Biomarkers Enhance Discrimination and Prognosis of Type 2 Myocardial Infarction.

BACKGROUND: The observed incidence of type 2 myocardial infarction (T2MI) is expected to increase with the implementation of increasingly sensitive cTn assays. However, it remains to be determined how to diagnose, risk-stratify, and treat patients with T2MI. We aimed to discriminate and risk-stratify T2MI using biomarkers. METHODS: Patients presenting to the emergency department with chest pain, enrolled in the CHOPIN study (Copeptin Helps in the early detection Of Patients with acute myocardial INfarction), were retrospectively analyzed. Two cardiologists adjudicated type 1 MI (T1MI) and T2MI. The prognostic ability of several biomarkers alone or in combination to discriminate T2MI from T1MI was investigated using receiver operating characteristic curve analysis. The biomarkers analyzed were cTnI, copeptin, MR-proANP (midregional proatrial natriuretic peptide), CT-proET1 (C-terminal proendothelin-1), MR-proADM (midregional proadrenomedullin), and procalcitonin. The prognostic utility of these biomarkers for all-cause mortality and major adverse cardiovascular event (a composite of acute myocardial infarction, unstable angina pectoris, reinfarction, heart failure, and stroke) at 180-day follow-up was also investigated. RESULTS: Among the 2071 patients, T1MI and T2MI were adjudicated in 94 and 176 patients, respectively. Patients with T1MI had higher levels of baseline cTnI, whereas those with T2MI had higher baseline levels of MR-proANP, CT-proET1, MR-proADM, and procalcitonin. The area under the receiver operating characteristic curve for the diagnosis of T2MI was higher for CT-proET1, MR-proADM, and MR-proANP (0.765, 0.750, and 0.733, respectively) than for cTnI (0.631). Combining all biomarkers resulted in a similar accuracy to a model using clinical variables and cTnI (0.854 versus 0.884, P=0.294). Addition of biomarkers to the clinical model yielded the highest area under the receiver operating characteristic curve (0.917). Other biomarkers, but not cTnI, were associated with mortality and major adverse cardiovascular event at 180 days among all patients, with no interaction between the diagnosis of T1MI or T2MI. CONCLUSIONS: Assessment of biomarkers reflecting pathophysiologic processes occurring with T2MI might help differentiate it from T1MI. All biomarkers measured, except cTnI, were significant predictors of prognosis, regardless of the type of myocardial infarction.

Necessity of hospitalization and stress testing in low risk chest pain patients.

BACKGROUND: Copeptin is a marker of endogenous stress including early myocardial infarction(MI) and has value in early rule out of MI when used with cardiac troponin I(cTnI). OBJECTIVES: The goal of this study was to demonstrate that patients with a normal electrocardiogram and cTnI<0.040µg/l and copeptin<14pmol/l at presentation and after 2 h may be candidates for early discharge with outpatient follow-up potentially including stress testing. METHODS: This study uses data from the CHOPIN trial which enrolled 2071 patients with acute chest pain. Of those, 475 patients with normal electrocardiogram and normal cTnI(<0.040µg/l) and copeptin<14pmol/l at presentation and after 2 h were considered "low risk" and selected for further analysis. RESULTS: None of the 475 "low risk" patients were diagnosed with MI during the 180day follow-up period (including presentation). The negative predictive value of this strategy was 100% (95% confidence interval(CI):99.2%-100.0%). Furthermore no one died during follow up. 287 (60.4%) patients in the low risk group were hospitalized. In the "low risk" group, the only difference in outcomes (MI, death, revascularization, cardiac rehospitalization) was those hospitalized underwent revascularization more often (6.3%[95%CI:3.8%-9.7%] versus 0.5%[95%CI:0.0%-2.9%], p=.002). The hospitalized patients were tested significantly more via stress testing or angiogram (68.6%[95%CI:62.9%-74.0%] vs 22.9%[95%CI:17.1%-29.6%], p<.001). Those tested had less cardiac rehospitalizations during follow-up (1.7% vs 5.1%, p=.040). CONCLUSIONS: In conclusion, patients with a normal electrocardiogram, troponin and copeptin at presentation and after 2 h are at low risk for MI and death over 180days. These low risk patients may be candidates for early outpatient testing and cardiology follow-up thereby reducing hospitalization.

