MSC may contribute to clinical decisionmaking for patients with ventricular paced rhythm.

Case series of 226 γ-hydroxybutyrate-associated deaths: lethal toxicity and trauma.

γ-Hydroxybutyrate (GHB) and its prodrugs are drugs of abuse that were also sold as "dietary supplements." Users present to emergency departments with overdose, impaired driving, withdrawal, and associated trauma. We compiled a series of GHB-associated deaths to elucidate lethal risks, GHB concentrations, cointoxicants, products, uses, and medical interventions. Death records were reviewed for toxicology, autopsy findings, and history. Inclusion cutoffs were as follows: 5/10 mg/L of GHB (antemortem blood/urine) and 50/20/7 mg/L of GHB (postmortem blood/urine/vitreous). Of 226 deaths included, 213 had cardiorespiratory arrest and 13 had fatal accidents. Seventy-eight deaths (35%) had no cointoxicants. Sixteen deaths involved "supplements" and 1 involved pharmaceutical GHB (Xyrem, Jazz Pharmaceuticals, Palo Alto, CA). Postmortem blood GHB was 18 to 4400 mg/L (median, 347 mg/L) in deaths negative for cointoxicants. Cardiorespiratory arrest occurred prehospital in 100% of 184 cases with available history. Of 72 cases with antemortem adverse effects reported, medical assistance was delayed or absent in 66; of these, acute GHB ingestion was known in 51, including 40 left to "sleep off" adverse effects. Thirty others were left "sleeping" and found dead. γ-Hydroxybutyrate is lethal even without cointoxicants, directly and through fatal accidents. Medical interventions were frequently delayed or absent despite known GHB ingestion, and witnessed adverse events and cardiorespiratory arrest occurred prehospital. Education is needed about the lethality of GHB and the necessity for prompt medical intervention.

Three deaths associated with use of Xyrem.

Fatalities resulting from popular use of gamma hydroxybutyrate (GHB) have previously been reported. We report three deaths associated with use of Xyrem (sodium oxybate), a pharmaceutical preparation of GHB initially approved for treatment of narcolepsy with cataplexy. One death appears associated with Xyrem abuse, with extremely high postmortem blood GHB levels documented. Although postmortem blood GHB levels in two other deaths are consistent with therapeutic levels, cause and effect cannot be established. We discuss these cases and factors which may have exerted contributory respiratory depressant effects, singly or in combination, including concurrent use of sedative hypnotics, obstructive sleep apnea, and obesity.

Physostigmine for gamma-hydroxybutyrate coma: inefficacy, adverse events, and review.

Physostigmine has been proposed as an antidote for gamma hydroxybutyrate (GHB) intoxication, based on associated awakenings in 1) patients anesthetized with GHB and 2) five of six patients administered physostigmine for GHB intoxication. However, there are neither well-supported mechanisms for physostigmine reversal of GHB effects, supportive animal studies, nor randomized, placebo-controlled trials demonstrating safety, efficacy, or improved outcomes. We sought to determine the outcomes of patients with GHB-induced coma after a physostigmine treatment protocol was instituted in an urban Emergency Department and ambulance service. Our search of medical records located five cases of GHB toxicity, all with co-intoxicants, who received physostigmine. None demonstrated response and, further, there were associated adverse events, including atrial fibrillation (2), pulmonary infiltrates (1) and significant bradycardia (1), and hypotension (1). We also reviewed 18 published GHB toxicity case series for incidence of adverse effects, stimulant co-intoxicants (which may heighten risk of physostigmine), complications, and outcomes of supportive care for GHB toxicity. We conclude that physostigmine is not indicated for reversal of GHB-induced alteration of consciousness; it is not efficacious, it may be unsafe, particularly in the setting of recreational polydrug use; and supportive care results in universally good outcomes.

Agitation is common in gamma-hydroxybutyrate toxicity.

Gamma-Hydroxybutyrate (GHB)-related compounds are most commonly described as depressants, with emphasis on somnolence, obtundation, stupor, and coma (SOSC). We sought to demonstrate the full spectrum of clinical presentations of GHB intoxication, including agitation and other nonsedative effects. Our observational study identified 66 patients with GHB toxicity, 40 of whom manifested agitation; 25 had agitation before or after SOSC, 10 had agitation alternating abruptly with SOSC, and 5 had agitation only. Fourteen presentations also included "bizarre" or self-injurious behaviors. Of 40 presentations with agitation, 19 had stimulant co-intoxicants confirmed by screen (14) or history (5). The remaining 21 patients with agitation were negative for stimulants by screen (12) or history (9). Gas chromatography/mass spectrometry detected GHB in 25 cases; 12 manifested agitation, 4 of which also screened negative for stimulants. Clinicians should broaden their definitions of GHB toxicity to include nonsedative effects such as agitation, combativeness, and bizarre or self-injurious behavior.