Initial Troponin I Research Articles

Utility of serial conventional troponin testing for emergency department patients stratified by HEART score and symptom timing

BackgroundThe HEART score for risk stratifying chest pain patients in the emergency department (ED) has been widely adopted in clinical practice, but is often employed with nonconformant serial troponin measurements. ObjectiveThe primary objective of this study was to examine the utility of obtaining a second conventional 3-h troponin I (TnI) level in ED patients presenting with potential acute coronary syndrome (ACS), stratified by HEART score and duration of symptoms. MethodsThis was a retrospective cohort study of consecutive adult ED patients with a complete HEART score. We assessed the utility of repeat TnI measurement by examining the positivity rate of ΔTnI = [Second TnI] – [Initial TnI] stratified by HEART score and time elapsed since onset or resolution of symptoms. Major adverse cardiac events (MACE) within 6 weeks of index visit were assessed. ResultsA total of 944 patients were included with 433 (45.9%) assigned a low risk HEART score 0–3. Of the 268 (61.9%) low risk HEART score patients receiving a second TnI, only 3 (1.1%, [0.2–3.2%]) resulted in a positive ΔTnI, one of which occurred in the setting of an elevated initial TnI. Overall, patients presenting within 3 h of symptoms were more likely to experience positive ΔTnI, index MACE and MACE at 6 weeks compared to patients presenting ≥3 h since symptoms onset/resolution and patients with unknown timing of symptoms (15.9% vs 11.0% vs 10.3%, p < 0.001; 10.0% vs 5.3% vs 4.6%, p = 0.021; 12.7% vs 6.6% vs 6.4%, p = 0.047). ConclusionOur data suggest serial measurement of conventional troponin provides limited added benefit in low risk HEART score patients, regardless of duration and timing of symptoms. Conversely, serial troponin measurement may confer utility in moderate/high risk HEART score patients, particularly those presenting within 3 h of symptoms.

Abstract 11581: False Positive Troponin Elevation Due to Heterophile Antibody

Introduction: While highly specific, false positive Troponin I (TnI) can be caused by heterophile antibodies, autoimmune phenomena, and fibrin interference. The overreliance on TnI levels can lead to unnecessary patient work-up. Here we present a case of chronically elevated troponin over several hospitalizations most consistent with viral heterophile antibody cross reactivity. Case: A 71-year-old man with diabetes and polio-related paraplegia was admitted for pharyngitis. Initial TnI assay was significantly elevated at &gt;90 (normal &lt; 0.04 ng/mL) with a CK-MB of 21.7 (normal &lt;20.0 U/L). ECG showed no evidence of ischemia (Figure 1). He had similar TnI elevation on two prior hospitalizations, with no significant coronary artery disease on angiography. Despite the absence of chest pain and normal ECG and TTE, myocardial perfusion stress test was performed due to the elevation in CK-MB, which was negative for ischemia (Figure 2). Troponin T, a sendout lab, was &lt;12 ng/L. Patient was later confirmed to have positive CMV IgG and positive EBV viral capsid and nuclear antigen IgG, supporting the mechanism of heterophile antibody cross reactivity as the mechanism for false positive troponin. Discussion: Our case demonstrates a growing literature of patients presenting with chronically elevated TnI unrelated to myocyte damage. Focus of troponin levels without consideration of overall clinical picture and previous medical history can lead to unnecessarily invasive and expensive testing. For this patient, elevated troponin led to unnecessary testing and prolonged hospital admissions despite consistently negative cardiac workup. Heterophile cross reactivity can lead to false positive TnI in 1:2000 patients. If elevated troponin is concerning for a false positive, evaluation through other markers should be considered before undergoing more invasive procedures.

Initially elevated troponin I in rapid atrial fibrillation should lead to coronary angiography

