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Résumé: Contexte: La mise en place de la sonde ventriculaire gauche dans une zone exempte de cicatrice myocardique est un facteur déterminant de la réponse au traitement de resynchronisation cardiaque. Nous avons cherché à développer et à valider une approche électrocardiographique (ECG) simple, concrète et novatrice afin de repérer de manière peropératoire la présence de tissu cicatriciel au ventricule gauche (VG). Nous avons émis l'hypothèse qu'il y aurait une diminution de l'amplitude du rythme de stimulation du ventricule gauche mesurée à la surface de la peau à l'ECG haute résolution (HR) lors de la stimulation de régions du VG présentant du tissu cicatriciel comparativement aux régions exemptes de cicatrices. Il s'agit de ce que nous appelons la méthode EASE (ECG Amplitude Signal Evaluation). Méthodologie: Des patients vus de manière consécutive qui présentaient une dysfonction systolique ischémique du VG et répondaient aux critères standard pour l'implantation de novo d'un dispositif de resynchronisation cardiaque ont été recrutés de manière prospective. Tous ont fait l'objet d'une résonance magnétique cardiaque améliorée par injection d'un produit de contraste avant l'implantation pour évaluer la présence de tissu cicatriciel. L'amplitude moyenne de l'impulsion de stimulation du VG a été échantillonnée sur l'ECG de surface HR réalisé pendant l'intervention, puis comparée aux résultats de la résonance magnétique cardiaque. Résultats: En tout, 38 points de stimulation du VG ont été évalués chez 13 receveurs. Le voltage médian mesuré sur l'ECG de surface HR dans les régions présentant du tissu cicatriciel était réduit de 41 % (intervalle interquartile : 17 % à 63 %), tandis qu'il n'y avait pas de changement mesurable du voltage (intervalle interquartile : 0 à 0 %) dans les régions exemptes de cicatrices par rapport à l'amplitude maximale (test de Wilcoxon, p < 0,0001). Conclusion: La méthode EASE semble avoir une utilité potentielle en tant que nouvel outil peropératoire pour guider la mise en place de la sonde ventriculaire gauche dans les régions exemptes de cicatrices. Il faudra réaliser d'autres travaux pour valider l'utilité de cette méthode dans une cohorte de patients plus importante. Abstract: Background: The placement of the left ventricular (LV) lead in an area free of myocardial scar is an important determinant of cardiac resynchronization therapy response. We sought to develop and validate a simple, practical, and novel electrocardiographic (ECG)-based approach to intraoperatively identify the presence of LV scar. We hypothesized that there would be a reduction in the measured amplitude of the LV pacing stimulus on the skin surface using a high-resolution (HR) ECG when pacing from LV regions with scar compared with regions without scar. We term this the ECG Amplitude Signal Evaluation (EASE) method. Methods: Consecutive patients with ischemic LV systolic dysfunction and standard criteria for de novo cardiac resynchronization therapy implantation were prospectively enrolled. All underwent a preimplant contrast-enhanced cardiac magnetic resonance study to assess for scar. The average amplitude of the LV pacing impulse was sampled on HR surface ECG intraprocedurally and then compared with the cardiac magnetic resonance results. Results: A total of 38 LV pacing sites were assessed among 13 recipients. The median voltage measured on the surface HR ECG in regions with scar was reduced by 41% (interquartile range, 17% to 63%), whereas there was no measurable change in voltage (interquartile range, 0 to 0%) in regions without scar compared with the maximal amplitude (Wilcoxon P < 0.0001). Conclusion: The EASE method appears to be of potential value as a novel intraoperative tool to guide LV lead placement to regions free of scar. Future work is required to validate the utility of this method in a larger patient cohort.

Key Points Question What proportion of patients with left ventricular dysfunction identified during hospitalization for acute myocardial infarction have follow-up assessment of left ventricular ejection fraction (LVEF)? Findings In this cohort study of 501 patients, 303 patients had undergone LVEF reassessment by 6 months, with significant variability according to patient-level and site-level characteristics. Meaning These findings suggest that programs to improve the quality of post–myocardial infarction care should include measures to ensure that indicated repeat cardiac imaging is performed., This cohort study assesses adherence with guideline-recommended left ventricular ejection fraction (LVEF) reassessment after myocardial infarction and studies the evolution of LVEF over 6 months of follow-up in the Acute Myocardial Infarction Quality Assurance (AMIQA) Canada study., Importance Persistently depressed left ventricular ejection fraction (LVEF) after myocardial infarction (MI) is associated with adverse prognosis and directs the use of evidence-based treatments to prevent sudden cardiac death and/or progressive heart failure. Objective To assess adherence with guideline-recommended LVEF reassessment and to study the evolution of LVEF over 6 months of follow-up. Design, Setting, and Participants This was a multicenter cohort study at Canadian academic and community hospitals with on-site cardiac catheterization services. Patients with type 1 acute MI and LVEF less than or equal to 45% during the index hospitalization were enrolled between January 2018 and August 2019 and were followed-up for 6 months. Data analysis was performed from May 2020 to September 2021. Exposures Baseline clinical factors, in-hospital care and LVEF, and site-specific features. Main Outcomes and Measures The main outcomes were receipt of repeat LVEF assessment by 6 months and the presence of a persistent LVEF reduction at 2 thresholds: LVEF less than or equal to 40%, prompting consideration of additional medical therapy for heart failure, or LVEF less than or equal to 35%, prompting referral for implanted cardioverter defibrillator in addition to medical therapy. Results This study included 501 patients (mean [SD] age, 63.3 [13.0] years; 113 women [22.6%]). Overall, 370 patients (73.4%) presented with STEMI, and 454 (90.6%) had in-hospital revascularization. The median (IQR) baseline LVEF was 40% (34%-43%). Of 458 patients (91.4%) who completed the 6-month follow-up, 303 (66.2%; 95% CI, 61.7%-70.5%) had LVEF reassessment, with a range of 46.7% to 90.0% across sites (χ213 = 19.6; P = .11). Participants from community hospitals were more likely than those from academic hospitals to undergo LVEF reassessment (73.6% vs 63.2%; χ21 = 4.50; P = .03), as were those with worse LVEF at baseline. Follow-up LVEF improved by an absolute median (IQR) of 8% (3%-15%). However, 103 patients (34.1%) met the definitions of clinically relevant LVEF reduction, including 52 patients (17.2%) with LVEF less than or equal to 35% and 51 patients (16.9%) with LVEF of 35.1% to 40.0%. Conclusions and Relevance In this cohort study, approximately 1 in 3 patients with at least mild LVEF reduction after acute MI did not undergo indicated LVEF reassessment within 6 months, suggesting that programs to improve the quality of post-MI care should include measures to ensure that indicated repeat cardiac imaging is performed. In those with follow-up imaging, clinically relevant persistent LVEF reduction was identified in more than one-third of patients.