Serial sampling of copeptin levels improves diagnosis and risk stratification in patients presenting with chest pain: results from the CHOPIN trial.

BACKGROUND: Copeptin has demonstrated a role in early rule out for acute myocardial infarction (AMI) in combination with a negative troponin. However, management of patients with chest pain with a positive copeptin in the setting of a negative troponin is unclear. METHODS: The multicentre CHOPIN trial enrolled 2071 patients with acute chest pain. Of these, 476 subjects with an initial negative troponin but an elevated copeptin (>14 pmol/L) were included in this study. Copeptin and troponin levels were rechecked at 2 h and the final diagnosis of AMI was made by two independent, blinded cardiologists. Follow-up at 30 days was obtained for major adverse cardiac events (MACEs), including death, AMI and urgent revascularisation. RESULTS: Of the 476 patients analysed, 365 (76.7%) had a persistently elevated copeptin at 2 h and 111 patients (23.3%) had a copeptin that fell below the cut-off of 14 pmol/L. When the second copeptin was elevated there were 18 AMIs (4.9%) compared with 0 (0%) when the second copeptin was negative (p=0.017), yielding a negative predictive value of 100% (95% CI 96.7% to 100%). On 30-day follow-up there were 36 MACEs (9.9%) in the positive second copeptin group and 2 (1.8%) MACEs in the negative second copeptin group (p=0.006). CONCLUSIONS: Patients with chest pain with an initial negative troponin but positive copeptin are common and carry an intermediate risk of AMI. A second copeptin drawn 2 h after presentation may help risk stratify and potentially rule out AMI in this cohort.

Comparison of conventional and high-sensitivity troponin in patients with chest pain: a collaborative meta-analysis.

BACKGROUND: Multiple studies have evaluated the diagnostic and prognostic performance of conventional troponin (cTn) and high-sensitivity troponin (hs-cTn). We performed a collaborative meta-analysis comparing cTn and hs-cTn for diagnosis of acute myocardial infarction (AMI) and assessment of prognosis in patients with chest pain. METHODS: MEDLINE/PubMed, Cochrane CENTRAL, and EMBASE were searched for studies assessing both cTn and hs-cTn in patients with chest pain. Study authors were contacted and many provided previously unpublished data. RESULTS: From 17 included studies, there were 8,644 patients. Compared with baseline cTn, baseline hs-cTn had significantly greater sensitivity (0.884 vs 0.749, P < .001) and negative predictive value (NPV; 0.964 vs 0.935, P < .001), whereas specificity (0.816 vs 0.938, P < .001) and positive predictive value (0.558 vs 0.759, P < .001) were significantly reduced. Based on summary receiver operating characteristic curves, test performance for the diagnosis of AMI was not significantly different between baseline cTn and hs-cTn (0.90 [95% CI 0.85-0.95] vs 0.92 [95% CI 0.90-0.94]). In a subanalysis of 6 studies that alternatively defined AMI based on hs-cTn, cTn had lower sensitivity (0.666, P < .001) and NPV (0.906, P < .001). Elevation of baseline hs-cTn, but negative baseline cTn, was associated with increased risk of death or nonfatal myocardial infarction during follow-up (P < .001) compared with both negative. CONCLUSION: High-sensitivity troponin has significantly greater early sensitivity and NPV for the diagnosis of AMI at the cost of specificity and positive predictive value, which may enable early rule in/out of AMI in patients with chest pain. Baseline hs-cTn elevation in the setting of negative cTn is also associated with increased nonfatal myocardial infarction or death during follow-up.

Derivation and validation of multimarker prognostication for normotensive patients with acute symptomatic pulmonary embolism.

