Prediction of postoperative atrial fibrillation with postoperative epicardial electrograms.

Objectives. New-onset postoperative atrial fibrillation (POAF) is a common complication after cardiac surgery. The arrhythmia often entails a longer hospital stay, greater risk of other complications, and higher mortality both short- and long-term. An investigation of the use of early atrial electrograms in predicting POAF in cardiac surgery was performed. Design. In this prospective observational study, a total of 99 consecutive adult patients undergoing coronary artery bypass grafting, valve surgery or both were included. On the first postoperative morning, standard 12-lead electrograms (ECG), unipolar atrial electrograms (aEG), and vital values were recorded. The outcome was new-onset POAF within one month postoperatively. Results. Three multivariable prediction models for POAF were formed using measurements derived from the ECG, aEG, and patient characteristics. Age, body mass index, and two unipolar electrogram measurements quantifying local activation time and fractionation were strongly associated with the outcome POAF. The performance of the POAF prediction models was assessed through receiver operating curve characteristics with cross-validation, and discrimination using the leave-one-out-method to internally validate the models. The cross-validated area under the receiver operating characteristic curve (AUC) was improved in a prediction model using atrial-derived electrogram variables (AUC 0.796, 95% CI 0.698-0.894), compared with previous ECG and clinical models (AUC 0.716, 95% CI 0.606-0.826 and AUC 0.718, 95% CI 0.613-0.822, respectively). Conclusions. This study found that easily obtainable measurements from atrial electrograms may be helpful in identifying patients at risk of POAF in cardiac surgery.

Plasma potassium concentration and cardiac repolarisation markers, Tpeak-Tend and Tpeak-Tend/QT, during and after exercise in healthy participants and in end-stage renal disease.

PURPOSE: The cardiac T-wave peak-to-end interval (Tpe) is thought to reflect dispersion in ventricular repolarisation, with abnormalities in Tpe associated with increased risk of arrhythmia. Extracellular K+ modulates cardiac repolarisation, and since arterial plasma K+ concentration ([K+]) rapidly increases during and declines following exercise, we investigated the relationship between [K+] and Tpe with exercise. METHODS: Serial ECGs (Tpe, Tpe/QT ratio) and [K+] were obtained from 8 healthy, normokalaemic volunteers and 22 patients with end-stage renal disease (ESRD), at rest, during, and after exhaustive exercise. RESULTS: Post-exercise [K+] nadir was 3.1 ± 0.1, 5.0 ± 0.2 and 4.0 ± 0.1 mmol.L-1 (mean ± SEM) for healthy participants and ESRD patients before and after haemodialysis, respectively. In healthy participants, compared to pre-exercise, recovery-induced low [K+] was associated with a prolongation of Tpe (110 ± 8 vs. 87 ± 5 ms, respectively, p = 0.03) and an increase in Tpe/QT ratio (0.28 ± 0.01 vs. 0.23 ± 0.01, respectively, p = 0.01). Analyses of serial data revealed [K+] as a predictor of Tpe in healthy participants (ß = -0.54 ±0.05, p < 0.0001), in ESRD patients (ß = -0.75 ± 0.06, p < 0.0001) and for all data pooled (ß = -0.61 ± 0.04, p < 0.0001). The [K+] was also a predictor of Tpe/QT ratio in healthy participants and ESRD patients. CONCLUSIONS: Tpe and Tpe/QT ratio are predicted by [K+] during exercise. Low [K+] during recovery from exercise was associated with increased Tpe and Tpe/QT, indicating accentuated dispersion of ventricular repolarisation. The findings suggest that variations in [K+] with physical exertion may unmask electrophysiological vulnerabilities to arrhythmia.

Preoperative Electrocardiogram Score for Predicting New-Onset Postoperative Atrial Fibrillation in Patients Undergoing Cardiac Surgery.