Introduction: Persistently reduced LVEF after acute MI predicts adverse prognosis and directs use of evidence-based treatments to prevent sudden death (SCD) and/or progressive heart failure. We conducted a multicentre, prospective, observational study to assess adherence with guideline recommendations to repeat imaging assessment post-MI in those with initially depressed LVEF. Methods: We enrolled 501 patients with type 1 acute MI and LVEF ≤45% during the index hospitalization, from 14 Canadian sites. Outcomes were the proportion having a repeat LVEF assessment by 6 months and the proportion with an actionable reduced LVEF in follow-up: Results: Mean age was 63.3 ± 13.0, and 113 (22.6%) were female. Overall, 370 (73.4%) presented with STEMI, and 454 (91.6%) had one or more in-hospital revascularization procedures. The mean baseline LVEF was 36.9% ± 6.7%. Over a median follow-up of 198 days, 18 (3.6%) patients died and 27 (5.3%) were lost to follow-up. Of 456 remaining patients, 303 (66.5%) had LVEF reassessment and significant variation was observed across sites (range 46.7-90.0%; p=0.035). Patients from community vs academic hospitals were more likely to undergo LVEF reassessment (73.6% vs. 63.2%, p=0.034), as were those with worse LVEF at baseline ( Figure, panel A ). In those with follow-up LVEF (n=302), 61.6% had an actionable persistent LVEF reduction: 13.9% had LVEF Figure, Panel B ). Conclusions: One in three patients with at least mild LVEF reduction after acute MI did not undergo indicated LVEF reassessment within 6 months. In those with follow-up imaging, clinically actionable persistent LVEF reduction was identified in over one quarter of patients.

Left ventricular (LV) dysfunction may be sustained or aggravated during the convalescent months following an acute myocardial infarction (MI) and is difficult to predict. We sought to determine current practice patterns of LV ejection fraction (LVEF) reassessment during the months following MI and evaluate the predictors and clinical significance of LVEF change in a prospective post-MI patient cohort.Patients with an acute MI between June 2010 and August 2014 were identified using the Alberta Provincial Project for Outcome Assessment in Coronary Heart Disease registry. Patients with initial LV dysfunction (LVEF40% with first MI or45% with multiple MI events) underwent a protocol-driven repeat LVEF assessment in follow-up if routine LVEF reassessment was not performed.Of 5,964 MI patients, follow-up LVEF assessments were attained for 442 of the 695 patients who had significant LV dysfunction. A sizable proportion (25%) had either no increase or a decline in LVEF. Adverse remodeling was associated with an anterior MI location, a greater peak serum troponin T, and a higher baseline LVEF at time of MI. Adverse LV remodeling conferred a 3-fold risk of death (hazard ratio 3.0, 95% CI 1.6-5.7, P=.001) adjusted for baseline LVEF, anterior MI location, and medication use.Current practice of LVEF reassessment during the convalescent months post-MI is suboptimal despite a sizeable proportion of patients that undergo adverse LV remodeling. Targeting processes affecting low rates of LVEF reassessment may reduce missed care opportunities and ensure that patients consistently receive appropriate evidence-based and guideline-recommended care.

Background Anti-platelet therapy is commonly used in patients receiving oral anticoagulation and may increase bleeding risk among patients undergoing cardiac implantable electronic device (CIED) surgery. We sought to determine the proportion of anticoagulated patients who are concomitantly receiving anti-platelet therapy, the associated risk of clinically significant hematoma (CSH), and the proportion of patients in whom anti-platelet usage is guideline-indicated. Methods A secondary analysis of the Bridge or Continue Coumadin for Device Surgery Randomized Controlled Trial (BRUISE CONTROL). Patients who were receiving warfarin, had an annual predicted risk of thromboembolism of ≥5% and were scheduled to undergo non-emergent CIED surgery were randomized to continued warfarin versus heparin bridging. In the current analysis, patients were divided into those receiving anti-platelet therapy and those not receiving anti-platelet therapy. The incidence of CSH was compared in both groups. The proportion of patients on potentially inappropriate and potentially interruptible antiplatelet therapy was estimated. Results All 681 patients enrolled in BRUISE CONTROL were included, of whom 280 received and 401 did not receive anti-platelet therapy. Anti-platelet therapy increased the risk of CSH (relative risk, 1.72; 95% confidence interval (CI), 1.09 to 2.72; P = 0.02). Of the 280 patients receiving anti-platelet therapy, 97 (34.6%) had no guideline indication for concomitant anti-platelet therapy and an additional 146 (52.1%) were on anti-platelet therapy that could potentially have been interrupted around CIED surgery. Conclusions Concomitant anti-platelet therapy in patients receiving anticoagulation is associated with a significant risk of CSH. The majority of concomitant anti-platelet therapy is potentially inappropriate or interruptible. Trial registration clinicaltrials.gov Identifier: (NCT00800137)

Background Recovery of left ventricular ejection fraction (LVEF) after acute myocardial infarction (MI) is not universal and is difficult to predict. Fragmented QRS (fQRS) complexes are thought to be markers of myocardial scar. We hypothesized that fQRS complexes on 12‑lead surface ECGs during the initial post-MI period would be associated with adverse LV remodeling over the following year. Methods Change in LVEF between the early (0–2 month) and later (2–12 month) post-MI periods was assessed in two independent cohorts of post-MI patients with initial LV dysfunction. A decline or no recovery in LVEF (ΔLVEF ≤0%) was used as a primary outcome. fQRS complexes were measured on 12‑lead ECGs within a week of acute MI. A subset of patients underwent cardiac magnetic resonance imaging (CMR) for scar quantification. Results Of 705 patients in the combined cohort, 27% experienced the primary outcome (average ΔLVEF of −4%). fQRS complexes were associated with a two-fold higher risk of no LVEF recovery, independent of prior MI or CABG, baseline LVEF, MI location and QRS duration or axis. Of 113 patients undergoing CMR, fQRS was associated with increased peri-infarct zone late gadolinium enhancement (13 ± 5% vs 11 ± 4%, p = 0.02), but not core infarct. Conclusions Despite contemporary post-MI therapy, >1 in 4 patients will show a decline in LVEF during follow-up. Fragmented QRS complexes on 12‑lead surface ECG early post-MI may be a valuable marker of unfavorable LV remodeling and correlate to increased peri-infarct scar on CMR imaging.