RATIONALE: Not all patients with acute pulmonary embolism (PE) have a high risk of an adverse short-term outcome. OBJECTIVES: This prospective cohort study aimed to develop a multimarker prognostic model that accurately classifies normotensive patients with PE into low and high categories of risk of adverse medical outcomes. METHODS: The study enrolled 848 outpatients from the PROTECT (PROgnosTic valuE of Computed Tomography) study (derivation cohort) and 529 patients from the Prognostic Factors for Pulmonary Embolism (PREP) study (validation cohort). Investigators assessed study participants for a 30-day complicated course, defined as death from any cause, hemodynamic collapse, and/or adjudicated recurrent PE. MEASUREMENTS AND MAIN RESULTS: A complicated course occurred in 63 (7.4%) of the 848 normotensive patients with acute symptomatic PE in the derivation cohort and in 24 patients (4.5%) in the validation cohort. The final model included the simplified Pulmonary Embolism Severity Index, cardiac troponin I, brain natriuretic peptide, and lower limb ultrasound testing. The model performed similarly in the derivation (c-index of 0.75) and validation (c-index of 0.85) cohorts. The combination of the simplified Pulmonary Embolism Severity Index and brain natriuretic peptide testing showed a negative predictive value for a complicated course of 99.1 and 100% in the derivation and validation cohorts, respectively. The combination of all modalities had a positive predictive value for the prediction of a complicated course of 25.8% in the derivation cohort and 21.2% in the validation cohort. CONCLUSIONS: For normotensive patients who have acute PE, we derived and validated a multimarker model that predicts all-cause mortality, hemodynamic collapse, and/or recurrent PE within the following 30 days.

Therapy and outcomes in massive pulmonary embolism from the Emergency Medicine Pulmonary Embolism in the Real World Registry.

STUDY AIM: Clinical guidelines recommend fibrinolysis or embolectomy for acute massive pulmonary embolism (PE) (MPE). However, actual therapy and outcomes of emergency department (ED) patients with MPE have not previously been reported. We characterize the current management of ED patients with MPE in a US registry. METHODS: A prospective, observational, multicenter registry of ED patients with confirmed PE was conducted from 2006 to 2008. Massive PE was defined as PE with an initial systolic blood pressure less than 90 mm Hg. We compared inpatient and 30-day mortality, bleeding complications, and recurrent venous thromboembolism. RESULTS: Of 1875 patients enrolled, 58 (3.1%) had MPE. There was no difference in frequency of parenteral anticoagulation (98.3% [95% confidence interval {CI}, 90.5-101.6] vs 98.5% [95% CI, 97.9-99.1], P = .902) between patients with and without MPE. Fibrinolytic therapy and embolectomy were infrequently used but were used more in patients with MPE than in patients without MPE (12.1% [95% CI, 3.7-20.5] vs 2.4% [95% CI, 1.7-3.1], P < .001, and 3.4% [95% CI, 0.0-8.1] vs 0.7% [95% CI, 0.3-1.1], P = .022, respectively). Comparison of outcomes revealed higher all-cause inpatient mortality (13.8% [95% CI, 4.9-22.7] vs 3.0% [95% CI, 2.2-3.8], P < .001), higher risk of inpatient bleeding complications (10.3% [95% CI, 2.5-18.1] vs 3.5% [95% CI, 2.7-4.3], P = .007), and a higher 30-day mortality (14.0% [95% CI, 4.4-23.6] vs 1.8% [95% CI, 1.2-2.4], P < .001) for patients with MPE. CONCLUSIONS: In a contemporary registry of ED patients, MPE mortality was 4-fold higher than patients without MPE, yet only 12% of the MPE cohort received fibrinolytic therapy. Variability exists between the treatment of MPE and current recommendations.

Finding acute coronary syndrome with serial troponin testing for rapid assessment of cardiac ischemic symptoms (FAST-TRAC): a study protocol.

OBJECTIVE: To determine the utility of a highly sensitive troponin assay when utilized in the emergency department. METHODS: The FAST-TRAC study prospectively enrolled >1,500 emergency department patients with suspected acute coronary syndrome within 6 hours of symptom onset and 2 hours of emergency department presentation. It has several unique features that are not found in the majority of studies evaluating troponin. These include a very early presenting population in whom prospective data collection of risk score parameters and the physician's clinical impression of the probability of acute coronary syndrome before any troponin data were available. Furthermore, two gold standard diagnostic definitions were determined by a pair of cardiologists reviewing two separate data sets; one that included all local troponin testing results and a second that excluded troponin testing so that diagnosis was based solely on clinical grounds. By this method, a statistically valid head-to-head comparison of contemporary and high sensitivity troponin testing is obtainable. Finally, because of a significant delay in sample processing, a unique ability to define the molecular stability of various troponin assays is possible. TRIAL REGISTRATION: ClinicalTrials.gov Identifier NCT00880802.

