Colum G. Owens

Novel biomarkers in early diagnosis of acute myocardial infarction compared with cardiac troponin T

AIMS To evaluate the role of novel biomarkers in early detection of acute myocardial infarction (MI) in patients admitted with acute chest pain. METHODS AND RESULTS A prospective study of 664 patients presenting to two coronary care units with chest pain was conducted over 3 years from 2003. Patients were assessed on admission: clinical characteristics, ECG (electrocardiogram), renal function, cardiac troponin T (cTnT), heart fatty acid binding protein (H-FABP), glycogen phosphorylase-BB, NT-pro-brain natriuretic peptide, D-dimer, hsCRP (high sensitivity C-reactive protein), myeloperoxidase, matrix metalloproteinase-9, pregnancy associated plasma protein-A, soluble CD40 ligand. A > or = 12 h cTnT sample was also obtained. MI was defined as cTnT > or = 0.03 microg/L. In patients presenting <4 h of symptom onset, sensitivity of H-FABP for MI was significantly higher than admission cTnT (73 vs. 55%; P = 0.043). Specificity of H-FABP was 71%. None of the other biomarkers challenged cTnT. Combined use of H-FABP and cTnT (either one elevated initially) significantly improved the sensitivities of H-FABP or cTnT (85%; P < or = 0.004). This combined approach also improved the negative predictive value, negative likelihood ratio, and the risk ratio. CONCLUSION Assessment of H-FABP within the first 4 h of symptoms is superior to cTnT for detection of MI, and is a useful additional biomarker for patients with acute chest pain.

Prognostic value of a multimarker approach for patients presenting to hospital with acute chest pain.

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). A >or=12-hour cTnT sample was also obtained. Myocardial infarction (MI) was defined as peak cTnT >or=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.

Comparison of the 80-lead body surface map to physician and to 12-lead electrocardiogram in detection of acute myocardial infarction☆

Diagnosis of non-ST-elevation acute myocardial infarction (AMI) by a 12-lead electrocardiogram has poor sensitivity and specificity and, therefore, relies on biochemical markers of myocardial necrosis, which can only be reliably detected within 14 to 16 hours from symptom onset. The body surface map (BSM) improves AMI detection but is limited by its interpretation by inexperienced medical staff. To facilitate interpretation, an automated BSM algorithm was developed and is evaluated in this study. One hundred three patients with ischemic-type chest pain were recruited for this study from December 2001 to April 2002. A 12-lead electrocardiogram (Marquette Mac 5K) and BSM (PRIME-ECG) were recorded at initial presentation, and cardiac troponin I and/or creatine kinase-MB levels measured at 12 hours after symptom onset. The admitting physicians 12-lead electrocardiographic (ECG) interpretation, 12-lead ECG algorithm (Marquette 12 SL V233) diagnosis, and BSM algorithm diagnosis were documented for each patient. AMI, defined by elevation of troponin I to >1 microg/L and/or creatine kinase-MB to >25U/L, occurred in 53 patients. The admitting physician diagnosed 24 patients with AMI (sensitivity 45%, specificity 94%), the 12-lead ECG algorithm diagnosed 17 patients with AMI (sensitivity 32%, specificity 98%), and the BSM algorithm diagnosed 34 patients with AMI (sensitivity 64%, specificity 94%). The BSM algorithm improved the diagnostic sensitivity by 2.0 (p <0.001) and 1.4 (p = 0.002) compared with the 12-lead ECG algorithm or the admitting physician, respectively. There was no significant difference in specificity. Thus, the BSM algorithm improves detection of AMI compared with the 12-lead ECG algorithm or physicians 12-lead ECG interpretation.

How should I treat a patient to remove a fractured jailed side branch wire

BACKGROUND A 53-year-old female was sent for diagnostic angiography after successful reperfusion therapy for an anterior ST-elevation myocardial infarct. The culprit lesion was a LAD/D1 bifurcation stenosis. INVESTIGATIONS Coronary angiography, intravascular ultrasound. DIAGNOSIS Left anterior descending artery/first diagonal artery bifurcation stenosis, fractured jailed side branch wire. TREATMENT Provisional stenting strategy for bifurcation stenosis. Consideration of surgical and percutaneous options to retrieve fractured, jailed, side branch wire. Wire and balloon catheter wrap technique for retrieval of fractured wire.

Heart fatty acid–binding protein in combination with the 80-lead body surface potential map improves early detection of acute myocardial infarction in patients who are cardiac troponin T–negative at presentation

UNLABELLED Of patients who present with ischemic-type chest pain and a negative cardiac troponin T (cTnT) at first medical contact, there are patients at a very early stage of infarction. The aim of this research was to assess heart fatty acid-binding protein (H-FABP), a novel marker of myocyte necrosis, in combination with the 80-lead body surface potential map (BSPM) in the early diagnosis of acute myocardial infarction (AMI). METHODS In this prospective study, consecutive patients presenting with acute ischemic-type chest pain between 2003 and 2006 were enrolled. At first medical contact, blood was sampled for cTnT and H-FABP; in addition, a 12-lead electrocardiogram (ECG) and BSPM were recorded. A second cTnT was sampled 12 hours or more after presentation. Peak cTnT 0.03 μg/L or higher diagnosed AMI. Elevated H-FABP was 5 ng/mL or higher. A cardiologist blinded to both the clinical details and 12-lead ECG interpreted the BSPM. RESULTS Enrolled were 407 patients (age 62 ± 13 years; 70% men). Of these 407, 180 had cTnT less than 0.03 μg/L at presentation. Acute myocardial infarction occurred in 52 (29%) of 180 patients. Of these 180 patients, 27 had ST-segment elevation (STE) on ECG, 104 had STE on BSPM (sensitivity, 88%; specificity, 55%), and 95 (53%) had H-FABP elevation. The proportion with elevated H-FABP was higher in the AMI group compared with non-AMI group (P < .001). Body surface potential map STE was significantly associated with H-FABP elevation (P < .001). Of those with initial cTnT less than 0.03 μg/L, the c-statistic for the receiver operating characteristic curve distinguishing AMI from non-AMI using H-FABP alone was 0.644 (95% confidence interval [CI], 0.521-0.771), using BSPM alone was 0.716 (95% CI, 0.638-0.793), and using the combination of BSPM and H-FABP was 0.812 (95% CI, 0.747-0.876; P < .001). CONCLUSION In patients with acute ischemic-type chest pain who have a normal cTnT at presentation, the combination of H-FABP and BSPM at first assessment identifies those with early AMI (c-statistic, 0.812; P < .001), thus allowing earlier triage to reperfusion therapy and secondary prevention.