Background Patients with diabetes mellitus (DM) have a higher risk of sudden cardiac death. Factors associated with the risk profiles of coronary artery disease (CAD) patients with DM are not well established. Heart rate turbulence (HRT) and T-wave alternans (TWA) are often used to predict arrhythmia events. Methods and Results HRT and TWA were measured in two independent groups: the ARTEMIS cohort study and the REFINE-ICD randomized trial. ARTEMIS assesses risk 3–12 months after coronary angiography in patients with CAD. The initial 1001 patients in ARTEMIS, 526 with and 475 without DM, are included in this analysis. REFINE-ICD compares usual care versus usual care plus ICD therapy in patients with left ventricular (LV) ejection fraction (EF) values of 36–50% assessed 2–15 months after myocardial infarction. The initial 275 patients screened in REFINE ICD are included in this analysis. Abnormal HRT plus TWA was more common in patients with versus without DM in ARTEMIS (125/526, 24% vs 63/475, 13%; P < 0.001) and REFINE-ICD (43/55, 78% vs 55/220, 25%; P < 0.001), respectively. Abnormal HRT plus TWA was also more common in patients with LVEF values < 50% (28%) vs ≥ 50% (18%; P < 0.001) in ARTEMIS and LVEF values below the population median of 42% (60/138, 43%) versus above the median (38/137, 28%; P < 0.01) in REFINE-ICD. Conclusions Abnormal HRT plus TWA is more common in CAD patients with DM compared with the patients without DM and is related to the severity of LV dysfunction. Clinical Trial Registration Information http://www.clinicaltrials.gov, NCT01426685; http://www.clinicaltrials.gov, NCT00673842.

This study hypothesizes that a lack of left ventricular ejection fraction (LVEF) recovery after myocardial infarction (MI) would be associated with a poor outcome.A reduced LVEF early after MI identifies patients at risk of adverse outcomes. Whether the change in LVEF in the weeks to months following MI provides additional information on prognosis is less certain.Change in LVEF between the early (2 to 7 days) and later (2 to 12 weeks) post-MI periods in patients with a first MI was assessed in 3 independent cohorts (REFINE [Risk Estimation Following Infarction Noninvasive Evaluation]; CARISMA [Cardiac Arrhythmia and Risk Stratification after Myocardial Infarction]; ISAR [Improved Stratification of Autonomy Regulation]). Patients were categorized as having no recovery (Δ ≤0%), a modest increase (Δ 1% to 9%), or a large increase (Δ ≥10%) in LVEF. The relationship between change in LVEF and risk of sudden cardiac arrest (SCA) and all-cause mortality were assessed in Cox multivariable models.In REFINE, patients with no LVEF recovery had a higher risk of sudden cardiac arrest (hazard ratio: 5.8; 95% confidence interval: 2.1 to 16.6; p = 0.001) and death (hazard ratio: 3.9; 95% confidence interval: 1.5 to 10.1; p 0.001), independent of revascularization, baseline LVEF, and medical therapy compared with patients with recovery. Similar findings were observed in the other cohorts. LVEF reassessments beyond 6 weeks post-MI were more predictive of outcome than were earlier reassessments.The degree of LVEF recovery after a first MI provides important prognostic information. Patients with no recovery in LVEF after MI are at high risk of sudden cardiac arrest events and death.

Canadian electrophysiology (EP) fellowship programs have evolved in an ad hoc fashion over 30 years. This evolution has occurred in many fields in medicine and is natural when innovators and pioneers attract research fellows who help change the status quo from predominantly research to a predominantly clinical application and focus. Fellows not only push their supervisors and their centres into new areas of inquiry but also function at the most advanced level to encourage and teach junior trainees and to provide examples of excellence to residents, medical students, and other health professionals. Funding for fellows has never been provided in the traditional way through the Ministry of Health or the Ministry of Advanced Education. Each Canadian centre has over the years found novel ways to fund fellowship programs, and many centres have used value-adds from procurement programs. These sources of funding are eroding as provincial government agencies are beginning to assume procurement responsibilities and local flexibility to fund fellowships is lost. In particular, provincial government agencies feel that valuable financial resources should be restricted to Canadian trainees only, despite the international consensus that fellowship is an essential time for advanced trainees to travel abroad to acquire a broad a range of experience, learn new techniques and approaches, make lifelong research connections, and hopefully return home with these skills and expertise. This article summarizes the long history of EP fellowship training in Canada, as well as EP fellowship experiences at home and abroad by Canadian electrophysiologists, in an attempt to contextualize these new realities.

Background Whether patients with persistent atrial fibrillation (AF) obtain the same degree of benefit with cardiac resynchronization therapy (CRT) as those in sinus rhythm remains unclear. Methods We enrolled 93 patients undergoing CRT implantation, 20 (22%) of whom had rate-controlled persistent AF. The primary endpoint was CRT response defined as 1 class improvement in Specific Activity Scale and 15% reduction in left ventricular end-systolic volume (LVESV) during 12 months. Other endpoints included changes in 6-minute walk distance, quality of life, B-type natriuretic peptide, and survival. Results Baseline characteristics were similar in those with and without AF. Response to CRT was observed in 42% vs 54% of those with and without AF, respectively (P = 0.3). Both groups had significant improvements in 6-minute walk distance, quality of life, and LVESV, but the improvement in LVESV was smaller in those with AF (13.7% ± 14.9% vs 27.7% ± 23.7%; P = 0.02). During 2.8 ± 1.4 years of follow-up, AF was associated with a 2.2-fold increased risk of death or transplantation (95% confidence interval, 1.2-3.9; P = 0.01). Conclusions Compared with patients without rate-controlled persistent AF, those with rate-controlled persistent AF had similar rates of clinical improvement but less left ventricular reverse remodelling in the first year after CRT. AF was associated with a markedly higher risk of death or transplantation in long-term follow-up. Given these findings, randomized studies assessing CRT efficacy in those with AF are warranted.