Prognosis is worse with elevated cardiac troponin in nonacute coronary syndrome compared with acute coronary syndrome.

BACKGROUND: Cardiac troponin (cTn) can be elevated in many patients presenting to the emergency department (ED) with chest pain but without a diagnosis of acute coronary syndrome (ACS). We compared the prognostic significance of cTn in these different populations. METHODS: We retrospectively analyzed the CHOPIN study, which enrolled patients who presented to the ED with chest pain. Patients were grouped as ACS, non-ACS cardiovascular disease, noncardiac chest pain and chest pain not otherwise specified (NOS). We examined the prognostic ability of cTnI for the clinical endpoints of mortality and major adverse cardiovascular event (MACE; a composite of acute myocardial infarction, unstable angina, revascularization, reinfarction, and congestive heart failure and stroke) at 180-day follow-up. RESULTS: Among 1982 patients analyzed, 14% had ACS, 21% had non-ACS cardiovascular disease, 31% had a noncardiac diagnosis and 34% had chest pain NOS. cTnI elevation above the 99th percentile was observed in 52, 18, 6 and 7% in these groups, respectively. cTnI elevation was associated with mortality and MACE, and their relationships were more prominent in noncardiac diagnosis and chest pain NOS than in ACS and non-ACS cardiovascular diagnoses for mortality, and in non-ACS patients than in ACS patients for MACE (hazard ratio for doubling of cTnI 1.85, 2.05, 8.26 and 4.14, respectively; P for interaction 0.011 for mortality; 1.04, 1.23, 1.54 and 1.42, respectively; P for interaction <0.001 for MACE). CONCLUSION: In patients presenting to the ED with chest pain, cTnI elevation was associated with a worse prognosis in non-ACS patients than in ACS patients.

Accuracy of a novel stress echocardiography pattern for myocardial bridging in patients with angina and no obstructive coronary artery disease - A retrospective and prospective cohort study.

BACKGROUND: Myocardial bridge (MB) may cause angina in patients with no obstructive coronary artery disease (CAD). We previously reported a novel stress echocardiography (SE) pattern of focal septal buckling with apical sparing in the end-systolic to early-diastolic phase that is associated with the presence of an MB. We evaluated the diagnostic accuracy of this pattern, and prospectively validated our results. METHODS: The retrospective cohort included 158 patients with angina who underwent both SE and coronary CT angiography (CCTA). The validation cohort included 37 patients who underwent CCTA in the emergency department for angina, and prospectively underwent SE. CCTA was used as a reference standard for the presence/absence of an MB, and also confirmed no obstructive CAD. RESULTS: In the retrospective cohort, an MB was present in 107 (67.7%). The sensitivity, specificity, positive predictive value (PPV) and negative predictive value (NPV) were 91.6%, 70.6%, 86.7% and 80%, respectively. On logistic regression, focal septal buckling and Duke treadmill score were associated with an MB. In the validation cohort, an MB was present in 31 (84%). The sensitivity, specificity PPV and NPV were 90.3%, 83.3%, 96.5% and 62.5%, respectively. On logistic regression, focal septal buckling was associated with an MB. CONCLUSION: Presence of focal septal buckling with apical sparing on SE is an accurate predictor of an MB in patients with angina and no obstructive CAD. This pattern can reliably be used to screen patients who may benefit from advanced non-invasive/invasive testing for an MB as a cause of their angina.

A multicenter randomized controlled trial comparing central laboratory and point-of-care cardiac marker testing strategies: the Disposition Impacted by Serial Point of Care Markers in Acute Coronary Syndromes (DISPO-ACS) trial.