Early detection of acute posterior myocardial infarction using body surface mapping and SPECT scanning.

BackgroundMany patients with non-ST elevation myocardial infarction (NSTEMI) may have posterior STEMI, which should be emergently treated with reperfusion strategies but is difficult to identify by 12-lead ECG. ObjectivesTo compare the initial ECG and body surface map (BSM) for the diagnosis of posterior MI as verified by single-photon emission computed tomography (SPECT) and cTroponin T. MethodsPatients with chest pain greater than 20 min at rest with either ST depression of at least 0.1 mV in at least one of leads I, aVL or V1–V6 on ECG or STE at least 0.05 mV in at least one posterior lead on the BSM which underwent early SPECT scan. ResultsSixty patients (87%, 60 out of 69 with interpretable SPECT) had a posterior wall perfusion defect, all had cTroponinT (>0.09 ng/ml) and thus had posterior MI. Initial ECG showed STE in 24 (40%, 24 out of 60): 36 were non-diagnostic (60%, 36 out of 60). STE on BSM identified inferior MI in seven patients (12%, 7 out of 60), posterior in 32 patients (53%, 32 out of 60), and nine patients had right ventricular (15%, 9 out of 60). Twelve had no STE (20%, 12 out of 60). Of the patients with posterior MI and non-diagnostic ECGs, 53% (19 out of 36) were posterior MI by the BSM and six (17%, 6 out of 36) right ventricular MI only. The BSM correctly identified 53% (32 out of 60) (95% confidence interval 40–66%) of posterior MI. Of the 60 patients with posterior MI, 60% (36) had non-diagnostic ECGs: the BSM identified 42% (25) either as posterior MI or right ventricular MI only. ConclusionWe have shown that the BSM diagnoses significantly more posterior MI than the 12-lead ECG, allowing early identification of these patients so that maximum benefit from early reperfusion strategies can be gained.

Optimization of the precordial leads of the 12-lead electrocardiogram may improve detection of ST-segment elevation myocardial infarction

BACKGROUND For the assessment of patients with chest pain, the 12-lead electrocardiogram (ECG) is the initial investigation. Major management decisions are based on the ECG findings, both for attempted coronary artery revascularization and risk stratification. The aim of this study was to determine if the current 6 precordial leads (V(1)-V(6)) are optimally located for the detection of ST-segment elevation in ST-segment elevation myocardial infarction (STEMI). METHODS We analyzed 528 (38% anterior [200], 44% inferior [233], and 18% lateral [95]) patients with STEMI with both a 12-lead ECG and an 80-lead body surface map (BSM) ECG (Prime ECG, Heartscape Technologies, Bangor, Northern Ireland). Body surface map was recorded within 15 minutes of the 12-lead ECG during the acute event and before revascularization. ST-segment elevation of each lead on the BSM was compared with the corresponding 12-lead precordial leads (V(1)-V(6)) for anterior STEMI. In addition, for lateral STEMI, leads I and aVL of the BSM were also compared; and limb leads II, III, aVF of the BSM were compared with inferior unipolar BSM leads for inferior STEMI. Leads with the greatest mean ST-segment elevation were selected, and significance was determined by analysis of variance of the mean ST segment. RESULTS For anterior STEMI, leads V(1), V(2), 32, 42, 51, and 57 had the greatest mean ST elevation. These leads are located in the same horizontal plane as that of V(1) and V(2). Lead 32 had a significantly greater mean ST elevation than the corresponding precordial lead V(3) (P = .012); and leads 42, 51, and 57 were also significantly greater than corresponding leads V(4), V(5), V(6), respectively (P < .001). Similar findings were also found for lateral STEMI. For inferior STEMI, the limb leads of the BSM (II, III, and aVF) had the greatest mean ST-segment elevation; and lead III was significantly superior to the inferior unipolar leads (7, 17, 27, 37, 47, 55, and 61) of the BSM (P < .001). CONCLUSION Leads placed on a horizontal strip, in line with leads V(1) and V(2), provided the optimal placement for the diagnosis of anterior and lateral STEMI and appear superior to leads V(3), V(4), V(5), and V(6). This is of significant clinical interest, not only for ease and replication of lead placement but also may lead to increased recruitment of patients eligible for revascularization with none or borderline ST-segment elevation on the initial 12-lead ECG.

A method for the ECG inverse problem in the frequency domain

The Inverse ECG problem is ill-conditioned and its solution requires a relatively high computing effort. Additional constraints are required in order to obtain a stable solution. A method is proposed in which the solution of the inverse ECG problem is approached in the frequency domain, taking advantage of the assumption that propagation delays may be ignored and the quasi-periodicity of ECG. In this method usual Tikhonov zero-order constraints are applied to the amplitudes of the signals for a selected frequency domain. This method ensures faster solutions that are spatially and temporally well behaved. Calculation of epicardial electrograms is compared to a basic method.