Autonomic dysfunction tends to improve over time after acute myocardial infarction (MI), but the clinical significance of autonomic remodeling is not well known.The purpose of this study was to test the hypothesis that the amount of recovery of autonomic function early after MI is associated with a risk for serious arrhythmias.The prognostic significance of autonomic remodeling after MI was assessed in one post-MI cohort [Cardiac Arrhythmia and Risk Stratification after Myocardial Infarction (CARISMA)] and validated in a second cohort [Risk Estimation After Infarction, Noninvasive Evaluation (REFINE)]. Changes in heart rate variability (DeltaHRV) and heart rate turbulence (DeltaHRT) were measured from 24-hour ECG recordings performed early (5-21 days) and later (6 weeks) after MI in CARISMA (n = 312). DeltaHRV and DeltaHRT were similarly measured from early (2-4 weeks) and later (10-14 weeks) post-MI recordings in REFINE (n = 322).HRV and HRT increased over time in both cohorts. Attenuated recovery of autonomic function, defined as DeltaHRT slope2.0 ms/RR, was associated with a 9.4-fold (95% confidence interval 1.2-71.6; P = .03) higher risk of ECG-documented sustained ventricular tachycardia or ventricular fibrillation in CARISMA and a 7.0-fold (95% confidence interval 1.6-29.6; P = .009) higher risk of fatal or near-fatal events in REFINE. Changes in HRV and HRT were not predictive of nonarrhythmic death in either cohort.Attenuated recovery of autonomic function early after MI consistently predicts a higher risk of fatal or near-fatal arrhythmic events. A lack of improvement in HRT early after MI appears to be a specific marker for serious arrhythmic events.

Objectives We sought to evaluate the utility of T-wave alternans (TWA) assessment in the immediate post-exercise period to identify and validate cutpoints for the modified moving average (MMA) assessment method. Background The presence of TWA is associated with an increased risk of cardiovascular death (CVD). The immediate post-exercise period, where increased physiologic stress and minimal surface artifact coexist, appears ideal to implement the MMA method. Methods A test (n = 322) and validation cohort (n = 681) provided 1,003 patients with coronary artery disease (CAD). We assessed TWA immediately after exercise. The outcomes, CVD and mortality, were adjudicated independent of the TWA results. Results During 48 months of follow-up 85 deaths, 54 categorized as CVD (64%), were observed. A linear relationship between the magnitude of TWA and the risk of CVD was identified. As a continuous measure TWA voltage was equivalent to ejection fraction in predicting the risk of CVD. To facilitate clinical application, a sensitive, modest predictive accuracy (20 μV) and a specific, greater predictive accuracy MMA cutpoint (60 μV) were identified and validated. Each cutpoint was associated with a 2.5-fold greater risk of CVD, independent of other important variables, including ejection fraction. Conclusions Post-exercise assessment of TWA using the MMA method is a strong, independent predictor of risk in patients with CAD. The 20-μV cutpoint (87% sensitivity) appears to be most suitable in higher-risk patients, whereas the 60-μV cutpoint (95% specificity) appears more appropriate when TWA is used as a single screening test in those at lower risk. (Assessment of Noninvasive Methods to Identify Patients at Risk of Serious Arrhythmias After a Heart Attack; NCT00399503 )

Aims Data suggest that atrial pacing, statins, angiotensin-converting enzyme-inhibitors and angiotensin receptor blocking drugs prevent atrial tachycardia/atrial fibrillation (AT/AF) in some patients. The clinical predictors of AT/AF recurrence following dual-chamber pacemaker insertion were examined in 185 consecutive patients with paroxysmal AF. Methods and results Predictors of AT/AF recurrence were evaluated in this observational cohort study. The time to first AT/AF recurrence and AT/AF burden (h/day) was retrieved at each follow-up visit by interrogating the pacemaker. AT/AF recurred following pacemaker implantation in 157 (85%) patients. At 1 year of follow-up, patients without recurrence were more likely to be on statin therapy (54%) when compared with patients without statin therapy (25%, χ = 12.31, P = 0.0004). Statin therapy was the only significant predictor of AT/AF recurrence in a multivariate logistic regression model (adjusted odds ratio 0.33, 95% confidence interval 0.14–0.74, P = 0.007). AT/AF burden was significantly lower in the group on statin therapy (median 0.10 h/day) when compared with the group not on statin therapy (median 0.39 h/day, P = 0.0059). Conclusion AT/AF recurs frequently following pacemaker implantation in patients with sinus node disease. The progression to permanent AF remains low over time. Statin therapy was significantly associated with AT/AF suppression.

Objectives This study sought to determine whether combined assessment of autonomic tone plus cardiac electrical substrate identifies most patients at risk of serious events after myocardial infarction (MI) and to compare assessment at 2 to 4 weeks versus 10 to 14 weeks after MI. Background Methods to identify most patients at risk of serious events after MI are required. Methods Patients (n = 322) with an ejection fraction (EF) Results Mean EF significantly increased over the initial 8 weeks after MI. Testing 2 to 4 weeks after MI did not reliably identify patients at risk, whereas testing at 10 to 14 weeks did. The 20% of patients with impaired HRT, abnormal exercise TWA, and an EF Conclusions Impaired HRT, abnormal TWA, and an EF http://www.clinicaltrials.gov/ct/show/NCT00399503?order=1 ; NCT00399503 )

The present report describes an unusual case of pulmonary edema after adenosine cardioversion of a supraventricular tachycardia. Despite a structurally normal heart, a 52-year-old woman presented with pulmonary edema on two separate occasions, having had her atrioventricular nodal re-entrant tachycardia terminated with 12 mg of intravenous adenosine. A third similar episode of tachycardia that was terminated with verapamil was not complicated by pulmonary edema.

The critical points (also known as phase singularities) in the heart reflect the pathological change of the heart tissue, and hence can be used to describe and analyze the dynamics of the cardiac electrical activity. As a result, the detection of these critical points can lead to correct understanding and effective therapy of the tachycardia. In this paper, we propose a novel approach to address this problem. The proposed approach includes four stages: image smoothing, motion estimation, motion decomposition, and detection of the critical points. In the image smoothing stage, the noisy cardiac optical data are smoothed using anisotropic diffusion equation. The conduction velocity fields of the cardiac electrical patterns can then be estimated from two consecutive smoothed images. Using the recently developed discrete Hodge-Helmholtz motion decomposition technique, the curl-free and divergence-free potential surfaces of an estimated velocity field are extracted. Finally, hierarchically searching the minima and maxima on the potential surfaces, the sources, sinks, and rotational centers are located with high accuracy. Experimental results with four real cardiac videos show that the proposed approach performs satisfactorily, especially for the cardiac electrical patterns with simple propagations.

