Biomedical subjects
Publications and source records attributed to Francis M Fesmire.
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BACKGROUND: The threshold of troponin elevation that stimulates changes in clinical decision making for patients with non-ST-segment elevation acute coronary syndromes (NSTE ACSs) has not been previously evaluated. METHODS: A total of 23 298 patients with NSTE ACSs from the CRUSADE (Can Rapid Risk Stratification of Unstable Angina Patients Suppress Adverse Outcomes With Early Implementation of the ACC/AHA Guidelines) initiative were separated into categories of maximum troponin ratios (ratio of the highest recorded troponin value in the first 24 hours to the local laboratory troponin assay upper limit of normalization [ULN]). RESULTS: Unadjusted rates of in-hospital mortality increased from the group with troponin levels below the reference limit (maximum troponin ratio 0-1 x ULN; n = 5291) to those with minor (1-2 x ULN; n = 2499), intermediate (2-5 x ULN; n = 3825), and major (>5 x ULN; n = 11 683) elevations (-2.8% vs 4.6% vs 4.7% vs 6.0%). The use of early (<24 hours) aspirin, heparin, glycoprotein IIb/IIIa inhibitors, and beta-blockers was similar for the group with troponin levels below the reference limit compared with those with minor troponin elevations, and greater use of medications was demonstrated in patients with intermediate and major troponin elevations. Use of cardiac catheterization and percutaneous coronary intervention was higher in patients with troponin levels below the reference limit compared with those with minor troponin elevations, and procedures were used most frequently in patients with major troponin elevations. Similar patterns of care were demonstrated after excluding patients with chronic renal insufficiency. CONCLUSIONS: Any degree of troponin elevation is associated with a higher risk of mortality for patients with NSTE ACSs, but guideline-recommended medical therapies are used more commonly only in patients with intermediate and major troponin elevations, whereas patients with troponin levels below the reference limit underwent invasive procedures more frequently than those with mild troponin elevations.
STUDY OBJECTIVE: Previous studies in clinical trial populations have demonstrated that patients presenting with positive troponin levels have a higher risk of mortality than patients with later positive troponin levels, but the influence of the timing of troponin elevation has not been previously characterized. We evaluate the impact of the timing of troponin elevation on clinical outcomes and adherence to the American College of Cardiology/American Heart Association acute care guidelines for patients with non-ST-segment elevation acute coronary syndromes. METHODS: We examined inhospital outcomes and use of acute (<24 hours) medications and invasive cardiac procedures in 23,184 high-risk patients with non-ST-segment elevation acute coronary syndromes (positive cardiac markers or ischemic ST-segment changes) during 2001 to 2002 from 396 US hospitals participating in the Can Rapid Risk Stratification of Unstable Angina Patients Suppress ADverse Outcomes with Early Implementation of the American College of Cardiology/American Heart Association Guidelines (CRUSADE) Initiative. Baseline and peak troponin values were recorded and were designated as positive if above the cutoff value used at each institution to designate definite myocardial necrosis. RESULTS: In the study cohort, 53.2% of patients presented with baseline positive troponin levels, 30.6% had baseline negative/later positive troponin levels, and 16.2% had negative troponin levels during the entire hospitalization. Patients with baseline positive troponin levels had a higher risk of inhospital mortality than patients with baseline negative/later positive troponin levels (6.5% versus 4.1%) and were less likely to undergo early cardiac catheterization or percutaneous coronary intervention. The use of acute aspirin (in approximately 91% of patients), heparin (85%), and beta-blockers (78%) was similar in patients with baseline-positive versus later-positive troponin levels. CONCLUSION: These findings demonstrate that evidence-based therapies and interventions for non-ST-segment elevation acute coronary syndromes are underused in patients with elevated troponin levels, but baseline troponin elevations, which are associated with a higher risk of inhospital mortality, do not stimulate more aggressive care.