OBJECTIVE: To investigate if electrocardiogram (ECG) markers from routine preoperative ECGs can be used in combination with clinical data to predict new-onset postoperative atrial fibrillation (POAF) following cardiac surgery. DESIGN: Retrospective observational case-control study. SETTING: Single-center university hospital. PARTICIPANTS: One hundred consecutive adult patients (50 POAF, 50 without POAF) who underwent coronary artery bypass grafting, valve surgery, or combinations. INTERVENTIONS: Retrospective review of medical records and registration of POAF. MEASUREMENTS AND MAIN RESULTS: Clinical data and demographics were retrieved from the Western Denmark Heart Registry and patient records. Paper tracings of preoperative ECGs were collected from patient records, and ECG measurements were read by two independent readers blinded to outcome. A subset of four clinical variables (age, gender, body mass index, and type of surgery) were selected to form a multivariate clinical prediction model for POAF and five ECG variables (QRS duration, PR interval, P-wave duration, left atrial enlargement, and left ventricular hypertrophy) were used in a multivariate ECG model. Adding ECG variables to the clinical prediction model significantly improved the area under the receiver operating characteristic curve from 0.54 to 0.67 (with cross-validation). The best predictive model for POAF was a combined clinical and ECG model with the following four variables: age, PR-interval, QRS duration, and left atrial enlargement. CONCLUSION: ECG markers obtained from a routine preoperative ECG may be helpful in predicting new-onset POAF in patients undergoing cardiac surgery.

Algorithm for the automatic computation of the modified Anderson-Wilkins acuteness score of ischemia from the pre-hospital ECG in ST-segment elevation myocardial infarction.

BACKGROUND: The acuteness score (based on the modified Anderson-Wilkins score) estimates the acuteness of ischemia based on ST-segment, Q-wave and T-wave measurements obtained from the electrocardiogram (ECG) in patients with ST Elevation Myocardial Infarction (STEMI). The score (range 1 (least acute) to 4 (most acute)) identifies patients with substantial myocardial salvage potential regardless of patient reported symptom duration. However, due to the complexity of the score, it is not used in clinical practice. Therefore, we aimed to develop a reliable algorithm that automatically computes the acuteness score. METHODS: We scored 50 pre-hospital ECGs from STEMI patients, manually and by the automated algorithm. We assessed the reliability test between the manual and automated algorithm by interclass correlation coefficient (ICC) and Bland-Altman plot. RESULTS: The ICC was 0.84 (95% CI 0.72-0.91), P<0.0001. The mean difference between manual and automated acuteness score was 0.17±0.66. In only two cases, there was a major disagreement between the two scores. There was an excellent agreement between the scores for the remaining 48 ECGs, all within the upper (1.46) and lower (-1.12) limits of agreement. CONCLUSION: In conclusion, we have developed an automated algorithm for measurement of the modified Anderson-Wilkins ECG acuteness score from the pre-hospital ECG in STEMI patients. This automated algorithm is highly reliable, can be applied in daily practice for research purposes and may be implemented in commercial automated ECG analysis programs to achieve practical use for decision support in the acute phase of STEMI.

Minimizing a Wireless Passive LC-Tank Sensor to Monitor Bladder Pressure: A Simulation Study.

In this simulation study, a wireless passive LC-tank sensor system was characterized. Given the application of continuous bladder monitoring, a specific system was proposed in terms of coil geometries and electronic circuitry. Coupling coefficients were spatially mapped by simulation, as a function of both coil distance, and longitudinal and transverse translation of the sensor relative to the antenna. Further, two interrogation schemes were outlined. One was an auto-balancing bridge for computing the sensor-system impedance. In this case, the theoretical noise limit of the analogue part of the system was found by simulations. As the full system is not necessary for obtaining a pressure reading from the sensor, a simplified circuit more suited for an implantable system was deduced. For this system, both the analogue and digital parts were simulated. First, the required ADC resolution for operating the system at a given coupling was found by simulations in the noise-free case. Then, for one selected typical operational point, noise was added gradually, and through Monte-Carlo type simulations, the system performance was obtained. Combining these results, it was found that it at least is possible to operate the proposed system for distances up to 12 mm, or equivalently for coupling coefficients above 0.005. In this case a 14 bit ADC is required, and a carrier SNR of 27 dB can be tolerated.