STUDY OBJECTIVE: Point-of-care testing reduces time to cardiac marker results in patients evaluated for acute coronary syndromes, yet evidence this translates to a decreased length of stay is lacking. We hypothesized that point-of-care testing decreases length of stay in patients being evaluated for acute coronary syndromes in the emergency department (ED). METHODS: Patients being evaluated for possible acute coronary syndromes at 4 EDs in the United States were randomized to having point-of-care markers as well as central laboratory markers, or central laboratory markers only (laboratory arm). Point-of-care markers were obtained using early serial testing at presentation and at 90, 180, and 360 minutes as required by the treating physician. Evaluation, treatment, and disposition decisions were at the treating physician's discretion. Length of stay was from presentation to the time of departure from the ED, either to an inpatient setting or to home. RESULTS: There were 1,000 patients in each study arm. There were 520 patients discharged home from the ED. Median (interquartile range) time to discharge home was 4.6 hours (3.5 to 6.1 hours) in laboratory patients and 4.5 hours (3.5 to 6.1 hours) in point-of-care patients. Median (interquartile range) time to transfer to an inpatient setting for admitted patients was 5.5 hours (4.2 to 7.5 hours) in laboratory patients, and 5.4 hours (4.1 to 7.3 hours) in point-of-care patients. At one site, time to transfer to the floor was reduced in the point-of-care arm compared with the laboratory arm (difference in medians 0.45 hours; 95% confidence interval [CI] -0.14 to 1.04 hours). At one site, time to ED departure for discharged patients was higher in the point-of-care arm than the laboratory arm (difference in medians 1.25 hours; 95% CI 0.13 to 2.36 hours). CONCLUSION: The effect of point-of-care testing on length of stay in the ED varies between settings. At one site, point-of-care testing decreased time to admission, whereas at another, point-of-care testing increased time to discharge. Potential effects of point-of-care testing on patient throughput should be considered in the full context of ED operations.

Copeptin to rule out myocardial infarction in Blacks versus Caucasians.

BACKGROUND: Copeptin in combination with troponin has been shown to have incremental value for the early rule-out of myocardial infarction, but its performance in Black patients specifically has never been examined. In light of a potential for wider use, data on copeptin in different relevant cohorts are needed. This is the first study to determine whether copeptin is equally effective at ruling out myocardial infarction in Black and Caucasian races. METHODS: This analysis of the CHOPIN trial included 792 Black and 1075 Caucasian patients who presented to the emergency department with chest pain and had troponin-I and copeptin levels drawn. RESULTS: One hundred and forty-nine patients were diagnosed with myocardial infarction (54 Black and 95 Caucasian). The negative predictive value of copeptin at a cut-off of 14 pmol/l (as in the CHOPIN study) for myocardial infarction was higher in Blacks (98.0%, 95% confidence interval (CI) 96.2-99.1%) than Caucasians (94.1%, 95% CI 92.1-95.7%). The sensitivity at 14 pmol/l was higher in Blacks (83.3%, 95% CI 70.7-92.1%) than Caucasians (53.7%, 95% CI 43.2-64.0%). After controlling for age, hypertension, heart failure, chronic kidney disease and body mass index in a logistic regression model, the interaction term had a P value of 0.03. A cut-off of 6 pmol/l showed similar sensitivity in Caucasians as 14 pmol/l in Blacks. CONCLUSIONS: This is the first study to identify a difference in the performance of copeptin to rule out myocardial infarction between Blacks and Caucasians, with increased negative predictive value and sensitivity in the Black population at a cut-off of 14 pmol/l. This also holds true for non-ST-segment elevation myocardial infarction and, although numbers were small, similar trends exist in the normal troponin population. This may have significant implications for early rule-out strategies using copeptin.

Statin-induced rhabdomyolysis.

Simvastatin and other HMG-CoA reductase inhibitors (statins) are one of the most frequently prescribed class of medications in the United States, with over 15 million Americans taking these drugs. Relatively rare adverse effects related to the known toxic effects of these drugs are more common than generally realized. Clinically significant statin-induced rhabdomyolysis is an uncommon but life-threatening adverse effect. We describe a case of simvastatin-induced rhabdomyolysis. Current knowledge of the pharmacology of the HMG-CoA reductase inhibitors and the drug interactions that potentiate these adverse effects are discussed. The clinical features of rhabdomyolysis and current treatment recommendations are presented.

Paroxysmal atrial fibrillation precipitated by amiodarone-induced thyrotoxicosis five months after cessation of therapy.

Amiodarone is currently indicated for the treatment of life-threatening ventricular dysrhythmias. It is also used for the treatment of supraventricular dysrhythmias and as maintenance therapy after successful cardioversion of atrial flutter or atrial fibrillation. Adverse effects related to its expanded use are increasingly common. We describe a case of amiodarone-induced thyrotoxicosis occurring 5 months after cessation of therapy and discuss the pathophysiology and treatment of this disorder.

