Peak CK-MB has a strong association with chronic scar size and wall motion abnormalities after revascularized non-transmural myocardial infarction - a prospective CMR study.

BACKGROUND: Large myocardial infarction (MI) is associated with adverse left ventricular (LV) remodeling (LVR). We studied the nature of LVR, with specific attention to non-transmural MIs, and the association of peak CK-MB with recovery and chronic phase scar size and LVR. METHODS: Altogether 41 patients underwent prospectively repeated cardiovascular magnetic resonance at a median of 22 (interquartile range 9-29) days and 10 (8-16) months after the first revascularized MI. Transmural MI was defined as ≥75% enhancement in at least one myocardial segment. RESULTS: Peak CK-MB was 86 (40-216) µg/L in median, while recovery and chronic phase scar size were 13 (3-23) % and 8 (2-19) %. Altogether 33 patients (81%) had a non-transmural MI. Peak CK-MB had a strong correlation with recovery and chronic scar size (r ≥ 0.80 for all, r ≥ 0.74 for non-transmural MIs; p < 0.001). Peak CK-MB, recovery scar size, and chronic scar size, were all strongly correlated with chronic wall motion abnormality index (WMAi) (r ≥ 0.75 for all, r ≥ 0.73 for non-transmural MIs; p < 0.001). There was proportional scar size and LV mass resorption of 26% (0-50%) and 6% (- 2-14%) in median. Young age (< 60 years, median) was associated with greater LV mass resorption (median 9%vs.1%, p = 0.007). CONCLUSIONS: Peak CK-MB has a strong association with chronic scar size and wall motion abnormalities after revascularized non-transmural MI. Considerable infarct resorption happens after the first-month recovery phase. LV mass resorption is related to age, being more common in younger patients.

Fibrosis and wall thickness affect ventricular repolarization dynamics in hypertrophic cardiomyopathy.

BACKGROUND: Hypertrophic cardiomyopathy (HCM) is characterized by ventricular repolarization abnormalities and risk of ventricular arrhythmias. Our aim was to study the association between the phenotype and ventricular repolarization dynamics in HCM patients. METHODS: HCM patients with either the MYBPC3-Q1061X or TPM1-D175N mutation (n = 46) and control subjects without mutation and hypertrophy (n = 35) were studied with 24-hr ambulatory ECG recordings by measuring time intervals of rate-adapted QT (QTe), maximal QT, and T-wave apex to wave end (TPE) intervals and the QTe/RR slope. Findings were correlated to specified echocardiographic and cardiac magnetic resonance imaging (CMRI) findings. RESULTS: Rate-adapted QTe interval was progressively longer in HCM patients with decreasing heart rates compared to control subjects (p = 0.020). The degree of hypertrophy correlated with measured QTe values. HCM patients with maximal wall thickness higher than the mean (20.6 mm) had longer maximum QTe and median TPE intervals compared to control subjects and HCM patients with milder hypertrophy (p < 0.001 and p = 0.014, respectively). HCM patients with late gadolinium enhancement (LGE) on CMRI had steeper QTe/RR slopes compared to HCM patients without LGE and control subjects (p = 0.044 and p = 0.001, respectively). LGE was an independent predictor of QTe/RR slope (p = 0.023, B = 0.043). CONCLUSION: Dynamics of ventricular repolarization in HCM are affected by hypertrophy and fibrosis. LGE may confer an independent effect on QT dynamics which may increase the arrhythmogenic potential in HCM.

Slowed depolarization and irregular repolarization in catecholaminergic polymorphic ventricular tachycardia: a study from cellular Ca2+ transients and action potentials to clinical monophasic action potentials and electrocardiography.