Novel non-invasive ECG imaging method based on the 12-lead ECG for reconstruction of ventricular activation: A proof-of-concept study.

Aim: Current non-invasive electrocardiographic imaging (ECGi) methods are often based on complex body surface potential mapping, limiting the clinical applicability. The aim of this pilot study was to evaluate the ability of a novel non-invasive ECGi method, based on the standard 12-lead ECG, to localize initial site of ventricular activation in right ventricular (RV) paced patients. Validation of the method was performed by comparing the ECGi reconstructed earliest site of activation against the true RV pacing site determined from cardiac computed tomography (CT). Methods: This was a retrospective study using data from 34 patients, previously implanted with a dual chamber pacemaker due to advanced atrioventricular block. True RV lead position was determined from analysis of a post-implant cardiac CT scan. The ECGi method was based on an inverse-ECG algorithm applying electrophysiological rules. The algorithm integrated information from an RV paced 12-lead ECG together with a CT-derived patient-specific heart-thorax geometric model to reconstruct a 3D electrical ventricular activation map. Results: The mean geodesic localization error (LE) between the ECGi reconstructed initial site of activation and the RV lead insertion site determined from CT was 13.9 ± 5.6 mm. The mean RV endocardial surface area was 146.0 ± 30.0 cm2 and the mean circular LE area was 7.0 ± 5.2 cm2 resulting in a relative LE of 5.0 ± 4.0%. Conclusion: We demonstrated a novel non-invasive ECGi method, based on the 12-lead ECG, that accurately localized the RV pacing site in relation to the ventricular anatomy.

Non-invasive estimation of QLV from the standard 12-lead ECG in patients with left bundle branch block.

Background: Cardiac resynchronization therapy (CRT) is a treatment for patients with heart failure and electrical dyssynchrony, i.e., left bundle branch block (LBBB) ECG pattern. CRT resynchronizes ventricular contraction with a right ventricle (RV) and a left ventricle (LV) pacemaker lead. Positioning the LV lead in the latest electrically activated region (measured from Q wave onset in the ECG to LV sensing by the left pacemaker electrode [QLV]) is associated with favorable outcome. However, optimal LV lead placement is limited by coronary venous anatomy and the inability to measure QLV non-invasively before implantation. We propose a novel non-invasive method for estimating QLV in sinus-rhythm from the standard 12-lead ECG. Methods: We obtained 12-lead ECG, LV electrograms and LV lead position in a standard LV 17-segment model from procedural recordings from 135 standard CRT recipients. QLV duration was measured post-operatively. Using a generic heart geometry and corresponding forward model for ECG computation, the electrical activation pattern of the heart was fitted to best match the 12-lead ECG in an iterative optimization procedure. This procedure initialized six activation sites associated with the His-Purkinje system. The initial timing of each site was based on the directions of the vectorcardiogram (VCG). Timing and position of the sites were then changed iteratively to improve the match between simulated and measured ECG. Noninvasive estimation of QLV was done by calculating the time difference between Q-onset on the computed ECG and the activation time corresponding to centroidal epicardial activation time of the segment where the LV electrode is positioned. The estimated QLV was compared to the measured QLV. Further, the distance between the actual LV position and the estimated LV position was computed from the generic ventricular model. Results: On average there was no difference between QLV measured from procedural recordings and non-invasive estimation of QLV ( Δ Q L V = - 3.0 ± 22.5 m s , p = 0.12 ). Median distance between actual LV pacing site and the estimated pacing site was 18.6 mm (IQR 17.3 mm). Conclusion: Using the standard 12-lead ECG and a generic heart model it is possible to accurately estimate QLV. This method may potentially be used to support patient selection, optimize implant procedures, and to simulate optimal stimulation parameters prior to pacemaker implantation.

Clinical implications of electrocardiographic bundle branch block in primary care.