Abstract Funding Acknowledgements Type of funding sources: None. Background In patients admitted to the emergency department (ED) with rapid atrial fibrillation (AF), the decision to undergo coronary angiography is usually due to elevated cardiac biomarkers. However, a study evaluating the rentability of this approach has never been done. Purpose Evaluate the predictors of a positive coronary angiography performed in patients with rapid AF and elevated cardiac biomarkers. Methods We retrospectively studied patients admitted to the ED between January 2016 and December 2018 with rapid AF who have undergone coronary angiography. We analysed symptoms, risk factors, initial value, peak value and curve of troponin I (TnI) and ST-T segment abnormalities. We evaluated the presence of significant coronary artery stenosis with the need of revascularization at coronary angiography and we used logistic regression to assess the predictors of a positive result. Results From 2265 patients admitted to the ED with rapid AF, 46 patients, 60.9% (28) male, median age 73 (IQR 14.75) years, were submitted to coronary angiography. Significant coronary artery stenosis was present in 24 (52.2%) patients. Regarding cardiovascular risk factors, 39 (85.6%) patients had hypertension, 15 (32.6%) had type 2 diabetes mellitus, 36 (78.3%) had dyslipidaemia, 25 (54.3%) were obese or overweight and 12 (26.1%) had a previous history of CAD. Twenty-eight (60.9%) patients presented with chest pain and 27 (58.7%) had ST-T segment abnormalities. Of note, in 17 (37.0%) cases high-sensitivity TnI was measured. In univariable analysis, ST-T segment abnormalities, the presence of typical TnI curve and an elevated initial TnI predicted the presence of significant CAD in coronary angiography. In multivariable analysis, an initial TnI value above the upper reference limit (URL) was the only independent predictor of significant CAD in coronary angiography. Conclusion In this group of patients with rapid AF an initial elevated TnI was the only independent predictor of the presence of significant CAD. Therefore, maybe it would be advisable to perform coronary angiography in these patients. Without CADWith CADUnivariate analysisOR (95% CI), p-valueMultivariate analysisOR (95% CI), p-valueAge in years, median (IQR)69 (15)77.5 (17)1.045 (0.988-1.106), 0.1270.967 (0.882-1.062), 0.484Type 2 diabetes mellitus, n (%)5 (23.8)10 (41.7)2.286 (0.629-8.313), 0.2095.865 (0.566-60.806), 0.138ST-T segment abnormalities, n (%)8 (36.4)19 (79.2%)6.650 (1.788-24.730), 0.0055.338 (0.491-58.063), 0.169Typical TnI curve, n (%)10 (52.6)20 (90.9)9.000 (1.628-49.756), 0.01217.900 (0.475-674.480), 0.119Elevated initial TnI, n (%)10 (45.5)18 (75.0)3.600 (1.033-12.542), 0.04415.167 (1.363-168.778), 0.027Peak TnI elevation &amp;gt;2 times URL, n (%)11 (50.0)18 (75.0)3.000 (0.863-10.428), 0.0840.169 (0.005-5.298), 0.312

Abstract 15975: Association of Maximum Troponin Levels With Myocardial Infarction Diagnosis and Higher Mortality

Introduction: Cardiac troponin I (TnI) is a sensitive and specific marker of acute myocardial infarction (AMI). However, a wide range of non-AMI conditions can also cause significant elevations in cardiac troponins. Given the deleterious impact of misdiagnosis, the ability to risk stratify patients who present with an elevated troponin is paramount. Hypothesis: We hypothesized that maximum TnI would be more predictive of mortality and the diagnosis of AMI than the initial or change in TnI. Methods: Records of 30,173 patients from a nine-hospital system in Texas were reviewed over a 24-month period 2016-2018. Data were collected on patients &gt; 40 years of age and included international classification of disease (ICD-10) diagnoses, TnI, demographic data (age, sex, race, smoking status, chronic medical conditions), death during hospitalization, and readmission within 30 days. Results: Notable finding include TnI as a significant predictor of death with odds of death increased by 0.9% (1.009, 95% CI 1.004-1.013) for initial, and 0.7% (1.007, 95% CI 1.005-1.009) for delta and maximum TnI. An ROC curve demonstrated a statistically significant predictive ability of death for the maximum TnI level (0.6782, 95% CI (0.6576, 0.6989)) when compared to the initial and change in TnI. We analyzed the initial TnI as a significant predictor of AMI demonstrating the odds of AMI increased by 7.4% as initial TnI values increased (1.074, 95% CI 1.063-1.085), and 3.1% for delta and maximum TnI (1.031, 95% CI 1.028-1.034). A separate ROC curve demonstrated that the maximum TnI level 0.9401, 95% CI (0.9353, 0.9449) showed a statistically significant predictive ability to predict an AMI compared to initial change in TnI. Conclusions: Regardless of TnI level, a detectable TnI results in an increased risk of in-hospital mortality. Our study demonstrates that the maximum TnI level is a more sensitive and specific predictor of mortality when compared to delta or initial TnI. Similarly, the maximum TnI is the most predictive of an AMI versus other causes of TnI elevation. Further studies are needed to correlate TnI levels and clinical manifestations, which may be helpful in redefining AMI to better distinguish AMI from non-AMI diagnoses.