AIMS: Spontaneous Ca2+ release leads to afterdepolarizations and triggered arrhythmia in catecholaminergic polymorphic ventricular tachycardia (CPVT). Irregular Ca2+ release is hypothesized to manifest as slowed depolarization and irregular repolarization. Our goal was to study depolarization and repolarization abnormalities in CPVT, as they remain largely uninvestigated. METHODS AND RESULTS: We studied intracellular Ca2+ handling and action potentials (APs) in an induced pluripotent stem cell (iPSC) model of CPVT. Induced pluripotent stem cell cardiomyocytes from a RyR2-P2328S patient showed increased non-alternating variability of Ca2+ transients in response to isoproterenol. ß-Agonists decreased AP upslope velocity in CPVT cells and in monophasic AP recordings of CPVT patients. We compared 24 h electrocardiograms (ECGs) of 19 CPVT patients carrying RyR2 mutations and 19 healthy controls. Short-term variability (STV) of the QT interval was 6.9 ± 0.5 ms in CPVT patients vs. 5.5 ± 0.4 ms in controls (P < 0.05) and associated with a history of arrhythmic events. Mean T-wave alternans (TWA) was 25 ± 1.4 µV in CPVT patients vs. 31 ± 2.0 µV in controls (P < 0.05). Older CPVT patients showed lower maximal upslope velocity of the ECG R-spike than control patients. CONCLUSION: Catecholaminergic polymorphic ventricular tachycardia patients show higher STV of repolarization but lower TWA on the 24 h ECG than control patients, which is likely to reflect increased non-alternating variability of Ca2+ release by mutant RyR2s as observed in vitro. ß-Agonists slow depolarization in RyR2-mutant cells and in CPVT patients. These findings may constitute a marker of arrhythmogenicity.

Sensitivity and specificity of automated detection of early repolarization in standard 12-lead electrocardiography.

BACKGROUND: Early repolarization (ER) is defined as an elevation of the QRS-ST junction in at least two inferior or lateral leads of the standard 12-lead electrocardiogram (ECG). Our purpose was to create an algorithm for the automated detection and classification of ER. METHODS: A total of 6,047 electrocardiograms were manually graded for ER by two experienced readers. The automated detection of ER was based on quantification of the characteristic slurring or notching in ER-positive leads. The ER detection algorithm was tested and its results were compared with manual grading, which served as the reference. RESULTS: Readers graded 183 ECGs (3.0%) as ER positive, of which the algorithm detected 176 recordings, resulting in sensitivity of 96.2%. Of the 5,864 ER-negative recordings, the algorithm classified 5,281 as negative, resulting in 90.1% specificity. Positive and negative predictive values for the algorithm were 23.2% and 99.9%, respectively, and its accuracy was 90.2%. Inferior ER was correctly detected in 84.6% and lateral ER in 98.6% of the cases. CONCLUSIONS: As the automatic algorithm has high sensitivity, it could be used as a prescreening tool for ER; only the electrocardiograms graded positive by the algorithm would be reviewed manually. This would reduce the need for manual labor by 90%.

Assessment of myocardial infarct size with body surface potential mapping: validation against contrast-enhanced cardiac magnetic resonance imaging.

BACKGROUND: Assessment of myocardial infarct (MI) size is important for therapeutic and prognostic reasons. We used body surface potential mapping (BSPM) to evaluate whether single-lead electrocardiographic variables can assess MI size. METHODS: We performed BSPM with 120 leads covering the front and back chest (plus limb leads) on 57 patients at different phases of MI: acutely, during healing, and in the chronic phase. Final MI size was determined by contrast-enhanced cardiac magnetic resonance imaging (DE-CMR) and correlated with various computed depolarization- and repolarization-phase BSPM variables. We also calculated correlations between BSPM variables and enzymatic MI size (peak CK-MBm). RESULTS: BSPM variables reflecting the Q- and R wave showed strong correlations with MI size at all stages of MI. R width performed the best, showing its strongest correlation with MI size on the upper right back, there representing the width of the "reciprocal Q wave" (r = 0.64-0.71 for DE-CMR, r = 0.57-0.64 for CK-MBm, P < 0.0001). Repolarization-phase variables showed only weak correlations with MI size in the acute phase, but these correlations improved during MI healing. T-wave variables and the QRSSTT integral showed their best correlations with DE-CMR defined MI size on the precordial area, at best r = -0.57, P < 0.0001 in the chronic phase. The best performing BSPM variables could differentiate between large and small infarcts at all stages of MI. CONCLUSIONS: Computed, single-lead electrocardiographic variables can estimate the final infarct size at all stages of MI, and differentiate large infarcts from small.

Performance comparison of 6 in-hospital patient monitoring systems in the detection and alarm of ventricular cardiac arrhythmias.