OBJECTIVES: Electrocardiographic bundle branch block (BBB) is common but the prognostic implications in primary care are unclear. We sought to investigate the relationship between electrocardiographic BBB subtypes and the risk of cardiovascular (CV) outcomes in a primary care population free of major CV disease. METHODS: Retrospective cohort study of primary care patients referred for electrocardiogram (ECG) recording between 2001 and 2011. Cox regression models were used to estimate hazard ratios (HR) as well as absolute risks of CV outcomes based on various BBB subtypes. RESULTS: We included 202 268 individuals with a median follow-up period of 7.8 years (Inter-quartile range [IQR] 4.9-10.6). Left bundle branch block (LBBB) was associated with heart failure (HF) in both men (HR 3.96, 95% CI 3.30 to 4.76) and women (HR 2.51, 95% CI 2.15 to 2.94) and with CV death in men (HR 1.80, 95% CI 1.38 to 2.35). Right bundle branch block (RBBB) was associated with pacemaker implantation in both men (HR 3.26, 95% CI 2.74 to 3.89) and women (HR 3.69, 95% CI 2.91 to 4.67), HF in both sexes and weakly associated with CV death in men. Regarding LBBB, we found an increasing hazard of HF with increasing QRS-interval duration (HR 1.25, 95% CI 1.11 to 1.42 per 10 ms increase in men and HR 1.23, 95% CI 1.08 to 1.40 per 10 ms increase in women). Absolute 10-year risk predictions across age-specific and sex-specific subgroups revealed clinically relevant differences between having various BBB subtypes. CONCLUSIONS: Opportunistic findings of BBB subtypes in primary care patients without major CV disease should be considered warnings of future HF and pacemaker implantation.

A History of Drug-Induced Torsades de Pointes Is Associated With T-wave Morphological Abnormalities.

The hypothesis of the study is that Torsades de pointes (TdP) history can be better identified using T-wave morphology compared to Fridericia-corrected QT interval (QTcF) at baseline. ECGs were recorded at baseline and during sotalol challenge in 20 patients with a history of TdP (+TdP) and 16 patients without previous TdP (-TdP). The QTcF and T-wave morphology combination score (MCS) were calculated. At baseline, there was no significant difference in QTcF between the groups (+TdP: QTcF = 446 ± 9 ms; -TdP: QTcF = 431 ± 9 ms, P = 0.27). In contrast, MCS was significantly different between the groups at baseline (+TdP: MCS = 1.07 ± 0.095; -TdP: MCS = 0.74 ± 0.07, P = 0.012). Both QTcF and MCS could be used to discriminate between +TdP and -TdP after sotalol but only MCS reached statistical significance at baseline. Combining QTcF with MCS provided a significantly larger difference between groups than QTcF alone.

Automatic electrocardiographic algorithm for assessing severity of ischemia in ST-segment elevation myocardial infarction.

BACKGROUND: Terminal QRS distortion on the electrocardiogram (ECG) is a sign of severe ischemia in patients with STEMI and can be quantified by the Sclarovsky-Birnbaum Severity of Ischemia. Due to score complexity, it has not been applied in clinical practice. Automatic scoring of digitally recorded ECGs could facilitate clinical application. We aimed to develop an automatic algorithm for the severity of ischemia. METHODS: Development set: 50 STEMI ECGs were manually (Manual-score) and automatically (Auto-score) scored by our designed algorithm. The agreement between Manual- and Auto-score was assessed by kappa statistics. Test set: ECGs from 199 STEMI patients were assigned a severity grade (severe or non-severe ischemia) by the Auto-score. Infarct size estimated by median peak Troponin T (TnT) and Creatinine Kinase Myocardial Band (CKMB) was tested between the groups. RESULTS: The agreement between Manual- and Auto-score was 0.83 ((95% CI 0.55-1.00), p < 0.0001), sensitivity 75% and specificity 100%, PPV 100% and NPV 94.6%. In the test set 152 (76%) patients were male, mean age 61 ±â€¯12 years. The Auto-score designated severe ischemia in 42 (21%) and non-severe ischemia in 157 (79%) patients. Patients with ECG signs of severe vs. non-severe ischemia had significantly higher levels of biomarkers of infarct size. In multiple linear regression, ECG sign of severe ischemia was an independent predictor for higher TnT and CKMB levels. CONCLUSION: The automatic ECG algorithm for severity of ischemia in STEMI performs adequately for clinical use. Severe ischemia obtained by the Auto-score was associated with biomarker estimated larger infarct size.

