John M. Morgan

HRS/EHRA Expert Consensus on the Monitoring of Cardiovascular Implantable Electronic Devices (CIEDs): Description of Techniques, Indications, Personnel, Frequency and Ethical Considerations

Developed in partnership with the Heart Rhythm Society (HRS) and the European Heart Rhythm Association (EHRA); and in collaboration with the American College of Cardiology (ACC), the American Heart Association (AHA), the European Society of Cardiology (ESC), the Heart Failure Association of ESC (HFA), and the Heart Failure Society of America (HFSA). Endorsed by the Heart Rhythm Society, the European Heart Rhythm Association (a registered branch of the ESC), the American College of Cardiology, the American Heart Association

EHRA Expert Consensus Statement on the management of cardiovascular implantable electronic devices in patients nearing end of life or requesting withdrawal of therapy

The purpose of this Consensus Statement is to focus on implantable cardioverter-defibrillator (ICD) deactivation in patients with irreversible or terminal illness. This statement summarizes the opinions of the Task Force members, convened by the European Heart Rhythm Association (EHRA) and the Heart Rhythm Society (HRS), based on ethical and legal principles, as well as their own clinical, scientific, and technical experience. It is directed to all healthcare professionals who treat patients with implanted ICDs, nearing end of life, in order to improve the patient dying process. This statement is not intended to recommend or promote device deactivation. Rather, the ultimate judgement regarding this procedure must be made by the patient (or in special conditions by his/her legal representative) after careful communication about the deactivations consequences, respecting his/her autonomy and clarifying that he/she has a legal and ethical right to refuse it. Obviously, the physician asked to deactivate the ICD and the industry representative asked to assist can conscientiously object to and refuse to perform device deactivation.

Comprehensive risk reduction in patients with atrial fibrillation: emerging diagnostic and therapeutic options-a report from the 3rd Atrial Fibrillation Competence NETwork/European Heart Rhythm Association consensus conference

While management of atrial fibrillation (AF) patients is improved by guideline-conform application of anticoagulant therapy, rate control, rhythm control, and therapy of accompanying heart disease, the morbidity and mortality associated with AF remain unacceptably high. This paper describes the proceedings of the 3rd Atrial Fibrillation NETwork (AFNET)/European Heart Rhythm Association (EHRA) consensus conference that convened over 60 scientists and representatives from industry to jointly discuss emerging therapeutic and diagnostic improvements to achieve better management of AF patients. The paper covers four chapters: (i) risk factors and risk markers for AF; (ii) pathophysiological classification of AF; (iii) relevance of monitored AF duration for AF-related outcomes; and (iv) perspectives and needs for implementing better antithrombotic therapy. Relevant published literature for each section is covered, and suggestions for the improvement of management in each area are put forward. Combined, the propositions formulate a perspective to implement comprehensive management in AF.

Mutations in the Lamin A/C gene mimic arrhythmogenic right ventricular cardiomyopathy.

AIMS Arrhythmogenic right ventricular cardiomyopathy (ARVC) is an inherited heart muscle disease predominantly caused by mutations in desmosomal protein genes. Lamin A/C gene (LMNA) mutations are associated with dilated cardiomyopathy, conduction abnormalities and high incidence of sudden cardiac death. In this study, we screened a large cohort of ARVC patients for LMNA mutations. METHODS AND RESULTS One hundred and eight patients from unrelated families with borderline (n = 27) or definite (n = 81) diagnosis of ARVC were genetically tested for five desmosomal genes and LMNA. Sixty-one (56.5%) were positive for desmosomal gene mutations. Standard polymerase chain reaction (PCR) amplification of the 12 protein-coding LMNA exons was performed and mutational screening performed by direct sequencing. Four patients (4%) without desmosomal gene mutations carried LMNA variants. Three had severe right ventricular involvement, and during follow-up three died (two suddenly and one from congestive heart failure); all three had conduction abnormalities on resting 12-lead electrocardiogram (ECG). Myocardial tissue from two patients showed myocyte loss and fibro-fatty replacement. In one of these, immunohistochemical staining with antibody to plakoglobin showed reduced/absent staining of the intercalated discs in the myocardium. CONCLUSION Lamin A/C gene mutations can be found in severe forms of ARVC. Lamin A/C gene should be added to desmosomal genes when genetically testing patients with suspected ARVC, particularly when they also have ECG evidence for conduction disease.

Pulmonary embolectomy for acute massive pulmonary embolism: an analysis of 71 cases.