Background: Patient monitoring devices are critical for alerting of potential cardiac arrhythmias during hospitalization; however, there are concerns of alarm fatigue due to high false alarm rates. Objective: The purpose of this study was to evaluate the sensitivity and false alarm rate of hospital-based continuous electrocardiographic (ECG) monitoring technologies. Methods: Six commonly used multiparameter bedside monitoring systems available in the United States were evaluated: B125M (GE HealthCare), ePM10 and iPM12 (Mindray), Efficia and IntelliVue (Philips), and Life Scope (Nihon Kohden). Sensitivity was tested using ECG recordings containing 57 true ventricular tachycardia (VT) events. False-positive rate testing used 205 patient-hours of ECG recordings containing no cardiac arrhythmias. Signals from ECG recordings were fed to devices simultaneously; high-severity arrhythmia alarms were tracked. Sensitivity to true VT events and false-positive rates were determined. Differences were assessed using Fisher exact tests (sensitivity) and Z-tests (false-positive rates). Results: B125M raised 56 total alarms for 57 annotated VT events and had the highest sensitivity (98%; P <.05), followed by iPM12 (84%), Life Scope (81%), Efficia (79%), ePM10 (77%), and IntelliVue (75%). B125M raised 20 false alarms, which was significantly lower (P <.0001) than iPM12 (284), Life Scope (292), IntelliVue (304), ePM10 (324), and Efficia (493). The most common false alarm was VT, followed by nonsustained VT. Conclusion: We found significant performance differences among multiparameter bedside ECG monitoring systems using previously collected recordings. B125M had the highest sensitivity in detecting true VT events and lowest false alarm rate. These results can assist in minimizing alarm fatigue and optimizing patient safety by careful selection of in-hospital continuous monitoring technology.

U wave features in body surface potential mapping in post-myocardial infarction patients.

BACKGROUND: The data on U wave features in post-myocardial infarction (MI) remain sparse. We employed 120-lead body surface potential mapping (BSPM) to explore the U wave in patients with remote MI. METHODS: Sixty post-MI patients and 46 healthy controls were examined. After signal averaging, the polarity changes of U wave related to the T wave were analyzed, and the spatial and temporal U wave parameters were computed. RESULTS: Four types of patterns based on T and U polarity were recognized. A pattern with positive T and U waves was related to better ventricular function. The study groups did not differ as regards to Tend-Uapex and Tapex-Uapex intervals whereas Uapex-Uend was significantly longer in MI patients (110 ± 20 ms vs. 100 ± 13 ms, P = 0.004). MI patients had significantly higher U wave maximum amplitude (70 ± 30 µV vs. 50 ± 20 µV, P < 0.001), and U integral area (3.96 ± 1.50 µV·s vs. 3.17 ± 0.99 µV·s, P = 0.002), but lower corresponding T wave parameter values, thus resulting into higher U/T maximum amplitude and area ratios (0.16 ± 0.10 vs. 0.09 ± 0.04, P < 0.001; and 0.13 ± 0.06 vs. 0.09 ± 0.03, P < 0.001). In comparison to 12-lead ECG, BSPM covering the entire thorax enhanced the detection of U waves. CONCLUSION: MI tends to increase the U amplitude and prolong the later part of U wave duration thus augmenting the U wave. The size and location of infarction were associated with specific T and U wave polarity patterns.

Predicting recovery of myocardial function by electrocardiography after acute infarction.

BACKGROUND: In acute ischemic left ventricular (LV) dysfunction, distinguishing viable myocardium is clinically important. METHODS: Body surface potential mapping (Electrocardiography [ECG] with 123 leads), was recorded in 62 patients with acute coronary syndrome (ACS). ECG variables were computed from de- and repolarization phases. LV segmental wall motion was assessed by echocardiography acutely and after 1 year. RESULTS: The number of dysfunctional segments (DFS) diminished during follow-up in 37 patients (recovery group) and remained the same or increased in 25 patients (nonrecovery group). Acutely, DFS was 5.7 ± 2.1 versus 4.4 ± 2.4 (P = 0.02), and peak CK-MBm 141 ± 157 versus 156 ± 167 µg/L (P = 0.78) in the recovery versus nonrecovery group. At follow-up, DFS was 1.9 ± 1.7 versus 6.5 ± 2.6 (P < 0.001). The best ECG variable to predict decrease in DFS depended on the region of acute LV dysfunction: The best variable in the left anterior descending region was the integral of the first QRS integral (area under the curve [AUC] 0.82, P = 0.002); in the right coronary artery region, this was the integral of the ST segment (AUC 0.98, P = 0.003); and in the left circumflex region, the area including the ST segment and the T wave (AUC 0.97, P = 0.006). CONCLUSIONS: In ACS patients, computed ECG variables predict recovery of LV function from ischemic myocardial injury, even in the presence of comparable CK-MBm release and LV dysfunction.