Predictive factors for acute brain lesions on magnetic resonance imaging in acute carbon monoxide poisoning

BackgroundAcute brain lesions on diffusion-weighted-magnetic resonance imaging (MRI) after acute carbon monoxide (CO) poisoning were associated with delayed neurological sequelae. This study was conducted to identify the risk factors associated with acute brain lesions on MRI after acute CO poisoning and to help select patients who need acute-phase brain MRI after acute CO poisoning in the emergency department (ED). MethodsThis retrospective observational study included 103 adult patients who were hospitalized at a tertiary-care hospital between November 2016 and September 2019 and underwent brain MRI because of acute CO poisoning. Multivariable logistic regression analysis was applied to identify predictive factors for acute brain lesions on MRI after acute CO poisoning. ResultsMultivariable logistic regression analysis showed that Glasgow Coma Scale (GCS) score of <9 at ED presentation (odds ratio [OR] 17.749, 95% confidence interval [CI] 3.098–101.690, P = 0.001) and the initial troponin-I level at presentation in the ED (OR 13.657, 95% CI 1.415–131.834, P = 0.024) were predictive factors for acute brain lesions on MRI in acute CO poisoning. The receiver operating characteristics curve for initial troponin-I showed an area under the curve of 0.761 (95% CI 0.638–0.883, P < 0.001) and the optimal cutoff value was 0.105 ng/mL. ConclusionsAcute-phase brain MRI in acute CO poisoning can be considered for patients who present at the ED with a GCS score <9 or troponin-I level >0.105 ng/mL.

Troponin I as an early biomarker of cardiopulmonary parameters during the first 24 h of intensive care unit treatment in isolated traumatic brain injury patients

ObjectiveCardiopulmonary (CP) complications are well-known phenomena after an isolated traumatic brain injury (iTBI) and they may be associated with an elevated serum troponin I (TnI) value. However, the influence of an elevated TnI level on CP parameters within the first 24 h after an iTBI is still unknown. The current study was conducted to assess the associations between the initial TnI value on admission and CP parameters during the first 24 h of intensive care unit (ICU) treatment in iTBI patients. Patients and MethodsA total of 288 patients with iTBIs, who were admitted to our emergency department between January 2010 and November 2016 were retrospectively analyzed. Blood samples were taken on admission to determine TnI value. Each patient's demographic data, treatment regime, computed tomography results, and intra-hospital outcomes were evaluated, as well as several CP parameters, within the first 24 h of ICU treatment. The entire study population was stratified into patients with an initial TnI elevation (TnI positive) and without an initial TnI elevation (TnI negative). ResultsIncreased TnI values on admission were found in 59 (20.5%) patients. There were significant correlations between an initially elevated TnI value and a lower Glasgow Coma Scale score (p = 0.003), higher head Abbreviated Injury Scale score (p<0.0001), and higher Acute Physiology and Chronic Health Evaluation II score (p = 0.005) on admission, as well as a lower Glasgow Outcome Scale score (p = 0.0002) and higher modified Rankin Scale score (p = 0.0001) at discharge. In addition, a significantly higher norepinephrine application rate (NAR) (p<0.0001) and inspiratory oxygen fraction (FiO2) (p = 0.028) were needed in the TnI positive group. ConclusionPatients with elevated TnI values on admission require more circulation support (NAR and FiO2) within the first 24 h of ICU treatment after an iTBI. Therefore, the TnI may be a useful biomarker to improve ICU treatment of these patients.