This study assessed in vivo temporal and spatial electrophysiological properties of murine hearts and the effect of manipulation of transmural action potential durations (APDs) on T wave morphology. Monophasic action potentials (MAPs) were acquired from multiple left ventricular sites. All MAPs exhibited a plateau phase, with a spike and dome appearance being present in epicardial recordings. Activation occurred from endocardial apex to epicardial apex and apex to base while repolarization occurred from base (shortest 90 eta0 level of repolarization (MAP90), 95.4 +/- 8.9 ms) to apex and epicardium to endocardium (longest MAP90, 110.77 +/- 10.6 ms). The peak of phase 0 of the epicardial base MAP correlated with the return to baseline of the initial and usually dominant waveform of the QRS and the onset of the second usually smaller wave, which clearly occurred in early repolarization, thus establishing where depolarization ended and repolarization began on the murine ECG. This second waveform was similar to the J wave seen in larger animals. Despite temporal and spatial electrophysiological similarities, a T wave is frequently not seen on a murine ECG. There are several determinants of T wave morphology, including transmural activation time, slope of phase 3 repolarization and differences in epicardial, endocardial and M cell APDs. Experimental manipulation of murine transmural gradients by shortening epicardial MAP(90) to 84% of endocardial MAP90 the epicardial/endocardial ratio in larger mammals when a positive T wave is present, resulted in a positive murine T wave. Thus, manipulation of the transmural gradients such that they are similar to larger mammals can result in T waves with similar morphology.

A line of nonobese diabetic (NOD) mice expressing the human diabetes-associated HLA-DQ8 transgene in the absence of mouse IAβfailed to show spontaneous insulitis or diabetes, but rather developed dilated cardiomyopathy, leading to early death from heart failure. Pathology in these animals results from an organ- and cell-specific autoimmune response against normal cardiomyoctes in the atrial and ventricular walls, as well as against very similar myocytes present in the outermost muscle layer surrounding the pulmonary veins. Progression of the autoimmune process could be followed by serial ECG measurements; irradiation of young animals significantly delayed disease progression, and this effect could be reversed by adoptive transfer of splenocytes taken from older animals with complete heart block. Disease progression could also be blocked by cyclosporin A treatment, but was accelerated by injection of complete Fruend's adjuvant. The constellation of findings of spontaneously arising destructive focal lymphocytic infiltrates within the myocardium, rising titers of circulating anticardiac autoantibodies, dilation of the cardiac chambers, and gradual progression to end-stage heart failure bears a striking resemblance to what is seen in humans with idiopathic dilated cardiomyopathy, a serious and often life-threatening medical condition. This transgenic strain provides a highly relevant animal model for human autoimmune myocarditis and postinflammatory dilated cardiomyopathy.

Background: Recovery of left ventricular ejection fraction (LVEF) after myocardial infarction (MI) is not universal and is difficult to predict. Fragmented QRS (fQRS) complexes are thought to be a marker of myocardial scar, and are defined as various RSR’ patterns on a 12-lead surface

The expression of calreticulin, a Ca(2+)-binding chaperone of the endoplasmic reticulum, is elevated in the embryonic heart, and because of impaired cardiac development, knockout of the Calreticulin gene is lethal during embryogenesis. The elevated expression is downregulated after birth. Here we have investigated the physiological consequences of continued high expression of calreticulin in the postnatal heart, by producing transgenic mice that overexpress the protein in the heart. These transgenic animals exhibit decreased systolic function and inward I(Ca,L), low levels of connexin43 and connexin40, sinus bradycardia, and prolonged atrioventricular (AV) node conduction followed by complete heart block and sudden death. We conclude that postnatal downregulation of calreticulin is essential in the development of the cardiac conductive system, in particular in the sinus and AV nodes, when an inward Ca(2+) current is required for activation. This work identifies a novel pathway of events, leading to complete heart block and sudden cardiac death, which involves high expression of calreticulin in the heart.

Background —Some clinical data suggest that atrial-based pacing prevents paroxysmal atrial fibrillation (AF). This study tested the hypothesis that DDDR pacing compared with VDD pacing prevents AF after atrioventricular (AV) junction ablation. Methods and Results —Patients were randomized to DDDR pacing (n=33) or to VDD pacing (n=34) after AV junction ablation and followed every 2 months for 6 months. Patients then crossed over to the alternate pacing mode and were followed for an additional 6 months. Primary analysis included the time to first recurrence of sustained AF (duration >5 minutes), total AF burden, and the development of permanent AF. The time to first episode of AF was similar in the DDDR group (0.37 days, 95% CI 0.1 to 1.3 days) and the VDD pacing group (0.5 days, 95% CI 0.2 to 1.7 days, P =NS). AF burden increased over time in both groups ( P P =NS). Twelve (35%) patients in the DDDR group and 11 (32%) patients in the VDD group had permanent AF within 6 months of ablation. Within 1 year of follow-up, 43% of patients had permanent AF. Conclusions —DDDR pacing compared with VDD pacing does not prevent paroxysmal AF over the long term in patients in the absence of antiarrhythmic drug therapy after total AV junction ablation. Many patients have permanent AF within the first year after ablation.

This study tests the hypothesis that moderate myocardial dysfunction is associated with altered myocardial anisotropic properties and structurally altered ventricular fibrillation (VF). Mongrel dogs were randomized to either a control group or a group that was rapidly paced at 250 beats/min until the left ventricular ejection fraction was [Formula: see text] 40%. Changes in anisotropic properties and the electrical characteristics of VF associated with the development of moderate myocardial dysfunction were assessed by microminiature epicardial mapping studies. In vivo conduction, refractory periods, and repolarization times were prolonged in both longitudinal and transverse directions in myopathic animals versus controls. VF was different in myopathic versus control animals. There were significantly more conducted deflections during VF in normal hearts compared with myopathic hearts. Propagated deflection-to-deflection intervals during VF were significantly longer in myopathic hearts compared with controls (125.5 ± 49.06 versus 103.4 ± 32.9 ms, p = 0.009). There were no abnormalities in cell size, cell shape, or the number of intercellular gap junctions and there was no detectable change in the expression of the gap junction proteins Cx43 and Cx45. Moderate myocardial dysfunction is associated with significant electrophysiological abnormalities in the absence of changes in myocardial cell morphology or intercellular connections, suggesting a functional abnormality in cell-to-cell communication.Key words: cardiomyopathy, anisotropy, fibrillation, defibrillation.