Optogenetic dephosphorylation of phosphatidylinositol 4,5 bisphosphate in Xenopus laevis oocytes.

Here, we present a protocol for optogenetic dephosphorylation of the phosphoinositide PI(4,5)P2 at the plasma membrane of Xenopus laevis oocytes. We first describe the co-injection of oocytes with cRNAs encoding (1) a light-activated PI(4,5)P2 5-phosphatase fusion protein, (2) its dimerization partner fused to the plasma membrane, and (3) the potassium channel reporter for PI(4,5)P2 dephosphorylation. We then detail blue light illumination to induce PI(4,5)P2 dephosphorylation, combined with simultaneous two-electrode voltage clamp electrophysiological recording to assess potassium channel current responses. For complete details on the use and execution of this protocol, please refer to Xu et al. (2022).1.

T-wave morphology after epinephrine bolus may reveal silent long QT syndrome mutation carriers.

BACKGROUND: Long QT syndrome (LQTS) gene mutation carriers with indeterminate electrocardiogram frequently escape clinical diagnosis. We assessed the use of epinephrine bolus injection in revealing T-wave abnormalities. METHODS: We recruited 30 genotyped asymptomatic LQTS gene carriers with nondiagnostic QT interval and 15 controls. Electrocardiogram was recorded with body surface potential mapping after an intravenous epinephrine bolus. T-wave morphology was determined as normal, biphasic, inverted, bifid, or combined pattern. RESULTS: Long QT syndrome carriers and healthy controls had different T-wave profiles (P = .027). Of controls, 12 (80%) of 15 had no change or biphasic appearance, whereas only 10 (33%) of 30 of LQTS carriers had so. Bifid or combined pattern occurred in 15 (50%) of 30 in LQTS and in 6 (60%) of 10 in the LQT3 subgroup but only in 1 (7%) of 15 of healthy. CONCLUSIONS: Modification of ventricular repolarization with low-dose epinephrine injection helps to distinguish silent LQTS mutation carriers. This concerns also the LQT3 subtype, which may escape tests.

Effects of ß-blockers on ventricular repolarization documented by 24-hour electrocardiography in long QT syndrome type 2.

BACKGROUND: Long QT syndrome (LQTS) is an inherited arrhythmia disorder characterized by ventricular repolarization abnormalities and a risk of sudden cardiac death. The electrophysiological components generating the high risk of arrhythmias in LQTS are prolonged repolarization, increased dispersion of repolarization, and early afterdepolarizations, which are clinically estimated as QT interval, T-wave peak to T-wave end (TPE) interval, and T2/T1-wave amplitude ratio, respectively. In experimental LQTS type 2 (LQT2) models, ß-blockers decrease dispersion of repolarization and prevent early afterdepolarizations. In clinical studies in patients with LQT2 , ß-blockers are more effective against exercise-induced than arousal-induced cardiac events. OBJECTIVES: The aim of the study was to investigate the effects of ß-blocker therapy on repolarization properties in LQT2. METHODS: QT and TPE intervals and maximal T2/T1-wave amplitude ratios recorded by 24-hour electrocardiograms before and during ß-blocker therapy were evaluated in 25 patients with LQT2. RESULTS: ß-Blocker therapy decreased the maximal T2/T1-wave amplitude ratio from 2.9 ± 1.1 to 1.8 ± 0.7 (P < .001), but did not change the pause-induced T2/T1-wave amplitude ratio. Under medication, abrupt maximal TPE intervals were shorter at heart rates of ≥75 beats/min and maximal QT intervals were shorter at a heart rate of 100 beats/min. CONCLUSION: ß-Blockers stabilize ventricular repolarization in LQT2 by reducing electrocardiographic early afterdepolarizations and by reducing abrupt prolongation of electrocardiographic dispersion of repolarization and ventricular repolarization duration at elevated heart rates. The effect of ß-blockers on pause-induced electrocardiographic early afterdepolarizations is weak. The findings provide electrocardiographic explanation for the protective effects of ß-blockers against exercise-induced cardiac events in LQT2.

Epinephrine bolus test in detecting long QT syndrome mutation carriers with indeterminable electrocardiographic phenotype.