EXTREME ECG AND TROPONIN ABNORMALITIES IN DIABETIC KETOACIDOSIS IN THE ABSENCE OF AN ACUTE CORONARY SYNDROME

SESSION TITLE: Monday Abstract Posters SESSION TYPE: Original Investigation Posters PRESENTED ON: 10/21/2019 02:30 PM - 03:15 PM INTRODUCTION: Although troponin I (TnI) elevation indicates myocardial injury, the majority of instances are not due to an acute coronary syndrome (ACS). CASE PRESENTATION: A 57 year old female presented with diabetic ketoacidosis (DKA) 5 months after CABG. She was hemodynamically stable with mild tachycardia and a normal cardiopulmonary examination. Serum glucose was > 1250, pH= 7.16, K+ =8.3. CXR and sepsis evaluation was negative. The ECG revealed ST elevation in V1-2 and aVR with diffuse ST segment depression and peaked T-waves (Figure 1A). Initial TnI (4th generation) was 0.079 and peaked at 63.2 ng/mL (Figure 1B). The patient had no cardiopulmonary complaints and an echocardiogram revealed hyperdynamic function with an LVEF of 70% without wall motion abnormalities. Treatment with IV fluid and insulin normalized K+ and pH, as the ECG returned to baseline. Myocardial infarction commonly causes death in the first 24 hours of DKA. This patient had known CAD, a markedly abnormal ECG and marked troponin elevation, but no clinical or imaging evidence of ACS. Cardiac catheterization was not pursued. DISCUSSION: Various metabolic derangements accompany DKA including hypo and hyperkalemia, hyponatremia and metabolic acidosis. Hyperkalemia is well known to present with ECG pseudoinfarct pattern including ST elevations and peaked T waves in the setting of severe academia. Likewise, hypokalemia can depress ST segments and cause T wave inversion. Free fatty acid elevation itself can disrupt cell membranes and release troponin. Our patient lacked other findings typically seen in demand ischemia. Such isolated troponin elevation has been seen in up to 27% of patients with DKA in the absence of ACS1. CONCLUSIONS: With the dawn of more sensitive troponin assays, caution will need to be taken interpreting troponin in non-ACS settings, as specificity for ACS may be reduced. Reference #1: Al-Mallah, M., Zuberi, O., Arida, M., & Kim, H. E. (2008). Positive Troponin in Diabetic Ketoacidosis without Evident Acute Coronary Syndrome Predicts Adverse Cardiac Events. Clinical Cardiology,31(2), 67-71. https://doi.org/10.1002/clc.20167 DISCLOSURES: No relevant relationships by Gilead Lancaster, source=Web Response No relevant relationships by Craig McPherson, source=Web Response No relevant relationships by Tony Roy, source=Web Response No relevant relationships by Kristin Stawiarski, source=Web Response No relevant relationships by stuart zarich, source=Web Response

Clinical utility of mean platelet volume and immature platelet fraction in acute coronary syndrome

BackgroundPlatelets play an important role in the pathogenesis of acute coronary syndrome (ACS). Patients with ACS have an increased mean platelet volume (MPV) and immature platelet fraction (IPF) resulting in elevation of thrombotic ability. In this study, we evaluated the diagnostic performance of MPV and IPF in identifying suspected ACS patients at emergency department. Moreover, we investigated the correlation between MPV or IPF with initial troponin I (TnI), one of the current ACS biomarkers. MethodsThis was a single-center study recruiting suspected ACS patients who had acute chest pain at the emergency department. Whole blood samples were obtained from all participants and MPV and IPF were measured by Sysmex XE-5000 hematology analyzer within 20 min of blood sampling. The diagnostic values of MPV and IPF in identifying ACS were analyzed retrospectively. ResultIn this study, 63 in 104 suspected ACS patients were diagnosed as ACS (65.3%). MPV and IPF were higher in ACS patients compared to non-ACS patients (MPV: 10.7 ± 0.80 fL vs 10.0 ± 0.64 fL, p < 0.001; IPF: 3.7 ± 2.64% vs 3.1 ± 2.69%, p = 0.030). MPV and IPF were similar in unstable angina and acute myocardial infarction patients. We showed that elevation of MPV could be an independent predictive factor of ACS (odds ratio: 5.038). At the optimal cut-off value of 10.55 fL (AUC 95% CI: 0.637–0.836), the diagnostic performance of MPV in predicting ACS had an area under a receiver operating characteristic curve (AUC) of 0.736 with sensitivity and specificity of 54.2% and 82.8%, respectively. Patients with both of initial TnI and MPV higher than the established cut-off value had increased incidence (3.792 fold) for ACS development compared to patients with TnI below the cut-off value. Furthermore, diagnosing ACS with both MPV and initial TnI increased the positive predictive value from 84.2% to 86.7%. No correlation was observed between MPV or IPF and the mortality rate of ACS patients (MPV: 3.8% vs 11.1%, p = 0.300; IPF: 12.0% vs 37.5%, p = 0.054). ConclusionHere we show that ACS patients have higher MPV and IPF compared to non-ACS patients. We further demonstrate that MPV can be utilized as an independent predictor for early diagnosis of low-risk ACS patients who have acute chest pain.