Patients who survive a tachyarrhythmic cardiac arrest in the first 6 months after acute myocardial infarction (AMI) are at risk for recurrent arrests, but the magnitude, timing and characteristics of this phenomenon are unknown. This study characterizes the nature of recurrent tachyarrhythmic cardiac arrests in the absence of reversible factors or new myocardial necrosis in patients between 3 and 180 days after AMI. We retrospectively assessed 28 patients (mean age 61 +/- 12 years) who survived an initial cardiac arrest a median of 10 days after AMI. Mean left ventricular ejection fraction was 36 +/- 9%. Fourteen patients (50%) had at least 1 recurrence of cardiac arrest, and 10 had > 2 arrests. Almost all (92%) recurrent cardiac arrests occurred within 5 days of the preceding arrest, and the high-risk periods were similar after the first, second or third cardiac arrest. Very fast ventricular tachycardia (mean cycle length 212 +/- 30 ms) was the documented responsible arrhythmia in 44 of 51 cardiac arrests. The morphology was either polymorphic, monomorphic or sinusoidal. No clinical or laboratory values could be found that predicted whether a patient would have a recurrent arrest. Nineteen patients (68%) survived to leave the hospital and have been followed for up to 96 months. For these, actuarial 5-year overall survival was 76% and actuarial 5-year arrhythmia-free probability was 80%. Thus, patients who survive a cardiac arrest in the first 6 months after AMI are at high risk of recurrent cardiac arrest for a further 5 days, and the arrests are due to characteristically fast ventricular tachycardias.(ABSTRACT TRUNCATED AT 250 WORDS)

Background The efficacy and safety of vernakalant, a relatively atrial-selective antiarrhythmic agent, in converting atrial fibrillation (AF) to sinus rhythm (SR) were evaluated in this multicenter, open-label study of patients with AF lasting >3 hours and ≤45 days (RCT no. NCT00281554 ). Methods Adult patients with AF and an indication for conversion to SR received a 10-minute intravenous infusion of vernakalant (3 mg/kg). If after a 15-minute observation period AF was present, a second 10-minute infusion of intravenous vernakalant (2 mg/kg) was given. The primary efficacy end point was the proportion of patients with recent-onset AF (AF lasting >3 hours to ≤7 days) who converted to SR within 90 minutes of the start of the first infusion. Safety evaluations included vital signs, telemetry and Holter monitoring, 12-lead electrocardiography, clinical laboratory tests, physical examinations, and adverse events (AEs). Results A total of 236 hemodynamically stable patients with AF received intravenous vernakalant. Among them, 167 (71%) had recent-onset AF and were eligible for the primary efficacy end point. Vernakalant rapidly converted recent-onset AF to SR in 50.9% of patients, with a median time to conversion of 14 minutes among responders. The most common AEs were dysgeusia, sneezing, and paresthesia. These occurred at the time of vernakalant infusion, were transient, and resolved spontaneously. Ten patients (4.2%) discontinued vernakalant treatment because of AEs, most commonly (in 4 of 10) hypotension. There were no episodes of torsades de pointes, ventricular fibrillation, or sustained ventricular tachycardia. Conclusions Vernakalant rapidly converted recent-onset AF to SR, was well tolerated, and may be a valuable therapeutic alternative for reestablishing SR in patients with recent-onset AF.

Background: A single, markedly elevated B-type natriuretic peptide (BNP) serum concentration predicts an increased risk of death after myocardial infarction (MI), though its sensitivity and predictive accuracy are low. We compared the predictive value of a modestly and persistently elevated, versus a single, markedly elevated measurement of N terminal pro-BNP (NT-BNP) early after MI. Methods and Results: NT-BNP was measured 2–4, 6–10, and 14–18 weeks after MI. The median age of the 100 patients was 61 years, median left ventricular ejection fraction (LVEF) was 0.40, and 88% were males. Over a median follow-up of 39 months, 10 patients died. The initial median NT-BNP was 802 pg/mL and declined over time (P = 0.002). An initial NT-BNP ≥2,300 pg/mL (upper quintile) was observed in 19 patients and predicted a 3.4-fold higher independent risk of death (P = 0.05), with modest sensitivity (30%) and positive predictive accuracy (16%). A NT-BNP consistently ≥1,200 pg/mL (upper tertile) was observed in 19 patients, and was associated with a 5.7-fold higher independent risk of death (P = 0.01), with a higher sensitivity (50%) and positive predictive accuracy (26%) than a single, markedly elevated NT-BNP measurement. Conclusions: A moderately and persistently elevated NT-BNP in the early post-MI period was associated with a 5.7-fold higher risk of death, independent of age, LVEF, and functional class. Compared with a single measurement, serial NT-BNP measurements early after MI were more accurate predictors of risk of death.

To determine how many electropharmacologic drug trials should be performed to select therapy for patients with ventricular tachyarrhythmias, the outcome of 150 consecutive patients with inducible ventricular tachyarrhythmias undergoing serial electropharmacologic testing was examined. The probability of identifying predicted effective therapy (inductive of fewer than five ventricular responses with three ventricular extrastimuli at three pacing cycle lengths) and the probability of that therapy preventing sustained ventricular tachyarrhythmia recurrences were determined as a function of the number of preceding trials. The probability ( +/- SE) of identifying predicted effective therapy by the first trial (0.23 +/- 0.03) was significantly higher than that of the second (0.09 +/- 0.04), third (0.08 +/- 0.04) and fourth (0.05 +/- 0.04) trials (p = 0.001). No patient had predicted effective therapy identified by subsequent trials. The 2 year actuarial probability of freedom from sustained ventricular tachyarrhythmias on predicted effective therapy was higher for the first (0.79 +/- 0.08), second (0.73 +/- 0.13) and third (0.86 +/- 0.13) trials than for the fourth (0.33 +/- 0.27) trial (p = 0.02). Thus, the probability of selecting therapy with long-term efficacy was highest for the first trial (0.18), intermediate for the second (0.07) and third (0.07) trials and lowest for the fourth (0.02) and subsequent (0.00) trials. Accordingly, the electropharmacologic approach to therapy selection should be abandoned after three unsuccessful trials.