BACKGROUND: In long QT syndrome (LQTS), prolonged and heterogeneous ventricular repolarization predisposes to serious arrhythmias. We examined how QT intervals are modified by epinephrine bolus in mutation carriers of three major LQTS subtypes with indefinite QT interval. METHODS: Genotyped, asymptomatic subjects with LQTS type 1 (LQT1; n = 10; four different KCNQ1 mutations), type 2 (LQT2; n = 10; three different HERG mutations), and type 3 (LQT3; n = 10; four different SCN5A mutations), and healthy volunteers (n = 15) were examined. Electrocardiogram was recorded with body surface potential mapping system. After an epinephrine 0.04 µg/kg bolus QT end, QT apex, and T-wave peak-to-end (Tpe) intervals were determined automatically as average of 12 precordial leads. Standard deviation (SD) of the 12 channels was calculated. RESULTS: Heart rate increased 26 ± 10 bpm with epinephrine bolus, and similarly in all groups. QT end interval lengthened, and QT apex interval shortened in LQTS and normals, leading to lengthening of Tpe interval. However, the lengthening in Tpe was larger in LQTS than in normals (mean 32 vs 18 ms; P < 0.05) and SD of QT apex increased more in LQTS than in normals (mean 23 vs 7 ms; P < 0.01). The increase in Tpe was most pronounced in LQT2, and in SD of QT apex in LQT1 and LQT2. CONCLUSIONS: Abrupt adrenergic stimulation with a moderate dose of exogenous epinephrine affects ventricular repolarization in genotype-specific fashion facilitating distinction from normals. This delicate modification may help in diagnosing electrocardiographically silent mutation carriers when screening LQTS family members.

Abnormal repolarization dynamics revealed in exercise test in long QT syndrome mutation carriers with normal resting QT interval.

AIMS: The identification of affected family members with long QT syndrome (LQTS) is often difficult due to their normal-or only marginally lengthened-QT interval duration. We examined whether physical exercise test could increase the ability to detect the mutation carrier status in phenotypically normal LQTS family members. METHODS AND RESULTS: Sixty-six subjects were included: 15 were carriers of KCNQ1 (LQT1); 15 of KCNH(2) (LQT2); and 9 of SCN5A (LQT3) gene mutations with no, or borderline, QT lengthening; and 27 were healthy controls. Multiple electrograms over the precordial area were recorded during workload and recovery phases of exercise test. QT intervals and T peak to T end intervals (Tpe intervals) were determined using an automatic algorithm at specified heart rates (HR).The LQT1 mutation carriers had QT interval most prolonged during exercise and recovery, whereas the LQT2 carriers had QT interval longest at low exercise HR. The LQT3 carriers had QT interval longest at rest. The Tpe interval remained nearly unchanged during exercise in LQT1, but shortened in LQT2 and in LQT3 carriers. The Tpe interval was longest in LQT2 carriers at the end of the recovery phase. Tentative dichotomizing values of QT and Tpe intervals improved sensitivity and specificity in distinguishing LQTS subtypes, compared with the QT interval duration alone. CONCLUSIONS: LQTS mutation carriers lacking diagnostic QT interval prolongation exhibit abnormal QT and Tpe interval adaptations during physical exercise test. Looking for subtype-specific adaptations might facilitate the identification of LQTS mutation carriers when molecular genetic analysis is not available.

Dynamic QT/RR relationship in post-myocardial infarction patients with and without cardiac arrest.

OBJECTIVES: Changes in QT interval dynamicity may be associated with susceptibility to ventricular fibrillation (VF) after myocardial infarction (MI). We tested the hypothesis that dynamic QT/RR relationship might differ between post-MI patients with and without a history of VF. We also evaluated the influence of negative T-waves on the assessment of QT/RR relationship. DESIGN: We reviewed Holter recordings from 37 post-MI patients resuscitated from VF not associated with new MI (VF group) and 30 patients after MI without known sustained ventricular arrhythmias (control group). With an automated computerized program, we measured QT interval dynamicity as the mean QT/RR slope and as the maximal QT/RR slope determined at stable heart rates. RESULTS: The mean QT/RR slope was 0.20 ± 0.08 in control group and 0.15 ± 0.09 in VF group (p=0.01) whereas corresponding maximal QT/RR slope values were 0.42 ± 0.20 and 0.33 ± 0.18 (p=0.01), respectively. Thirteen control patients (43%) and 22 VF patients (59%) showed only negative or both positive and negative T-waves (p=0.45). Mean QT/RR slope values were similar irrespective of T-wave polarity whereas maximal QT/RR slopes were steeper in cases with both positive and negative T-waves. Cases showing T-waves of both positive and negative polarity exhibited greatest intersubject variability of both QT/RR slope values. CONCLUSIONS: Lower mean QT/RR slope may be associated with a risk of VF after MI. A detailed assessment and definition of differing T-wave polarities is essential in evaluating the QT/RR relation in post-MI patients.

