This non-technical review introduces key concepts in personalized ECG monitoring (pECG), which aims to optimize the detection of clinical events and their warning signs as well as the selection of ...alarm thresholds. We review several pECG methods, including anomaly detection and adaptive machine learning (ML), in which learning is performed sequentially as new data are collected. We describe a distributed-network multiscale pECG system to show how the computational load and time associated with adaptive ML could be optimized. In this architecture, the limited analysis of ECG waveforms is performed locally (e.g., on a smart phone) to determine a small number of clinically important ECG elements, and an adaptive ML engine is located on a remote server (Internet cloud) to determine an individual's "fingerprint" basis patterns and to detect anomalies in those patterns.
Objectives This study sought to determine whether T-wave alternans (TWA) induced by anger in a laboratory setting predicts future ventricular arrhythmias in patients with implantable ...cardioverter-defibrillators (ICDs). Background Anger can precipitate spontaneous ventricular tachycardia/ventricular fibrillation and induce TWA. Whether anger-induced TWA predicts future arrhythmias is unknown. Methods Sixty-two patients with ICDs underwent ambulatory electrocardiography during a mental stress protocol, 3 months after the ICD was implanted. T-wave alternans was analyzed using time-domain methods. After a ≥1 year follow-up, ICD stored data was reviewed to determine incidence of ICD-terminated ventricular tachycardia/ventricular fibrillation. Results Patients with ICD-terminated arrhythmias during follow-up (n = 10) had higher TWA induced by anger, 13.2 μV (interquartile range IQR 9.3 to 16 μV), compared with those patients without future ventricular arrhythmias, 9.3 μV (IQR 7.5 to 11.5 μV, p < 0.01). Patients in the highest quartile of anger-induced TWA (>11.9 μV, n = 15) were more likely to experience arrhythmias by 1 year than those in the lower quartiles (33% vs. 4%) and during extended follow-up (40% vs. 9%, p < 0.01 for both). In multivariable regression controlling for ejection fraction, prior clinical arrhythmia, and wide QRS, anger-induced TWA remained a significant predictor of arrhythmia, with likelihood in the top quartile 10.8 times that of other patients (95% confidence interval: 1.6 to 113, p < 0.05). Conclusions Anger-induced TWA predicts future ventricular arrhythmias in patients with ICDs, suggesting that emotion-induced repolarization instability may be 1 mechanism linking stress and sudden death. Whether there is a clinical role for anger-induced TWA testing requires further study.
Rapid application of external defibrillation, a crucial first-line therapy for ventricular fibrillation and cardiac arrest, is currently unavailable in the setting of magnetic resonance imaging ...(MRI), raising concerns about patient safety during MRI tests and MRI-guided procedures, particularly in patients with cardiovascular diseases. The objective of this study was to examine the feasibility and safety of defibrillation/pacing for the entire range of clinically useful shock energies inside the MRI bore and during scans, using defibrillation/pacing outside the magnet as a control.
Experiments were conducted using a commercial defibrillator (LIFEPAK 20, Physio-Control, Redmond, Washington, USA) with a custom high-voltage, twisted-pair cable with two mounted resonant floating radiofrequency traps to reduce emission from the defibrillator and the MRI scanner. A total of 18 high-energy (200-360 J) defibrillation experiments were conducted in six swine on a 1.5 T MRI scanner outside the magnet bore, inside the bore, and during scanning, using adult and pediatric defibrillation pads. Defibrillation was followed by cardiac pacing (with capture) in a subset of two animals. Monitored signals included: high-fidelity temperature (0.01 °C, 10 samples/sec) under the pads and 12-lead electrocardiogram (ECG) using an MRI-compatible ECG system.
Defibrillation/pacing was successful in all experiments. Temperature was higher during defibrillation inside the bore and during scanning compared with outside the bore, but the differences were small (ΔT: 0.5 and 0.7 °C, p = 0.01 and 0.04, respectively). During scans, temperature after defibrillation tended to be higher for pediatric vs. adult pads (p = 0.08). MR-image quality (signal-to-noise ratio) decreased by ~ 10% when the defibrillator was turned on.
