Shared Decision Making in Cardiac Electrophysiology Procedures and Arrhythmia Management.

Shared decision making (SDM) has been advocated to improve patient care, patient decision acceptance, patient-provider communication, patient motivation, adherence, and patient reported outcomes. Documentation of SDM is endorsed in several society guidelines and is a condition of reimbursement for selected cardiovascular and cardiac arrhythmia procedures. However, many clinicians argue that SDM already occurs with clinical encounter discussions or the process of obtaining informed consent and note the additional imposed workload of using and documenting decision aids without validated tools or evidence that they improve clinical outcomes. In reality, SDM is a process and can be done without decision tools, although the process may be variable. Also, SDM advocates counter that the low-risk process of SDM need not be held to the high bar of demonstrating clinical benefit and that increasing the quality of decision making should be sufficient. Our review leverages a multidisciplinary group of experts in cardiology, cardiac electrophysiology, epidemiology, and SDM, as well as a patient advocate. Our goal is to examine and assess SDM methodology, tools, and available evidence on outcomes in patients with heart rhythm disorders to help determine the value of SDM, assess its possible impact on electrophysiological procedures and cardiac arrhythmia management, better inform regulatory requirements, and identify gaps in knowledge and future needs.

Into a Fluoroless Future: an Appraisal of Fluoroscopy-Free Techniques in Clinical Cardiac Electrophysiology.

PURPOSE OF REVIEW: There are risks to both patients and electrophysiology providers from radiation exposure from fluoroscopic imaging, and there is increased interest in fluoroscopic reduction. We review the imaging tools, their applications, and current uses to eliminate fluoroscopy. RECENT FINDINGS: Multiple recent studies provide supporting evidence for the transition to fluoroscopy-free techniques for both ablations and device implantation. The most frequently used alternative imaging approaches include intracardiac echocardiography, cardiac MRI guidance, and 3D electroanatomic mapping systems. Electroanatomic mapping and intracardiac echocardiography originally used to augment fluoroscopy imaging are now replacing the older imaging technique. The data supports that the future of electrophysiology can be fluoroscopy-free or very low fluoroscopy for the vast majority of cases. As provider and institution experience grows with these techniques, many EP labs may choose to completely forego the use of fluoroscopy. Trainees will benefit from early experience with these techniques.

P-Wave Amplitude and PR Changes in Patients With Inappropriate Sinus Tachycardia: Findings Supportive of a Central Mechanism.

BACKGROUND: The mechanism of inappropriate sinus tachycardia (IST) remains incompletely understood. METHODS AND RESULTS: We prospectively compared 3 patient groups: 11 patients with IST (IST Group), 9 control patients administered isoproterenol (Isuprel Group), and 15 patients with cristae terminalis atrial tachycardia (AT Group). P-wave amplitude in lead II and PR interval were measured at a lower and higher heart rate (HR1 and HR2, respectively). P-wave amplitude increased significantly with the increase in HR in the IST Group (0.16±0.07 mV at HR1=97±12 beats per minute versus 0.21±0.08 mV at HR2=135±21 beats per minute, P=0.001). The average increase in P-wave amplitude in the IST Group was similar to the Isuprel Group (P=0.26). PR interval significantly shortened with the increases in HR in the IST Group (146±15 ms at HR1 versus 128±16 ms at HR2, P<0.001). A similar decrease in the PR interval was noted in the Isuprel Group (P=0.6). In contrast, patients in the atrial tachycardia Group experienced PR lengthening during atrial tachycardia when compared with baseline normal sinus rhythm (153±25 ms at HR1=78±17 beats per minute versus 179±29 ms at HR2=140±28 beats per minute, P<0.01). CONCLUSIONS: We have shown that HR increases in patients with IST were associated with an increase in P-wave amplitude in lead II and PR shortening similar to what is seen in healthy controls following isoproterenol infusion. The increase in P-wave amplitude and absence of PR lengthening in IST support an extrinsic mechanism consistent with a state of sympatho-excitation with cephalic shift in sinus node activation and enhanced atrioventricular nodal conduction.

Cryoablation for AVNRT: importance of ablation endpoint criteria.

BACKGROUND: For ablation of atrioventricular nodal reentrant tachycardia (AVNRT), cryoablation has been shown to be a safe alternative to radiofrequency ablation. However, previous studies have shown a higher recurrence rate with cryoablation compared to radiofrequency ablation. OBJECTIVE: This study reviewed our experience using cryoablation for typical AVNRT using stringent endpoint criteria for slow pathway ablation, yet preserving the desirable safety profile of cryoablation. METHODS: Seventy-five consecutive cases of typical AVNRT underwent cryoablation. Ablation of the AV nodal slow pathway was performed with the goal of eliminating tachycardia, AH jump, and retrograde atrial echo beats. The primary efficacy endpoint was freedom of recurrent supraventricular tachycardia at follow-up. Analysis of AVN characteristics, number of lesions, and complications was performed. RESULTS: Seventy-two (96%) patients met the primary efficacy endpoint over an average follow-up of 34.6 (12.6-68.3) months. In patients who had complete elimination of the slow pathway, there were no recurrences. The presence of an AH jump with a single retrograde echo was highly associated with a recurrence (P = 0.0001). There were no complications, including AV conduction block. CONCLUSION: The efficacy of cryoablation for management of AVNRT can be comparable to radiofrequency energy if the suggested endpoint of elimination of tachycardia, AH jump with retrograde atrial beats, is met. Prior studies evaluating cryoablation in this setting did not require this endpoint, which could have contributed to the relatively higher rate of late recurrences.

KCNJ2 mutations in arrhythmia patients referred for LQT testing: a mutation T305A with novel effect on rectification properties.

BACKGROUND: Loss-of-function mutations in the KCNJ2 cause approximately 50% of Andersen-Tawil Syndrome (ATS) characterized by a classic triad of periodic paralysis, ventricular arrhythmia, and dysmorphic features. Do KCNJ2 mutations occur in patients lacking this triad and lacking a family history of ATS? OBJECTIVES: The purpose of this study was to identify and characterize mutations in the KCNJ2-encoded inward rectifier potassium channel Kir2.1 from patients referred for genetic arrhythmia testing. METHODS: Mutational analysis of KCNJ2 was performed for 541 unrelated patients. The mutations were made in wild type (WT) and expressed in COS-1 cells and voltage clamped for ion currents. RESULTS: Three novel missense mutations (R67Q, R85W, and T305A) and one known mutation (T75M) were identified in 4/249 (1.6%) patients genotype-negative for other known arrhythmia genes with overall incidence 4/541 (0.74%). They had prominent U-waves, marked ventricular ectopy, and polymorphic ventricular tachycardia but no facial/skeletal abnormalities. Periodic paralysis was present in only one case. Outward current was decreased to less than 5% of WT for all mutants expressed alone. Co-expression with WT (simulating heterozygosity) caused a marked dominant negative effect for T75M and R82W, no dominant negative effect for R67Q, and a novel selective enhancement of inward rectification for T305A. CONCLUSIONS: KCNJ2 loss of function mutations were found in approximately 1% of patients referred for genetic arrhythmia testing that lacked criteria for ATS. Characterization of three new mutations identified a novel dominant negative effect selectively reducing outward current for T305A. These results extend the range of clinical phenotype and molecular phenotype associated with KCNJ2 mutations.