Adjunctive platelet glycoprotein IIb/IIIa receptor inhibition with tirofiban before primary angioplasty improves angiographic outcomes: results of the TIrofiban Given in the Emergency Room before Primary Angioplasty (TIGER-PA) pilot trial.

BACKGROUND: Previous work has suggested that platelet glycoprotein IIb/IIIa receptor blockade may confer benefit in the treatment of acute myocardial infarction. The TIGER-PA pilot trial was a single-center randomized study to evaluate the safety, feasibility, and utility of early tirofiban administration before planned primary angioplasty in patients presenting with acute myocardial infarction. METHODS AND RESULTS: A total of 100 patients presenting with acute myocardial infarction were randomized to either early administration of tirofiban in the emergency room or later administration in the catheterization laboratory. The primary outcome measures were initial TIMI grade flow, corrected TIMI frame counts, and TIMI grade myocardial perfusion ("blush"). Thirty-day major adverse cardiac events were also assessed. Angiographic outcomes demonstrate a significant improvement in initial TIMI grade flow, corrected TIMI frame counts, and TIMI grade myocardial perfusion when patients are given tirofiban in the emergency room before primary angioplasty. The rate of 30-day major adverse cardiac events suggests that early administration may be beneficial. CONCLUSIONS: This pilot study suggests that early administration of tirofiban improves angiographic outcomes and is safe and feasible in patients undergoing primary angioplasty for acute myocardial infarction.

Surgical management of mycotic aneurysm of the left anterior descending artery.

Mycotic aneurysms of the coronary artery with underlying infective endocarditis are rare. The present report discusses the case of a 53-year-old woman with acute ST elevation myocardial infarction in the setting of native aortic valve endocarditis. Percutaneous transluminal coronary angioplasty was performed. Approximately four weeks after hospital admission, the patient had systemic embolization to the extremities with resulting cyanosis of the left toes. She was evaluated for replacement of the aortic valve and underwent a repeat angiogram, which demonstrated a mycotic aneurysm at the site of the angioplasty. She subsequently underwent successful excision of the aneurysm with coronary artery bypass grafting and replacement of the aortic valve with a 21 mm St Jude aortic valve prosthesis. The remaining hospital course was unremarkable.

Midregional proadrenomedullin predicts mortality and major adverse cardiac events in patients presenting with chest pain: results from the CHOPIN trial.

OBJECTIVES: Chest pain is a common complaint to emergency departments (EDs) and clinical risk factors are used to predict which patients are at risk for worse outcomes and mortality. The goal was to assess the novel biomarker midregional proadrenomedullin (MR-proADM) in prediction of mortality and major adverse cardiac events (MACE). METHODS: This was a subanalysis of the CHOPIN study, a 16-center prospective trial that enrolled 2,071 patients presenting with chest pain within 6 hours of onset. The primary endpoint was 6-month all-cause mortality and the secondary endpoint was 30-day and 6-month MACE: ED visits or hospitalization for acute myocardial infarction, unstable angina, reinfarction, revascularization, and heart failure. RESULTS: MR-proADM performed similarly to troponin (cTnI; c-statistic = 0.845 and 0.794, respectively) for mortality prediction in all subjects and had similar results in those with noncardiac diagnoses. MR-proADM concentrations were stratified by decile, and the cohort in the top decile had a 9.8% 6-month mortality risk versus 0.9% risk for those in the bottom nine deciles (p < 0.0001). MR-proADM, history of coronary artery disease (CAD), and hypertension were predictors of short-term MACE, while history of CAD, hypertension, cTnI, and MR-proADM were predictors of long-term MACE. CONCLUSIONS: In patients with chest pain, MR-proADM predicts mortality and MACE in all-comers with chest pain and has similar prediction in those with a noncardiac diagnosis. This exploratory analysis is primarily hypotheses-generating and future prospective studies to identify its utility in risk stratification should be considered.

Sex differences among children 2-13 years of age presenting at the emergency department with acute asthma.