Background. Changes in cardiac autonomic function have been documented after myocardial infraction (MI), but their significance is unknown. We assessed the amount of recovery of autonomic dysfunction after MI and its significance among the patients with depressed left ventricular ejection fraction (LVEF ≤ 0.40 - CARISMA and ≤ 0.50 - REFINE). Methods and Results. Changes in heart rate variability (dHRV) and turbulence (dHRT) were measured from 24-hour ECG recordings performed 5–21 days and again at six weeks post-MI in 312 patients included in the Cardiac Arrhythmias and Risk Stratification after Myocardial Infarction (CARISMA) study. The primary endpoint was sustained ventricular tachycardia (VT) or ventricular fibrillation (VF) recorded by an implantable device. Non-arrhythmic death was a secondary endpoint. HRV and HRT measures increased significantly from baseline to six weeks post-AMI (p Conclusions. Autonomic function undergoes a substantial improvement early after MI, which is associated with vulnerability to VT or VF. A marked recovery of autonomic dysfunction protects from the occurrence of fatal or near-fatal arrhythmic events after MI despite depressed LVEF

The Canadian Cardiovascular Society Access to Care Working Group recently published a series of commentaries on access to cardiovascular care in Canada. These commentaries included proposed minimally acceptable wait times for patients with atrial fibrillation (AF) to be assessed by a cardiologist or an electrophysiologist. To improve access to medical care for the patient with AF, a nurse clinician-based AF clinic was established in the Calgary Health Region (Alberta) in 2005. More than 330 patients had been referred at the time of writing. The time from referral to initial nurse assessment was 38+/-31 days, to physician review and establishment of a management plan was 66+/-49 days and to in-person specialist physician assessment was 80+/-55 days. These wait times are markedly shorter than historical wait times to see an arrhythmia specialist in the Calgary Region. As experience increased, wait times continued to shorten significantly. Preliminary data suggest that early assessment and patient education may reduce emergency department visits and hospitalizations for AF. This experience suggests that a nurse clinician-based AF clinic may provide earlier access to medical care and may improve health outcomes in the long term.

The purpose of the present study was to examine the effects of monophasic and biphasic stimulation under conditions of full and incomplete repolarization in an in vivo dog model and in an in vitro rabbit ventricular single cell model. Strength-interval curves were constructed with monophasic cathodal stimulation and biphasic subthreshold anodal followed by cathodal stimulation in dogs prior to and late after left anterior descending coronary artery occlusion. At the monophasic absolute refractory period plus 10 msec, less cathodal current was required for biphasic compared to monophasic stimulation (P = 0.04). Moreover, the biphasic absolute ventricular refractory period (116 +/- 8 msec) was significantly shorter than the monophasic absolute ventricular refractory period (136 +/- 15 msec) (P less than 0.02). At coupling intervals greater than 30 msec after the monophasic absolute ventricular refractory period, there was no distinction between monophasic and biphasic stimuli. Similarly enhanced excitability was observed with biphasic stimuli in infarcted hearts. Voltage clamp measurements mimicking conditions of the in vivo studies demonstrated that when repolarization is incomplete, a hyperpolarizing prepulse reactivates additional sodium current resulting in enhanced excitability. In conclusion, biphasic stimulation consisting of a hyperpolarizing anodal prepulse followed by a cathodal pulse decreases the current required for excitation compared to cathodal monophasic stimulation in a critical zone near the ventricular absolute refractory period.

Previous studies in animals and in humans have shown that melperone, a neuroleptic butyrophenone, has class III electrophysiologic activity. However, its antiarrhythmic activity has not been assessed in humans. Accordingly, the electrophysiologic and antiarrhythmic effects of melperone were assessed in 23 patients with symptomatic ventricular tachyarrhythmias. Seventeen patients had electrophysiologic testing while receiving melperone. At oral daily dosages greater than or equal to 240 mg, melperone produced significant prolongations of QT intervals (385 +/- 11 vs. 355 +/- 22 ms, p less than 0.05), ventricular effective refractory periods (263 +/- 18 vs. 243 +/- 28 ms, p less than 0.05; 260 +/- 18 vs. 235 +/- 27 ms, p less than 0.01; and 243 +/- 23 vs. 222 +/- 28 ms, p less than 0.01; at 600-, 500-, and 400-ms pacing cycle lengths, respectively) and ventricular tachycardia (VT) cycle lengths (286 +/- 46 vs. 239 +/- 70 ms, p less than 0.05). Inducible VT was suppressed entirely in one patient. In three other patients, inducible sustained VT became nonsustained. No significant negative inotropic effects were observed. The majority of patients (70%) experienced some adverse effect, the commonest of which was neurologic. In conclusion, melperone had significant class III electrophysiologic and antiarrhythmic activity in humans. Its clinical use may be limited by the high incidence of adverse effects.

Aims Previous studies showed that right ventricular (RV) endocardial pacing can be deleterious even in individuals with initially normal left ventricular (LV) function. The mechanism(s) by which RV endocardial pacing may cause LV dysfunction is unknown. This study compares the temporospatial LV transmyocardial activation profiles during sinus rhythm with normal His/Purkinje conduction vs. currently utilized and proposed cardiac pacing sites. Methods and results Mongrel dogs were instrumented with transmural electrodes that tracked transmyocardial activation sequences at five sites in the LV. Pacing/recording catheters were positioned in the RV apex and on the RV and LV sides of the ventricular septum. An epicardial pacing electrode was also sewn to the mid-lateral LV epicardium. Electrograms were recorded during sinus rhythm and pacing from the RV endocardium, LV septum, LV epicardium and during biventricular pacing. Compared to normal sinus/His/Purkinje rhythm (NSR), RV endocardial pacing significantly ( P < 0.05) prolonged transmural activation (NSR endocardium 6.1 ± 1 ms vs. RV endocardium 23.0 ± 2.6 ms). The highly ordered temporospatial pattern of transmural activation during sinus rhythm was replaced with dispersion and intermingling of endo-, mid-, and epicardial activation. LV epicardial and biventricular pacing did not correct these abnormalities. Only LV septal pacing achieved the transmural and transseptal activation sequences similar to sinus rhythm. Conclusion Clinically utilized pacing modalities, including biventricular pacing, cause abnormal transmyocardial activation. LV septal pacing results in transmyocardial activation patterns that closely resemble those seen in sinus rhythm.