Fragmented QRS in prediction of cardiac deaths and heart failure hospitalizations after myocardial infarction.

BACKGROUND: Increased QRS fragmentation in visual inspection of 12-lead ECG has shown association with cardiac events in postmyocardial infarction (MI) patients. We investigated user-independent computerized intra-QRS fragmentation analysis in prediction of cardiac deaths and heart failure (HF) hospitalizations after MI. METHODS: Patients (n = 158) with recent MI and reduced left ventricular ejection fraction (LVEF) were studied. A 120-lead body surface potential mapping was performed at hospital discharge. Intra-QRS fragmentation was computed as the number of extrema (fragmentation index FI) in QRS. QRS duration (QRSd) was computed for comparison. RESULTS: During a mean follow-up of 50 months 15 patients suffered cardiac death and 23 were hospitalized for HF. Using the mean + 1 SD as cut-point both parameters were univariate predictors of both end-points. In multivariate analysis including age, gender, LVEF, previous MI, bundle branch block, atrial fibrillation, and diabetes FI was an independent predictor for cardiac deaths (HR 8.7, CI 3.0-25.6) and HF hospitalizations (HR 3.8, CI 1.6-9.3) whereas QRSd only predicted HF hospitalizations (HR 4.6, CI 2.0-10.7). In comparison to QRSd, FI showed better positive (PPA) and equal negative (NPA) predictive accuracy for both end-points, and PPA was further improved when combined to LVEF < 40%. Limiting fragmentation analysis to 12-lead ECG or a randomly selected 8-lead set instead of all 120 leads resulted in an almost similar prediction. CONCLUSIONS: Increased QRS fragmentation in post-MI patients predicts cardiac deaths and HF progression. A computer-based fragmentation analysis is a stronger predictor than QRSd.

Primary cilia of human endothelial cells disassemble under laminar shear stress.

We identified primary cilia and centrosomes in cultured human umbilical vein endothelial cells (HUVEC) by antibodies to acetyl-alpha-tubulin and capillary morphogenesis gene-1 product (CMG-1), a human homologue of the intraflagellar transport (IFT) protein IFT-71 in Chlamydomonas. CMG-1 was present in particles along primary cilia of HUVEC at interphase and around the oldest basal body/centriole at interphase and mitosis. To study the response of primary cilia and centrosomes to mechanical stimuli, we exposed cultured HUVEC to laminar shear stress (LSS). Under LSS, all primary cilia disassembled, and centrosomes were deprived of CMG-1. We conclude that the exposure to LSS ends the IFT in cultured endothelial cells.

Complex T-wave morphology in body surface potential mapping in prediction of arrhythmic events in patients with acute myocardial infarction and cardiac dysfunction.

AIMS: Heterogeneous ventricular repolarization is associated with sudden cardiac death after myocardial infarction (MI). This prospective study investigated repolarization disparity with parameters based on T-wave morphology in body surface potential mapping (BSPM) in the assessment of arrhythmia risk in patients with a recent MI and cardiac dysfunction. METHODS AND RESULTS: Patients (n = 158) had 120-lead BSPM and 12-lead electrocardiogram (ECG) registered soon after acute MI. Principal component analysis (PCA) of the T-wave and T-wave vector loop descriptors were applied to compute parameters describing T-wave morphology and its variation. The study endpoints were arrhythmic events and all-cause mortality. During a mean follow-up of 50 months, 30 patients (19%) died and 16 (10%) had an arrhythmic event. Most of the parameters differed significantly between patients with and without arrhythmic events. In univariate analysis, T-wave vector loop length (TLL) and PCA parameter PCA(3) in BSPM and TLL in ECG were significant predictors of arrhythmic events. In multivariate analysis including several clinical variables, these parameters also showed an independent prediction, with parameters in BSPM performing somewhat better. None of the parameters predicted all-cause mortality. CONCLUSION: Complex T-wave morphology in BSPM is a marker of arrhythmia propensity in patients with a recent MI and cardiac dysfunction.