Hospitalization rates for asthma have been reported to be higher in males than females in children under age 15, but it is not clear whether this disparity reflects gender differences in prevalence, severity, or treatment. We performed a prospective cohort study as part of the Emergency Medicine Network. Patients aged 2-13 years who presented to the emergency department (ED) with acute asthma underwent a structured interview in the ED and another by telephone 2 weeks later. Of 1,602 patients, 61% (95% CI, 59-64%) were boys. Girls were slightly older than boys, although no material differences existed in acute presentation, chronic asthma characteristics, ED treatment, or ED course. There was no difference in admission rates for boys or girls (20% vs. 22%; P = 0.48). This finding persisted when adjusting for other factors in a multivariate logistic regression model. No sex differences were observed for relapse or ongoing exacerbation on univariate or multivariate analysis. These data suggest that asthma is not inherently more severe in boys with asthma compared to girls, and that the increased rate of hospitalizations in boys under age 13 is due to differences in prevalence, not severity.

Adverse cardiac events in emergency department patients with chest pain six months after a negative inpatient evaluation for acute coronary syndrome.

OBJECTIVE: To evaluate the impact of the diagnostic test setting-inpatient versus outpatient-on adverse cardiac events (ACEs) after six months in emergency department (ED) patients with chest pain who were admitted to the hospital and subsequently had a negative evaluation for acute coronary syndrome (ACS). METHODS: The authors retrospectively studied a consecutive sample of ED patients with chest pain over a nine-month period. All patients were admitted to the hospital and underwent negative evaluations for ACS, defined as the absence of diagnostic changes on serial electrocardiograms or cardiac markers (creatine kinase-MB and troponin T), and a negative diagnostic cardiac study. Subjects were classified according to cardiac diagnostic study setting-either inpatient or outpatient. Diagnostic testing included exercise treadmill, angiography, stress echocardiography, or stress thallium scans. Acute cardiac events at six months were defined as cardiac death, myocardial infarction, unstable angina, cardiac arrest, or emergent revascularization. RESULTS: The six-month rate of ACEs among 157 subjects was 14%, with 2% cardiac mortality. The outpatient group had higher ACE risk when compared with the inpatient group using multivariate logistic regression, both for the entire cohort (OR 3.5, p < 0.03) and for a subgroup excluding patients with prior coronary artery disease (OR 6.7, p < 0.05). The outpatient group included 19 of 52 (37%) noncompliant subjects who did not receive a diagnostic study. CONCLUSIONS: Long-term cardiac morbidity of patients after a negative ACS evaluation may be higher than previously thought. Risk of ACE is significantly higher in subjects scheduled for outpatient diagnostic tests. Inpatient diagnostic testing is justified for subjects at risk for poor compliance.

Ambulatory cardiac monitoring for discharged emergency department patients with possible cardiac arrhythmias.

INTRODUCTION: Many emergency department (ED) patients have symptoms that may be attributed to arrhythmias, necessitating outpatient ambulatory cardiac monitoring. Consensus is lacking on the optimal duration of monitoring. We describe the use of a novel device applied at ED discharge that provides continuous prolonged cardiac monitoring. METHODS: We enrolled discharged adult ED patients with symptoms of possible cardiac arrhythmia. A novel, single use continuous recording patch (Zio®Patch) was applied at ED discharge. Patients wore the device for up to 14 days or until they had symptoms to trigger an event. They then returned the device by mail for interpretation. Significant arrhythmias are defined as: ventricular tachycardia (VT) ≥4 beats, supraventricular tachycardia (SVT) ≥4 beats, atrial fibrillation, ≥3 second pause, 2nd degree Mobitz II, 3rd degree AV Block, or symptomatic bradycardia. RESULTS: There were 174 patients were enrolled and all mailed back their devices. The average age was 52.2 (± 21.0) years, and 55% were female. The most common indications for device placement were palpitations 44.8%, syncope 24.1% and dizziness 6.3%. Eighty-three patients (47.7%) had ≥1 arrhythmias and 17 (9.8%) were symptomatic at the time of their arrhythmia. Median time to first arrhythmia was 1.0 days (IQR 0.2-2.8) and median time to first symptomatic arrhythmia was 1.5 days (IQR 0.4-6.7). 93 (53.4%) of symptomatic patients did not have any arrhythmia during their triggered events. The overall diagnostic yield was 63.2% CONCLUSION: The Zio®Patch cardiac monitoring device can efficiently characterize symptomatic patients without significant arrhythmia and has a higher diagnostic yield for arrhythmias than traditional 24-48 hour Holter monitoring. It allows for longer term monitoring up to 14 days.