Protection against severe hypokalemia but impaired cardiac repolarization after intense rowing exercise in healthy humans receiving salbutamol.

Intense exercise induces pronounced hyperkalemia, followed by transient hypokalemia in recovery. We investigated whether the ß2 agonist salbutamol attenuated the exercise hyperkalemia and exacerbated the postexercise hypokalemia, and whether hypokalemia was associated with impaired cardiac repolarization (QT hysteresis). Eleven healthy adults participated in a randomized, counterbalanced, double-blind trial receiving either 1,000 µg salbutamol (SAL) or placebo (PLAC) by inhalation. Arterial plasma potassium concentration ([K+]a) was measured at rest, during 3 min of intense rowing exercise, and during 60 min of recovery. QT hysteresis was calculated from ECG ( n = 8). [K+]a increased above baseline during exercise (rest, 3.72 ± 0.7 vs. end-exercise, 6.81 ± 1.4 mM, P < 0.001, mean ± SD) and decreased rapidly during early recovery to below baseline; restoration was incomplete at 60 min postexercise ( P < 0.05). [K+]a was less during SAL than PLAC (4.39 ± 0.13 vs. 4.73 ± 0.19 mM, pooled across all times, P = 0.001, treatment main effect). [K+]a was lower after SAL than PLAC, from 2 min preexercise until 2.5 min during exercise, and at 50 and 60 min postexercise ( P < 0.05). The postexercise decline in [K+]a was correlated with QT hysteresis ( r = 0.343, n = 112, pooled data, P = 0.001). Therefore, the decrease in [K+]a from end-exercise by ~4 mM was associated with reduced QT hysteresis by ~75 ms. Although salbutamol lowered [K+]a during exercise, no additive hypokalemic effects occurred in early recovery, suggesting there may be a protective mechanism against severe or prolonged hypokalemia after exercise when treated by salbutamol. This is important because postexercise hypokalemia impaired cardiac repolarization, which could potentially trigger arrhythmias and sudden cardiac death in susceptible individuals with preexisting hypokalemia and/or heart disease. NEW & NOTEWORTHY Intense rowing exercise induced a marked increase in arterial potassium, followed by a pronounced decline to hypokalemic levels. The ß2 agonist salbutamol lowered potassium during exercise and late recovery but not during early postexercise, suggesting a protective effect against severe hypokalemia. The decreased potassium in recovery was associated with impaired cardiac QT hysteresis, suggesting a link between postexercise potassium and the heart, with implications for increased risk of cardiac arrhythmias and, potentially, sudden cardiac death.

The T-peak-T-end interval as a marker of repolarization abnormality: a comparison with the QT interval for five different drugs.

BACKGROUND AND OBJECTIVE: The T-peak to T-end (TpTe) interval has been suggested as an index of transmural dispersion and as a marker of drug-induced abnormal repolarization. In this study, we investigate the relation between TpTe and the QT interval. METHODS: Electrocardiograms (ECGs) from five different drugs (sotalol, sertindole, moxifloxacin, nalmefene, and Lu 38-135) and from a placebo group were analyzed. Semi-automatic measurements of T-peak, T-end, and QRS onset were obtained. The TpTe/QT ratio was calculated to investigate the proportional relationship of QT and TpTe. RESULTS: Although a significant increase of both TpTe and QT from baseline is apparent with QT-prolonging drugs, the TpTe/QT ratio remained the same at baseline and after drug administration, thus indicating that prolongation of TpTe is just a fractional part of total QT prolongation. In the presence of notched or flattened T-waves, the uncertainty associated with measurement of the TpTe interval increases. The errors in TpTe for individual subjects may be substantial, thus complicating the use of TpTe for follow-up of individuals. CONCLUSIONS: The duration of the QT interval and TpTe are closely related. Drugs appear to prolong the TpTe interval as a predictable fraction of the total QT prolongation.