Our study demonstrates the feasibility and safety of in-bore defibrillation for the full range of defibrillation energies used in clinical practice, as well as of transcutaneous cardiac pacing inside the MRI bore. Methods for Improving MR-image quality in the presence of a working defibrillator require further study.
Abstract Current guidelines recommend early reperfusion therapy for ST-elevation myocardial infarction (STEMI) within 90 min of first medical encounter. Telecardiology entails the use of advanced ...communication technologies to transmit the prehospital 12-lead electrocardiogram (ECG) to offsite cardiologists for early triage to the cath lab; which has been shown to dramatically reduce door-to-balloon time and total mortality. However, hospitals often find adopting ECG transmission technologies very challenging. The current review identifies seven major technical challenges of prehospital ECG transmission, including: paramedics inconvenience and transport delay; signal noise and interpretation errors; equipment malfunction and transmission failure; reliability of mobile phone networks; lack of compliance with the standards of digital ECG formats; poor integration with electronic medical records; and costly hardware and software pre-requisite installation. Current and potential solutions to address each of these technical challenges are discussed in details and include: automated ECG transmission protocols; annotatable waveform-based ECGs; optimal routing solutions; and the use of cloud computing systems rather than vendor-specific processing stations. Nevertheless, strategies to monitor transmission effectiveness and patient outcomes are essential to sustain initial gains of implementing ECG transmission technologies.
QT interval correction formulas are based on instantaneous heart rate (HR), but QT interval adaptation to sudden HR change occurs gradually. In humans, the QT interval has been reported to reach a ...new steady-state value in about 2 minutes.
This study sought to assess β-adrenergic stimulation effects on QT interval response to HR change.
Ten subjects (42.1 ± 15.3 years, 3 men) undergoing radiofrequency ablation of supraventricular tachycardia were studied. Atrial pacing for 5 minutes at an HR ranging from 60 to 140 beats/min was performed before and during dobutamine infusion (10 μg/kg/min). The QT response to sudden HR change was evaluated.
The QT response to sudden HR change consists of an immediate response (IR), followed by a gradual monoexponential course to the new steady-state value. Linear function results in inferior fit of QT adaptation course (P < .05 compared with exponential). The time constant of the exponential is approximately 1 minute (50.9 ± 11.4 seconds). The IR magnitude is approximately 3% of the RR interval change (2.97% ± 2.01%). Dobutamine shortens steady-state QT at given HR (from 301.8 ± 11.2 ms to 290.6 ± 13.2 ms at 120 beats/min; P < .001) and increases IR magnitude (to 13.28% ± 8.99% of RR change; P < .01). During sinus rhythm, QT variability and QT variability index were significantly increased by dobutamine.
QT adaptation has 2 distinct phases, which might have different mechanisms. The effect of β-adrenergic stimulation on IR may increase QT variability by increasing the immediate response to HR variability. These results may be important in the assessment of drug effects on repolarization and for understanding of QT variability.
Abstract only Studies have shown a higher risk of adverse outcomes after cardiac surgery in patients with reduced complexity of arterial-pressure dynamics (APD). We hypothesized that this effect is ...caused by age-related loss of vascular smooth-muscle activity (VSMA). This hypothesis was tested using data from 30 humans and a validated, large-scale theoretical model of circulation with VSMA blocked (T-model). The results were also verified in a realistic physical model of circulation (P-model, Fig.1). Methods: ECG and APD data were recorded using a high-fidelity system (APEX, PinMed, Inc.) during moderate physical activity (handgrip followed by leg lifts) in 30 subjects (age: 46±10y, 53% female; pressure ranges for systolic, diastolic, and mean: 90-210, 49-116, and 67-147mm, respectively). Results: T-model accurately predicted APD in older subjects ≥48y (n=13, r 2 =0.74; Fig.2); this effect was preserved in both females and males, but not in younger subjects (n=17, r 2 =0.13). The difference between the older and younger subjects was pronounced (40%) and significant (p=0.01, F-test). In P-model, changes in cardiac force produced changes in central arterial pressure that were in excellent agreement with those observed in humans ≥48y (r 2 =0.93, Fig.3). Conclusions: Loss of VSMA during physical activity could serve as an important prognostic/diagnostic indicator of cardiovascular aging and disease.