Between 1964 and 1986 a total of 71 pulmonary embolectomies were performed for acute massive pulmonary embolism. All patients were severely compromised haemodynamically. Sixteen (64%) of 25 patients who had sustained significant periods of cardiac arrest before operation died. The principal cause of death in this group was severe neurological damage. Five (11%) of the 46 who had not had a cardiac arrest died. The 50 (70%) patients who survived did so largely without morbidity during their hospital admission and in the follow up period. Most were not treated with long term anticoagulants and only two had another embolism. When a patient with acute massive pulmonary embolism is too ill to be given thrombolytic treatment, or when thrombolysis is either contraindicated or too slow in producing benefit, pulmonary embolectomy remains an effective alternative treatment with an acceptable mortality.

A Low-Complexity ECG Feature Extraction Algorithm for Mobile Healthcare Applications

This paper introduces a low-complexity algorithm for the extraction of the fiducial points from the electrocardiogram (ECG). The application area we consider is that of remote cardiovascular monitoring, where continuous sensing and processing takes place in low-power, computationally constrained devices, thus the power consumption and complexity of the processing algorithms should remain at a minimum level. Under this context, we choose to employ the discrete wavelet transform (DWT) with the Haar function being the mother wavelet, as our principal analysis method. From the modulus-maxima analysis on the DWT coefficients, an approximation of the ECG fiducial points is extracted. These initial findings are complimented with a refinement stage, based on the time-domain morphological properties of the ECG, which alleviates the decreased temporal resolution of the DWT. The resulting algorithm is a hybrid scheme of time- and frequency-domain signal processing. Feature extraction results from 27 ECG signals from QTDB were tested against manual annotations and used to compare our approach against the state-of-the art ECG delineators. In addition, 450 signals from the 15-lead PTBDB are used to evaluate the obtained performance against the CSE tolerance limits. Our findings indicate that all but one CSE limits are satisfied. This level of performance combined with a complexity analysis, where the upper bound of the proposed algorithm, in terms of arithmetic operations, is calculated as 2.423N+214 additions and 1.093N+12 multiplications for N ≤ 861 or 2.553N+102 additions and 1.093N+10 multiplications for N > 861 (N being the number of input samples), reveals that the proposed method achieves an ideal tradeoff between computational complexity and performance, a key requirement in remote cardiovascular disease monitoring systems.

Dispersion of monophasic action potential duration: Demonstrable in humans after premature ventricular extrastimulation but not in steady state

Abnormal dispersion of repolarization may contribute to the arrhythmogenic physiologic substrate of ventricular arrhythmia. Geographic dispersion of monophasic action potential duration was determined in steady state (drive cycle lengths 600 and 430 ms) between widely spaced right ventricular endocardial sites (geographic dispersion) in 10 control patients with right ventricular disease and complicating ventricular tachycardia (n = 9), 6 patients with right and left ventricular disease and complicating ventricular tachycardia and 7 patients with ischemic heart disease and complicating ventricular tachycardia. No significant difference in geographic dispersion could be demonstrated among the groups. Difference of monophasic action potential duration at adjacent right ventricular endocardial sites (adjacent dispersion) was determined after ventricular extrastimulation during construction of simultaneous electrical restitution curves in the same patient groups. Maximal adjacent dispersion over the electrical restitution curve was compared between disease and control groups. There was a significant difference in observations of maximal adjacent dispersion in patients with right ventricular disease and complicating ventricular tachycardia (range 5 to 85 ms, median 22.5; 14 pairs of sites; p less than 0.05) and patients with right and left ventricular disease and complicating ventricular tachycardia (range 5 to 50 ms, median 17.5; 14 pairs of sites; p less than 0.05) compared with control patients (range 5 to 20 ms, median 10; 15 pairs of sites). This difference was not evident when patients with ischemic heart disease and complicating ventricular tachycardia (range 5 to 25 ms, median 12.5; 12 pairs of sites) were compared with control patients. Maximal percent monophasic action potential shortening from steady state was significantly greater (p less than 0.001) in both groups with greater adjacent dispersions, and prolongation of activation time at monophasic action potential recording sites after premature extrastimulation tended to be greater in patients with right or right and left ventricular disease and complicating ventricular tachycardia. It is concluded that in disease, exaggeration of monophasic action potential shortening after premature ventricular extrastimulation may contribute to the electrophysiologic arrhythmogenic substrate.