Does undetectable troponin I at presentation using a contemporary sensitive assay rule out myocardial infarction? A cohort study

AimRecent evidence suggests that an undetectable troponin level at emergency department (ED) presentation can rule out the presence of myocardial infarction (MI) in low-risk patients. The aim of this study...

Evaluation of cardiac function using transthoracic echocardiography in patients with myocardial injury secondary to methomyl poisoning.

Generally, the mortality rate for cases of carbamate poisoning is low, but fatalities secondary to methomyl poisoning have been reported including a case report of cardiac toxicity following short-term exposure to methomyl. There have been no reports, however, regarding patterns of cardiac toxicity after exposure to methomyl. Therefore, we investigated the prevalence and patterns of myocardial injury using a biochemical marker, troponin I (TnI), and evaluated cardiac function using transthoracic echocardiography (TTE). We conducted a retrospective review of 14 consecutive methomyl poisoning cases that were diagnosed and treated at the emergency department of the Wonju Severance Christian Hospital between January 2009 and December 2013. On ECG analysis, ST depression and T-wave inversion were seen in five patients (35.7%) and one patient (7.1%), respectively. On cardiac biochemical marker analysis, initial TnI was elevated in 11 patients (78.6%). TTE was performed in nine patients among the 11 patients in whom TnI was found to be elevated. Of the nine patients that underwent TTE, three patients (33.3%) showed a reduced ejection fraction (EF), and RWMA was noted in two patients. There were two patients (22.2%) that had both reduced systolic function and RWMA. One patient did not regain normal systolic function on admission. None of the three patients with reduced EF received any specific treatment to support cardiac function. One patient expired due to pneumonia, and one patient was transferred as moribund. We followed up on 12 patients who survived to discharge for 6-44 months. One patient (8.3%) was died to follow-up, and 11 patients survived without any further complications. Methomyl exposure can cause direct myocardial injury and reversible cardiac dysfunction. Monitoring of TnI levels and TTE for evaluation of cardiac function may be useful in the workup of patients suffering from methomyl poisoning.

Predicting duration of mechanical ventilation in patients with carbon monoxide poisoning: A retrospective study

PurposePatients with severe carbon monoxide (CO) poisoning may develop acute respiratory failure, which needs endotracheal intubation and mechanical ventilation (MV). The objective of this study was to identify the predictors for duration of MV in patients with severe CO poisoning and acute respiratory failure. Materials and methodsThis is a retrospective observational study of 796 consecutive patients diagnosed with acute CO poisoning that presented to the emergency department. Patients who received MV were divided into 2 groups: the early extubation (EE) consisting of patients who were on MV for less than 72 hours and the nonearly extubation (NEE) consisting of patients who were on MV for more than 72 hours. Demographic and clinical data of the two groups were extracted for analysis. ResultsThe intubation rate of all CO-poisoned patients was 23.4%. A total of 168 patients were enrolled in this study. The main source of CO exposure was intentional CO poisoning by charcoal burning (137 patients). Positive toxicology screening result was found in 104 patients (61.9%). The EE group had 105 patients (62.5%). On arriving at the emergency department, high incidence of hypotension; high white blood cell count; and elevation of blood urea nitrogen, creatinine, aspartate aminotransferase, alanine aminotransferase, creatine kinase, and troponin-I levels were statistically significant in the NEE group (P < .05). Positive toxicology screening result was statistically significant in the EE group (P < .05). In a multivariate analysis, elevation of troponin-I level was an independent factor for NEE (odds ratio, 1.305; 95% confidence interval, 1.024-1.663; P = .032). Positive toxicology screening result was an independent factor for EE (odds ratio, 0.222; 95% confidence interval, 0.101-0.489; P = .001). ConclusionsA positive toxin screen predicts extubation within the first 72 hours for patients with severe CO poisoning and acute respiratory failure. On the other hand, elevation of initial troponin-I level is a predictor for a longer duration of MV.