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STUDY OBJECTIVE: Limited information is available about the diagnostic performance of creatine kinase (CK)-MB and myoglobin levels during the early evaluation of chest pain patients using cardiac troponins as the criterion standard for diagnosing acute myocardial infarction. In this study, we compare the sensitivity and specificity of the baseline, 2-hour absolute, and 2-hour delta values of myoglobin and CK-MB mass assay for detection of acute myocardial infarction using cardiac troponin I (troponin) as the sole marker of myocardial necrosis. METHODS: A prospective observational study was conducted of 975 chest pain patients with a baseline troponin level of 1.0 ng/mL or less (Abbott Axsym Assay) and an initial ECG nondiagnostic for injury. CK-MB, myoglobin, and troponin levels were all measured on the Abbott Axsym immunoassay. Acute myocardial infarction was diagnosed if there was at least 20 minutes of chest pain and any one of the following criteria within 24 hours of ED presentation: a serial increase in troponin to more than 1.0 ng/mL, new Q-wave formation in 2 contiguous leads, or patient death by cardiac or unknown cause. The optimal values of CK-MB and myoglobin were chosen at the most accurate value on the receiver operating characteristic (ROC) curve (ie, value with lowest false-negative and false-positive rate) of the 2-hour absolute and 2-hour delta value for predicting acute myocardial infarction. RESULTS: Acute myocardial infarction was diagnosed in 44 (4.5%) of the 975 study patients. ROC curve analysis revealed no statistically significant differences in areas for myoglobin and CK-MB values at baseline and 2 hours for determination of acute myocardial infarction. However, the ROC curve area of the delta CK-MB level significantly outperformed the ROC curve area of the delta myoglobin level for early identification of acute myocardial infarction (0.97 versus 0.81; 95% confidence interval [CI] for difference between areas 0.09 to 0.24). At the most accurate cutoff value, a 2-hour delta CK-MB level more than 0.7 ng/mL had a sensitivity of 93.2% (95% CI 81.3% to 98.5%), a specificity of 94.4% (95% CI 92.7% to 95.8%), a positive likelihood ratio of 16.7, and a negative likelihood ratio of 0.07. CONCLUSION: A 2-hour delta CK-MB level outperforms myoglobin level in the early identification and exclusion of acute myocardial infarction in non-ST-segment elevation chest pain patients. This finding suggests that myoglobin may no longer be the optimal early marker of acute myocardial infarction when troponins are used as the criterion standard.
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BACKGROUND: Vectorcardiographic (VCG) measurements of ST-vector magnitude (VM) and QRS-vector difference (VD) have been demonstrated to be independent predictors of adverse outcome (AO) and acute myocardial infarction (AMI) in emergency department (ED) chest pain patients with absence of bundle branch block or left ventricular hypertrophy (LVH) on the initial 12-lead electrocardiogram (ECG). The prognostic value of ST-VM and QRS-VD in ED chest pain patients with LVH on the initial 12-lead ECG has not been previously investigated. METHODS: A prospective observational study was performed in 196 consecutive ED chest pain patients with suspected AMI and presence of voltage criteria for LVH on initial ECG who underwent continuous VCG monitoring during the initial evaluation. The optimal baseline ST-VM value and 2-hour QRS-VD value were defined as the most accurate value on the receiver operator characteristic curve (value with lowest false-negative and false-positive rate). Thirty-day AO was defined as AMI, percutaneous coronary intervention, coronary artery bypass grafting (CABG), or cardiac death occurring within 30 days of initial ED visit. RESULTS: Fourteen patients (7.1%) were diagnosed as 24-hour AMI and 28 patients (14.3%) experienced 30-day AO. The optimal cut-off value for predicting 30-day AO was > 124 microV for ST-VM and > 21.7 microV for QRS-VD. Patients with either a positive ST-VM or a positive QRS-VD had 8.8 times increased odds of AMI (95% confidence interval, CI, 1.9-40.3; P = 0.003); 4.3 times increased odds of 30-day PTCA/CABG (95% CI 1.3-13.8; P = 0.019); and 3.8 times increased odds of 30-day AO (95% CI 1.6-9.3; P = 0.003). CONCLUSIONS: Baseline ST-VM and 2-hour QRS-VD risk stratifies ED chest pain patients with LVH voltage criteria on the initial 12-lead ECG.