Increased variability of QT interval (QTV) has been linked to arrhythmias in animal experiments and multiple clinical situations. Congenital long QT syndrome (LQTS), a pure repolarization disease, ...may provide important information on the relationship between delayed repolarization and QTV.
Twenty-four-hour Holter monitor tracings from 78 genotyped congenital LQTS patients (52 females; 51 LQT1, 23 LQT2, 2 LQT5, 2 JLN, 27 symptomatic; age, 35.2±12.3 years) were evaluated with computer-assisted annotation of RR and QT intervals. Several models of RR-QT relationship were tested in all patients. A model assuming exponential decrease of past RR interval contributions to QT duration with 60-second time constant provided the best data fit. This model was used to calculate QTc and residual "intrinsic" QTV, which cannot be explained by heart rate change. The intrinsic QTV was higher in patients with long QTc (r=0.68; P<10(-4)), and in LQT2 than in LQT1/5 patients (5.65±1.28 vs 4.46±0.82; P<0.0002). Both QTc and intrinsic QTV were similar in symptomatic and asymptomatic patients (467±52 vs 459±53 ms and 5.10±1.19 vs 4.74±1.09, respectively).
In LQTS patients, QT interval adaptation to heart rate changes occurs with time constant ≈60 seconds, similar to results reported in control subjects. Intrinsic QTV correlates with the degree of repolarization delay and might reflect action potential instability observed in animal models of LQTS.
Abstract Unstable (cyclical alternating pattern, or CAP) sleep is associated with surges of sympathetic nervous system activity, increased blood pressure and vasoconstriction, heightened baroreflex ...sensitivity, and unstable heart rhythm and breathing. In susceptible persons, CAP sleep provokes clinically significant events, including hypertensive crises, sleep-disordered breathing, and cardiac arrhythmias. Here we explore the neurophysiology of CAP sleep and its impact on cardiovascular and respiratory functions. We show that: (i) an increase in neurophysiological recovery rate can explain the emergence of slow, self-sustained, hypersynchronized A1 CAP-sleep pattern and its transition to the faster A2-A3 CAP-sleep patterns; (ii) in a two-dimensional, continuous model of cardiac tissue with heterogeneous action potential duration (APD) distribution, heart rate accelerations during CAP sleep may encounter incompletely recovered electrical excitability in cell clusters with longer APD. If the interaction between short cycle length and incomplete, spatially heterogeneous repolarization persists over multiple cycles, irregularities and asymmetry of depolarization front may accumulate and ultimately lead to a conduction block, retrograde conduction, breakup of activation waves, reentrant activity, and arrhythmias; and (iii) these modeling results are consistent with the nighttime data obtained from patients with structural heart disease (N = 13) that show clusters of atrial and ventricular premature beats occurring during the periods of unstable heart rhythm and respiration that accompany CAP sleep. In these patients, CAP sleep is also accompanied by delayed adaptation of QT intervals and T-wave alternans.
Introduction: Psychological stress can precipitate ventricular arrhythmias in patients with ICDs, as well as sudden death. However, the physiologic pathways remain unknown. We sought to determine ...whether psychological stress induced in the laboratory setting alters indices of repolarization associated with arrhythmogenesis.
Methods and Results: Patients with ICDs and a history of ventricular arrhythmia underwent ambulatory ECG monitoring during a laboratory mental stress protocol (anger recall and mental arithmetic). Continuous changes in repolarization indices which have correlated with temporal and spatial myocardial heterogeneity of repolarization, including T‐wave alternans (TWA), T‐wave amplitude (Tamp), and T‐wave area (Tarea) were analyzed in the time domain. In the 33 patients (85% male, 88% with coronary artery disease, mean ejection fraction 30%), norepinephrine, epinephrine, BP, and HR increased during mental stress. TWA increased from 22 (interquartile range 16–27) at baseline to 29 (21–38) uV during mental stress (P < 0.001). Changes in TWA correlated with changes in HR, systolic BP, and catecholamines. Tamp and Tarea also increased with mental stress (P < 0.01) but did not correlate with changes in other variables.
Conclusion: Psychological stress increased TWA, Tamp, and Tarea. Autonomically mediated repolarization changes may be a pathophysiologic link between emotion and arrhythmia in susceptible patients.
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