The Extent of Left Ventricular Scar Quantified by Late Gadolinium Enhancement MRI Is Associated With Spontaneous Ventricular Arrhythmias in Patients With Coronary Artery Disease and Implantable Cardioverter-Defibrillators

Background—Characterization of sudden cardiac death (SCD) risk remains a challenge in the application of implantable cardioverter-defibrillator (ICD) therapy. Late gadolinium enhancement cardiac MRI (LGE-CMR) can accurately identify myocardial scar. We performed a retrospective, single-center observational study to evaluate the association between the extent and distribution of left ventricular scar, quantified using LGE-CMR, and the burden of ventricular arrhythmias in patients with coronary artery disease and ICDs. Methods and Results—All patients included (2006 to 2009) had undergone LGE-CMR before ICD implantation. Scar (defined as myocardium with a signal intensity ≥50% of the maximum in scar tissue) was characterized in terms of percent scar, scar surface area, and number of transmural left ventricular scar segments. The end point was appropriate ICD therapy. Sixty-four patients (mean age, 66±11 years; male sex, 51) were included. During 19±10 months follow-up, appropriate ICD therapy occurred in 19 (30%) patients. In Cox regression analyses, both percent scar (hazard ratio per 10%, 1.75; 95% CI, 1.09 to 2.81; P=0.02) and number of transmural scar segments (hazard ratio per segment, 1.40; 95% CI, 1.15 to 1.70; P=0.001) were significantly associated with the occurrence of appropriate ICD therapy. Conclusions—In this pilot study, the extent of myocardial scar characterized by LGE-CMR was significantly associated with the occurrence of spontaneous ventricular arrhythmias. We hypothesize that scar quantification by LGE-CMR may prove a valuable risk stratification tool for the occurrence of ventricular arrhythmias, which may have implications for patient selection for ICD therapy.

Electrophysiological Mapping and Ablation of Intra-Atrial Reentry Tachycardia After Fontan Surgery With the Use of a Noncontact Mapping System

BACKGROUND Atrial tachyarrhythmias are a complication of Fontan surgery. Conventional electrophysiological mapping and ablation techniques are limited by the complex anatomic and surgical substrate and a high arrhythmia recurrence rate. This study investigates the use of noncontact mapping to identify arrhythmia circuits and guide ablation in Fontan patients. METHODS AND RESULTS Eleven arrhythmias were recorded in 6 patients. Noncontact mapping improved recognition of the anatomic and surgical substrate and identified exit sites from zones of slow conduction in all clinical arrhythmias. Radiofrequency linear lesions were targeted across these critical zones in 5 patients. One patient underwent surgical cryotherapy. Although immediate success was achieved in 3 of 5 patients with radiofrequency ablation, 2 patients had a recurrence after a mean of 6.4 months of follow-up. The patient who underwent cryoablation remains free of arrhythmias. CONCLUSIONS Noncontact mapping can identify arrhythmia circuits in the Fontan atrium and guide placement of ablation lesions. Arrhythmia recurrence is high, possibly because of inadequate lesion creation rather than inaccurate mapping and lesion targeting.

Determination of Human Ventricular Repolarization by Noncontact Mapping Validation With Monophasic Action Potential Recordings

Background—Noncontact mapping (NCM) has not been validated as a clinical technique to measure ventricular repolarization. We used NCM to determine repolarization characteristics by analysis of reconstructed unipolar electrograms (UEs) at the same sites as monophasic action potential (MAP) recordings in the human ventricle. Methods and Results—MAPs were recorded from a total of 355 beats at 46 sites in the left or right ventricle of 9 patients undergoing ablation of ventricular tachycardia guided by NCM (EnSite system). Measurements were made during sinus rhythm, constant right ventricular pacing, and ventricular extrastimuli during restitution-curve construction. The EnGuide locator signal was used to document MAP catheter locations on the endocardial geometry. UE-determined activation-recovery interval (ARI) measured at the maximum derivative of the T wave (Wyatt method) and the minimum derivative of the positive T wave (alternative method) was correlated with MAP measured at 90% repolarization (MAP90%) at the same sites. ARI correlated with MAP90% during steady state by the Wyatt method (r=0.83, P<0.001) and the alternative method (r=0.94, P<0.001). Restitution curves constructed from MAP and UE data exhibited the same characteristics, with a mean correlation coefficient of 0.95 (range, 0.90 to 0.99, P<0.001). The error between ARI and MAP90% was greater over a shorter diastolic coupling interval but was not influenced by distance of the sampling site from the multielectrode array. Conclusions—NCM accurately determines steady-state and dynamic endocardial repolarization in humans. Global, high-density, NCM data could be used to characterize abnormalities of human ventricular repolarization.