BACKGROUND: The acute benefits of platelet glycoprotein IIb/IIIa inhibitors for non-ST-segment elevation acute coronary syndromes (NSTE ACS) remain unclear. METHODS: In this pilot trial, 311 patients with NSTE ACS were randomly assigned in the emergency department to double-blinded therapy with eptifibatide or placebo for 12 to 24 hours before crossover to open-label eptifibatide. Serial creatine-kinase MB (CK-MB) and quantitative cardiac troponin T levels were collected during the first 24 hours to assess the impact of early platelet glycoprotein IIb/IIIa blockade on infarct size as measured by cardiac markers. RESULTS: Median peak CK-MB (10.3 vs 11.8 ng/mL; P =.71) and peak quantitative cardiac troponin T levels (0.2 vs 0.3 ng/mL; P =.95) were similar between treatment groups, respectively. Median calculated peak CK-MB values (41 vs 40 ng/mL; P =.72) and area under the CK-MB curve measurements (980 vs 764 microg/min/L; P =.68) from curve-fitting analyses that could be performed in 106 of 311 patients were also similar. CONCLUSIONS: In this pilot trial, early administration of eptifibatide in the emergency department did not modulate serologic measurements of infarct size in patients with NSTE ACS.
A prospective observational study was conducted in 2,007 patients experiencing chest pain to determine impact of local quality improvement (QI) measures on the use of glycoprotein (GP) IIb/IIIa inhibitors in the ED treatment of high-risk patients with non-ST-segment elevation acute coronary syndromes (ACS). Patients with injury on the initial ECG or new sustained injury on continuous ECG were excluded. QI interventions were as follows: control (0-4 mo): no interventions (standardized protocols and prewritten orders in place 4 months prior); phase I (5-8 mo): simple education/awareness program with posted drug information pamphlets and eligibility criteria; phase II (9-12 mo): mandated QI form with real-time feedback and focused one-on-one physician education championed by an ED physician QI advocate. A total of 179 (8.9%) of the study patients met predefined high-risk criteria. Of these, a total of 41 (23.0%) patients had GP IIb/IIIa inhibitor therapy initiated in the ED. Percent of high-risk patients receiving therapy increased from 6.0% during the control phase to 16.1% during phase I and 50.9% during phase II. After controlling for patient demographics, patients treated during phase I had a 2.8 times increased odds (95% confidence interval CI: 0.8-10.3; P =.11 [not significant]) of receiving GP IIb/IIIa inhibitor relative to the control phase, and patients treated during phase II had a 20.2 times increased odds (95% CI: 6.1-66.9; P <.0001) of treatment. In conclusion, local QI measures incorporating standardized protocols, preprinted orders, physician education, and interactive feedback championed by an ED QI physician advocate can increase early use of GP IIb/IIIa inhibitors in the ED treatment of high-risk patients presenting with chest pain.
It has been shown that the 2-h Stratus II delta creatine kinase-MB (CK-MB) is more sensitive and is equally specific compared to a 2-h Stratus II CK-MB and to a 2-h Stratus II delta cardiac troponin-I (DeltacTnI) for identification of acute myocardial infarction and adverse outcome (AO). Because the newest generation of Stratus (Stratus CS) cTnI assay has an analytical sensitivity of 0.03 ng/mL, compared to 0.35 ng/mL for the first generation assay, we undertook a small pilot study of 120 chest pain patients to compare sensitivities and specificities for 30-day AO of the Stratus CS DeltacTnI immunoassay to the DeltaCK-MB and DeltacTnI, as measured by the Abbott Axsym immunoassay, and to the DeltaCK-MB, as measured by the Stratus CS. A Stratus CS DeltacTnI > or = +0.02 ng/mL in 2 h was more sensitive (61.9%) than an Axsym DeltaCK-MB > or = +1.3 ng/mL (38.1%; p = 0.03), a Stratus CS DeltaCK-MB > or = +0.4 ng/mL (38.1%; p = 0.03), and an Axsym DeltacTnI > or = +0.3 ng/mL (33.3%; p = 0.03) for 30-day AO. There were no differences in specificities. Our data support enhanced identification of ACS with a second generation cTnI assay. Pending larger studies, patients with a rise in DeltacTnI of > or = +0.02 ng/mL in 2 h, as measured by the Stratus CS immunoassay, should receive consideration for aggressive anti-ischemic therapy and further diagnostic testing prior to making an exclusionary diagnosis of non-ischemic chest pain.