This study sought to determine whether combined assessment of autonomic tone plus cardiac electrical substrate identifies most patients at risk of serious events after myocardial infarction (MI) and to compare assessment at 2 to 4 weeks versus 10 to 14 weeks after MI.Methods to identify most patients at risk of serious events after MI are required.Patients (n = 322) with an ejection fraction (EF)0.50 in the initial week after MI were followed up for a median of 47 months. Serial assessment of autonomic tone, including heart rate turbulence (HRT), electrical substrate, including T-wave alternans (TWA), and EF was performed, interpreted blinded, and categorized using pre-specified cut-points where available. The primary outcome was cardiac death or resuscitated cardiac arrest. All-cause mortality and fatal or nonfatal cardiac arrest were secondary outcomes.Mean EF significantly increased over the initial 8 weeks after MI. Testing 2 to 4 weeks after MI did not reliably identify patients at risk, whereas testing at 10 to 14 weeks did. The 20% of patients with impaired HRT, abnormal exercise TWA, and an EF0.50 beyond 8 weeks post-MI had a 5.2 (95% confidence interval [CI] 2.4 to 11.3, p0.001) higher adjusted risk of the primary outcome. This combination identified 52% of those at risk, with good positive (23%; 95% CI 17% to 26%) and negative (95%; 95% CI 93% to 97%) accuracy. Similar results were observed for the secondary outcomes.Impaired HRT, abnormal TWA, and an EF0.50 beyond 8 weeks after MI reliably identify patients at risk of serious events. (Assessment of Noninvasive Methods to Identify Patients at Risk of Serious Arrhythmias After a Heart Attack; http://www.clinicaltrials.gov/ct/show/NCT00399503?order=1; NCT00399503).

A depressed left ventricular (LV) ejection fraction (EF) early after myocardial infarction (MI) identifies patients at risk of adverse outcomes. Whether the change in LVEF in the weeks to months following MI provides additional information on prognosis is less certain. We hypothesized that a lack of

A high-speed video camera and voltage-sensitive dyes were used to acquire high resolution (80times80 pixels) and high-speed (500mus/frame) optical signals of ventricular fibrillation in a Langendorff-perfused porcine heart. The resulting spatiotemporal dynamics were recorded before and after the application of a defibrillation shock in order to study the mechanism of defibrillation failure. We used recurrence plots as a tool to qualify the evolution of ordered behavior on the heart surface before fibrillation was reestablished in defibrillation failure. Such ordered periods may point to robust periods in which the defibrillation attempt has had the most effect and may provide a window in which a smaller, corrective shock may be applied to achieve defibrillation

A high-speed video camera and voltage-sensitive dyes were used to acquire high resolution (80 /spl times/ 80 pixels) and high-speed (1 ms/frame) optical signals of ventricular fibrillation in a Langendorff-perfused porcine heart. The resulting spatiotemporal dynamics were recorded before and after the application of a defibrillation shock in order to study the mechanism of defibrillation failure. We created time space cubes and calculated nonlinear synchronization index measures to qualify the evolution of different types of activity on the heart surface (focal, reentry). We observed changes with time in all types of analysis, thus establishing these techniques as viable methods for detecting defibrillation failure before reentry reestablishes itself.

In recent years radiofrequency energy sources have been utilized in patients with atrial fibrillation to ablate atrial tissue and restore normal sinus rhythm. Radiofrequency ablations significantly minimize time in surgery, and hence postoperative complications, but as yet do not duplicate the ablation transmurality achieved by "cut and sew" techniques. Studies of post-operative fibrillation recurrence attribute treatment failures to the lack of obtaining full lesion transmurality at the time of surgery. Unfortunately, no method or standard exists for validating in-vivo ablation transmurality. Using high-resolution optical mapping studies with Langendorff perfused heart preparations, we are able to correlate spatiotemporal electrical activity with ablation line transmurality, thus providing a means for validating ablation transmurality in order to quantify the type and number of ablation lines used in order to tailor ablation therapies to individual patient needs.

Objective: Overexpression of calcineurin causes cardiac hypertrophy and arrhythmic deaths. During disease development, sinus bradycardia followed by high degree atrioventricular (AV) block finally culminating in ventricular asystole has been observed over time in calcineurin hearts. AV block is associated with the development of pleomorphic ventricular tachycardia in mice and downregulation of potassium currents in ventricular myocytes. We tested the hypothesis that the abnormalities of AV block and propensity to ventricular tachycardia relate to overexpression of calcineurin independent of the development of hypertrophy. Methods: Cardiac electrophysiologic properties were compared in isolated perfused hearts with ventricular hypertrophy due to overexpression of calcineurin or NF-AT3 and in their corresponding wild types at 15 or 30 days of age. Results: Compared to wild-type hearts, significant prolongation of sinus node recovery times was noted in both NF-AT3 and calcineurin hearts. Compared to wild-type hearts, Wenckebach cycle length (WCL) and the left ventricular effective refractory period (LVERP) were significantly prolonged in the calcineurin hearts (pb0.05) but not NF-AT3 hearts. In calcineurin mice, left ventricular effective refractory period impinged on Wenckebach cycle length resulting in a significant correlation between left ventricular effective refractory period and Wenckebach cycle length (r 2 =0.56). No such correlation was observed for wild type or NF-AT3 hearts. At 30 days of development, ventricular tachycardia developed in 70% of calcineurin hearts compared to 0% wild-type hearts (p=0.003), whereas ventricular tachycardia was observed in 33% of NF-AT3 hearts and 10% of corresponding wild-type hearts (p=NS). Conclusions: The prolonged ventricular refractoriness, seen only in calcineurin hearts, impinges on Wenckebach cycle length resulting in heart block and is associated with propensity to ventricular tachycardia.

A high‐speed video camera and voltage‐sensitive dyes were used to acquire high resolution (80×80 pixels) and high‐speed (500 μs/frame) optical signals of ventricular fibrillation in a Langendorff‐perfused porcine heart. The resulting spatiotemporal dynamics were recorded before and after the application of a defibrillation shock in order to study the mechanism of defibrillation failure. We calculate nonlinear synchronization index measures to qualify the evolution of different types of activity on the heart surface (focal, reentry). We observe changes with time in the spatial distribution of the first Fourier mode, showing that two main types of activity compete on the heart surface during a failed defibrillation.

The electrophysiological mechanisms underlying cardiac arrhythmias are studied by determining the spatiotemporal progression of cardiac depolarization and repolarization, termed cardiac mapping. Analysis of transient events requires information to be obtained from multiple sites simultaneously. The most significant problem with the design of such systems has been the large amount of data storage required and the rapidity of the composite data stream. Mapping systems with 500 simultaneous channels are common, and 4,000 channel systems have been envisioned. The authors report a relatively simple approach to this data storage problem that uses commercially available frame grabber technology coupled to a personal computer. With this approach they have developed a storage system capable of 24,000 channels sampled at 1 kHz with 12 bit resolution. Hybrid mapping systems incorporating optical recording systems utilizing voltage sensitive dyes from devices such as CCD cameras as well as conventional extracellular electrograms can simultaneously utilize this approach.