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Epicardial electrical events were reconstructed using an inverse model for left ventricular (LV) pacing and during ventricular tachycardia (VT) induced during implantation of a biventricular pacemaker and/or internal defibrillator. The electrocardiographic position of the pacing lead, determined from the region of most negative potential 30 ms after the pacing spike, was compared with the radiographic position. Activation characterized by isochronal maps was correlated with the echocardiographic/myocardial scintigraphic data. Reconstructed epicardial isopotential/isochronal maps during VT were used to determine the presence of reentry. In 7 patients during LV pacing, epicardial isopotential maps located the maximum negative potentials anterolaterally (n = 3), posterolaterally (n = 2), and posteriorly (n = 2). Isochronal maps demonstrated activation patterns including regions of delayed activation that, in 5 patients, correlated with areas of akinesia/hypokinesia or fixed defects on echocardiography/myocardial scintigraphy. The mean difference between the radiographically measured right ventricular to LV pacing lead distance and calculated electrocardiographic right ventricular to LV pacing site distance was 1.7 cm. During VT, induced in 5 patients, single-loop reentry was observed in 3 and figure-of-8 reentry in 2. Exit site and regions of fast/slow conduction and conduction block that correlated with anatomic areas of infarction defined by echocardiography/myocardial scintigraphy were demonstrated. In conclusion, epicardial maps reconstructed from the body surface map can identify LV pacing sites and demonstrate reentry during VT. The body surface map could thus identify optimal pacing sites for LV pacing and targets for VT ablation.

To evaluate the prognostic role of novel biomarkers for the risk stratification of patients admitted with ischemic-type chest pain, a prospective study of 664 patients presenting to 2 coronary care units with ischemic-type chest pain was conducted over 3 years beginning in 2003. Patients were assessed on admission for clinical characteristics, electrocardiographic findings, renal function, cardiac troponin T (cTnT), markers of myocyte injury (heart fatty acid-binding protein [H-FABP] and glycogen phosphorylase BB), neurohormonal activation (N-terminal-pro-brain natriuretic peptide [NT-pro-BNP]), hemostatic activity (fibrinogen and D-dimer), and vascular inflammation (high-sensitivity C-reactive protein, myeloperoxidase, matrix metalloproteinase-9, pregnancy-associated plasma protein-A, and soluble CD40 ligand). Aor=12-hour cTnT sample was also obtained. Myocardial infarction (MI) was defined as peak cTnTor=0.03 microg/L. Patients were followed for 1 year from the time of admission. The primary end point was death or MI. Elevated fibrinogen, D-dimer, H-FABP, NT-pro-BNP, and peak cTnT were predictive of death or MI within 1 year (unadjusted odds ratios 2.5, 3.1, 5.4, 5.4, and 6.9, respectively). On multivariate analysis, H-FABP and NT-pro-BNP were selected, in addition to age, peak cTnT, and left ventricular hypertrophy on initial electrocardiography, as significant independent predictors of death or MI within 1 year. Patients without elevations of H-FABP, NT-pro-BNP, or peak cTnT formed a very low risk group in terms of death or MI within 1 year. A very high risk group had elevations of all 3 biomarkers. In conclusion, the measurement of H-FABP and NT-pro-BNP at the time of hospital admission for patients with ischemic-type chest pain adds useful prognostic information to that provided by the measurement of baseline and 12-hour cTnT.

We aimed to develop 12-lead electrocardiographic (ECG) models testing ST-elevation criteria with QRST variables and compare their performance with the 80-lead body surface map (BSM) in detection of acute myocardial infarction (AMI). Because the prevalence of non-ST-elevation AMI is increasing worldwide, advances in early ECG detection of AMI are urgently needed. The study population was 755 consecutive patients presenting with ischemic chest pain from January 2002 to June 2004. All patients had electrocardiography and body surface mapping performed at initial presentation. AMI occurred in 519 patients (69%, cardiac troponin T or I levelor =0.1 ng/ml). Of these 519 patients, 303 (58%) had no ST-elevation on the initial 12-lead electrocardiogram. Ten patients were classified as having an "aborted AMI" and were included in the AMI analysis. The American College of Cardiology/European Society of Cardiology criteria for ST-elevation on 12-lead electrocardiogram identified 236 patients with AMI (sensitivity 45%, specificity 92%). Additional QRST features improved sensitivity (51% to 68%) but with decreased specificity (71% to 89%), with the optimal multivariate ECG model having a c-statistic of 0.75. The optimal BSM model identified 402 patients as having AMI (sensitivity 76%, specificity 92%, c-statistic 0.84). This improvement in sensitivity over the 12-lead electrocardiogram was due mainly to detection of ST-elevation in the high right anterior, posterior, and right ventricular territories and AMI in the presence of left bundle branch block. In conclusion, QRST variables added to criteria for ST-elevation result in improvement in sensitivity of the 12-lead electrocardiogram, although with decreased specificity. The BSM is superior in detecting AMI and demonstrates the importance of electroanatomic evaluation of patients with acute coronary syndromes.