No information is currently available regarding optimal cut-off values of the ST-vector magnitude (ST-VM) for predicting acute myocardial infarction (AMI) in emergency department (ED) chest pain patients undergoing vectorcardiographic (VCG) monitoring. A prospective observational study was performed in 1,722 chest pain patients with suspected acute coronary syndrome and absence of bundle branch block (BBB) and left ventricular hypertrophy (LVH) on initial ECG who underwent continuous VCG ST-segment monitoring during the initial ED evaluation. Three cut-off values for baseline ST-VM are reported and represent the smallest values in which the positive likelihood ratio (+LR) for AMI is greater than 5, 10, and 20, respectively. AMI occurred in 158 of 1,722 patients (9.2%) without BBB or LVH on initial ECG. Optimal cut-off values at the predetermined +LR values of 5, 10, and 20, were 121 microV (sensitivity, 41.8%; specificity, 92.0%), 151 microV (sensitivity, 29.1%; specificity, 97.1%), and 175 microV (sensitivity, 25.9%; specificity, 98.7%), respectively. Combining the earlier-mentioned cut-off values with physician judgment of initial pretest probability (high, intermediate, or low, respectively) resulted in a relative increase in identification of injury of 37.5% as compared with the ED physician's interpretation of initial ECG (41.8% v 30.4%; P <.0001), and 65.2% as compared with the official ECG interpretation (41.8% v 25.3%; P <.0001). Increasing ST-VM results in increasing likelihood of AMI. Clinical studies need to be performed to determine if ST-VM cut-off values of 121, 151, and 175 microV in conjunction with physician pretest probability of AMI can be used as criterion for emergent reperfusion therapy in patients without LVH or BBB on the initial ECG.
STUDY OBJECTIVE: We determine the overall use of a 6-step accelerated chest pain protocol to identify and exclude acute coronary syndrome (ACS) and to confirm previous findings of the use of serial 12-lead ECG monitoring (SECG) in conjunction with 2-hour delta serum marker measurements to identify and exclude acute myocardial infarction (AMI). METHODS: A prospective observational study was conducted over a 1-year period from January 1, 1999, through December 31, 1999, in 2,074 consecutive patients with chest pain who underwent our accelerated evaluation protocol, which includes 2-hour delta serum marker determinations in conjunction with automated SECG for the early identification and exclusion of AMI and selective nuclear stress testing for identification and exclusion of ACS. In patients not undergoing emergency reperfusion therapy, physician judgment was used to determine patient disposition at the completion of the 2-hour evaluation period: admit for ACS, discharge or admit for non-ACS condition, or immediate emergency department nuclear stress scan for possible ACS. A positive protocol was defined as a positive result in 1 or more of the 6 incremental steps in our chest pain evaluation protocol: (1) initial ECG diagnostic of acute injury or reciprocal injury; (2) baseline creatine kinase (CK)-MB level of 10 ng/mL or greater and index of 5% or greater or cardiac troponin I level of 2 ng/mL or greater; (3) new/evolving injury or new/evolving ischemia on SECG; (4) increase in CK-MB level of +1.5 ng/mL or greater or cardiac troponin I level of +0.2 ng/mL or greater in 2 hours; (5) clinical diagnosis of ACS despite a negative 2-hour evaluation; and (6) reversible perfusion defect on stress scan compared with on resting scan. All patients were followed up for 30-day ACS, which was defined as myocardial infarction (MI), percutaneous coronary intervention/coronary artery bypass grafting, coronary arteriography revealing stenosis of major coronary artery of 70% or greater not amenable to percutaneous coronary intervention/coronary artery bypass grafting, life-threatening complication, or cardiac death within 30 days of ED presentation. RESULTS: Discharge diagnosis in the 2,074 study patients consisted of 179 (8.6%) patients with AMI, 26 (1.3%) patients with recent AMI (decreasing curve of CK-MB), and 327 (15.8%) patients with 30-day ACS. At 2 hours, sensitivity and specificity for MI (AMI or recent AMI) of SECG plus delta serum marker measurements was 93.2% and 93.9%, respectively (positive likelihood ratio 15.3; negative likelihood ratio 0.07). At the completion of the full ED evaluation protocol (positive result in >or=1 of the 6 incremental steps), sensitivity and specificity for 30-day ACS was 99.1% and 87.4%, respectively (positive likelihood ratio 7.9; negative likelihood ratio 0.01). CONCLUSION: An accelerated chest pain evaluation strategy consisting of SECG, 2-hour delta serum marker measurements, and selective nuclear stress testing in conjunction with physician judgment identifies and excludes MI and 30-day ACS during the initial evaluation of patients with chest pain.