Non-invasive detection of conduction pathways to left atrium using magnetocardiography: validation by intra-cardiac electroanatomic mapping.

AIMS: Alteration in conduction from right to left atrium (LA) is linked to susceptibility to atrial fibrillation (AF). We examined whether different inter-atrial conduction pathways can be identified non-invasively by magnetocardiographic mapping (MCG). METHODS AND RESULTS: In 27 patients undergoing catheter ablation of paroxysmal AF, LA activation sequence was determined during sinus rhythm using invasive electroanatomic mapping. Before this, 99-channel magnetocardiography was recorded over anterior chest. The orientation of the magnetic fields during the early (40-70 ms from P onset) and later part (last 50%) of LA depolarization was determined using pseudocurrent conversion. Breakthrough of electrical activation to LA occurred through Bachmann bundle (BB) in 14, margin of fossa ovalis (FO) in 3, coronary sinus ostial region (CS) in 2, and their combinations in 10 cases by invasive reference in total of 29 different P-waves. Based on the combination of pseudocurrent angles over early and late parts of LA activation, the MCG maps were divided to three types. These types correctly identified the LA breakthrough sites to BB, CS, FO, or their combinations in 27 of 29 (93%) cases. CONCLUSION: Magnetocardiographic mapping seems capable of distinguishing inter-atrial conduction pathways. Recognizing the inter-atrial conduction pattern may assist in understanding the pathogenesis of AF and identifying the subgroups for patient-tailored therapy.

Reversal of atrial remodeling after cardioversion of persistent atrial fibrillation measured with magnetocardiography.

BACKGROUND: Atrial fibrillation (AF) causes electrical, functional, and structural changes in the atria. We examined electrophysiologic remodeling caused by AF and its reversal noninvasively by applying a new atrial signal analysis based on magnetocardiography (MCG). METHODS: In 26 patients with persistent AF, MCG, signal-averaged electrocardiography (SAECG), and echocardiography were performed immediately after electrical cardioversion (CV), and repeated after 1 month in 15 patients who remained in sinus rhythm (SR). Twenty-four matched subjects without history of AF served as controls. P-wave duration (Pd) and dispersion (standard deviation of Pd values in individual channels) and root mean square amplitudes of the P wave over the last 40 ms portions (RMS40) were determined. RESULTS: In MCG Pd was longer (122.8 +/- 18.2 ms vs 101.5 +/- 14.6 ms, P < 0.01) and RMS40 was higher (60.4 +/- 28.2 vs 46.9 +/- 19.1 fT) in AF patients immediately after CV as compared to the controls. In SAECG Pd dispersion was increased in AF patients. Mitral A-wave velocity and left atrial (LA) contraction were decreased and LA diameter was increased (all P < 0.01). After 1 month, Pd in MCG still remained longer and LA diameter greater (both P < 0.05), while RMS40 in MCG, Pd dispersion in SAECG, mitral A-wave velocity, and LA contraction were recovered. CONCLUSIONS: Magnetocardiographically detected atrial electrophysiologic alterations in persistent AF diminish rapidly although incompletely during maintained SR after CV. This might be related to the known early high and late lower, but still existent tendency to AF relapses.

Single-lead electrocardiographic variables in the detection of prior myocardial infarction with respect to Q-wave status and infarct age.

OBJECTIVES: Conventionally, the detection of prior myocardial infarction (MI) is based on QRS abnormalities, which may ignore non-Q-wave MI (NQMI). We aimed at finding automatically applicable quantitative ECG variables for diagnosing prior MI. METHODS: Body surface potential mapping (BSPM) was registered and automatically analyzed in 144 patients with prior MI and in 75 healthy controls. The MI was defined according to its age as recent or old, and Q-wave status as Q-wave MI (QMI) or NQMI. RESULTS: The QRSSTT integral, the STT integral and the T-wave apex amplitude applied in single, selected leads were found to be the optimal parameters in the detection of prior MI. The areas under the receiver-operating characteristic curves (AUC) were 89% for each, and detection was equal in old and recent MI (AUCs from 87 to 90%), and in QMI and NQMI (AUCs from 88 to 90%). CONCLUSIONS: The quantitative, automatically applicable single-lead variables comprising ventricular repolarization was effective in detecting prior MI, irrespective of the time elapsed from MI or the Q-wave status. These variables could be suitable for population studies and health screening purposes and are applicable to automatic ECG diagnostics of prior MI.