Undetectable Troponin I at Presentation Using a Contemporary Assay does not Rule Out Myocardial Infarction

Objective Chest pain is a common reason for presentation to emergency departments (ED). Recent evidence suggests that an undetectable troponin level at ED presentation can rule out the presence of myocardial infarction (MI). The aim of this study was to externally validate that finding using a troponin I (TnI) assay. Methods Unplanned sub-study of a prospective observational cohort study of patients presenting to ED with chest pain without electrocardiogram evidence of ischaemia who underwent a ‘rule out’ acute coronary syndrome process. Clinical, investigational and outcome data were collected. Primary outcome of interest was diagnostic accuracy for type I MI at index visit. Results 685 patients were studied; median age 62, 60% male. Two hundred and seventeen had an undetectable TnI at ED presentation. There were two non-ST elevation myocardial infarctions in the group (2/217, 0.9%, 95% CI 0.16-3.6%). Sensitivity of undetectable TnI for ruling out type I MI was 98. 2% (99% CI 92.9-99.7%) with negative predictive value of 99.1% (96.4-99.8%). Conclusion Approximately 1% of patients with an undetectable TnI at ED presentation were diagnosed with a type I MI. An undetectable initial TnI using a contemporary sensitive TnI assay does not safely exclude MI in an ED chest pain cohort. (Hong Kong j.emerg.med. 2014;21:31-36)

Low-risk Chest Pain Patients Younger Than 40 Years Do Not Benefit From Admission and Stress Testing

A number of studies have suggested clinical decision rules for patients age <40 who are at low risk for acute coronary syndrome (ACS) and may be safe for discharge from the emergency department. Despite this, many such patients continue to be admitted for observation in low-risk observation units. We hypothesized that patients age <40 without coronary artery disease, with a nonischemic electrocardiogram (ECG), and normal initial troponin I (TnI) who are admitted to a CPU are at very low risk (<1%) for ACS or 30-day major adverse cardiac event (MACE) and would not benefit from observation care. This was a prospective, observational study of consecutive patients admitted to the CPU in a large-volume academic urban emergency department. Eligibility criteria included age >18 but <40, American Heart Association low-to-intermediate risk, nonischemic ECGs, and normal initial TnI. Standard descriptive statistics were used for demographics, cardiac comorbidities, and risk scores. Our primary outcomes were CPU ACS rate and 30-day MACE. MACE was defined as death, nonfatal AMI, revascularization, or out of hospital cardiac arrest. A sample size of at least 400 was chosen to have 1% precision about an expected outcome rate of 0.3% (based on prior CPU data of patients of all ages). Confidence intervals (CIs) were calculated using the refined Wilson simple asymptotic method with continuity correction. All patients were called at 30 days. All charts on index visit and any subsequent visit within 30 days were reviewed using standardized chart abstractions forms by 2 trained abstractors blinded to the hypothesis of the study. A Social Security Death Index search was performed on all patients. Three hundred eighty-four patients accounting for 403 CPU admissions were enrolled over a 28-month period. Mean age was 34.3 ± 4.5; 42% were women; and 89%, 8%, 2%, and 1% had Thrombolysis in Myocardial Infarction scores of 0, 1, 2, and 3, respectively. No patient had an abnormal TnI. The ACS rate was 0 (95% CI, 0-0.8%). The 30-day MACE rate was 0 (95% CI, 0-0.8%). Forty-two percentage of these patients received stress testing but 0 (95% CI, 0-1.8%) were positive. Patients age <40 with a normal ECG and normal first biomarker have <1% risk of ACS or 30-day MACE, such that admission and stress testing are of no benefit.

What is the incidence of major adverse cardiac events in emergency department chest pain patients with a normal ECG, Thrombolysis in Myocardial Infarction score of zero and initial troponin ≤99th centile: an observational study?

ObjectiveTo determine the rate of major adverse cardiac events (MACE) in patients assessed in an emergency department (ED) for chest pain with a non-ischaemic ECG, Thrombolysis in Myocardial Infarction (TIMI)...

An Unusual Pattern of ST-Segment Elevation

-amine-induced dilated cardiomyopathywas referred from clinic to the emer-gency department after having had anepisode of chest pain during his clinicvisit. The patient reported exertional chest discomfort,described as a pressurelike sensation accompanied bysweating.Thediscomfortresolvedwithrestandsublin-gual nitroglycerin. He admitted to recent methamphet-amine use. His blood pressure was 136/70 mm Hg, andhis heart rate was regular at 99 beats/min. The jugularvenous pressure was mildly elevated, and an S3 gallopwas audible at the apex. His initial troponin-I level was0.10 ng/mL (normal !0.10 ng/mL). An electrocardio-gram (ECG) showed normal sinus rhythm and left ven-tricular hypertrophy with associated repolarizationabnormalities.Thepatientwasadmittedtothehospitalforserialcar-diacenzymedeterminations.Onthesecondhospitalday,the patient suddenly became profusely diaphoretic andcomplained of chest pain. An ECG was obtained(