This case series describes 2 women on prolonged therapy with class III antiarrhythmics who developed torsades de pointes polymorphic ventricular tachycardia in the setting of catheter ablation for atrial fibrillation as a result of QTc prolonging factors. Clinicians must exercise increased vigilance in the perioperative period in patients on QTc-prolonging medications. (Level of Difficulty: Intermediate.).

Multiple techniques have been developed in addition to pulmonary vein isolation (PVI) to improve the outcomes of catheter ablation in patients with persistent atrial fibrillation (AF). We sought to evaluate the long-term efficacy of alternative techniques used in our laboratory for the treatment of persistent AF, including spatiotemporal dispersion (SD) and low-voltage isolation (LVI). Consecutive patients with persistent AF who underwent catheter ablation with the studied techniques between July 2016 and December 2019 were included in the study. PVI alone was compared with PVI plus SD and PVI plus LVI in terms of long-term freedom from atrial tachycardia (AT) and AF recurrence. Follow-up data were obtained from clinical records and hospital visits, which included a 7-day Holter monitor and electrocardiograms. The study was approved by the institutional review board of Rhode Island Hospital. A total of 382 patients underwent catheter ablation at our institution during the study period. One hundred seventy-two patients had paroxysmal AF and were excluded from the study. The remaining 210 patients had persistent AF and were included in the study. One hundred and three patients underwent PVI alone, while 48 had the addition of LVI and 59 had SD. Additionally, freedom from AT/AF recurrence at 18 months was 68% in the group that underwent LVI, 49% in the SD group, and 40% in the group that underwent PVI alone (log-rank P = .014). Freedom from AF recurrence was 74% in the LVI group, 71% in the SD group, and 43% in the PVI-alone group (log-rank P = .002). On multivariate Cox regression, LVI and left atrial size were found to be independent predictors of recurrence (hazard ratio, 0.39; 95% confidence interval, 0.206-0.760; P = .005 and hazard ratio, 1.4; 95% confidence interval, 1.105-1.923; P = .008, respectively). LVI and SD in addition to PVI were associated with greater freedom from AT/AF recurrence at 18 months compared to PVI alone.

The cardiac T-wave peak-to-end interval (Tpe) is thought to reflect dispersion in ventricular repolarisation, with abnormalities in Tpe associated with increased risk of arrhythmia. Extracellular K+ modulates cardiac repolarisation, and since arterial plasma K+ concentration ([K+]) rapidly increases during and declines following exercise, we investigated the relationship between [K+] and Tpe with exercise. Serial ECGs (Tpe, Tpe/QT ratio) and [K+] were obtained from 8 healthy, normokalaemic volunteers and 22 patients with end-stage renal disease (ESRD), at rest, during, and after exhaustive exercise. Post-exercise [K+] nadir was 3.1 ± 0.1, 5.0 ± 0.2 and 4.0 ± 0.1 mmol.L−1 (mean ± SEM) for healthy participants and ESRD patients before and after haemodialysis, respectively. In healthy participants, compared to pre-exercise, recovery-induced low [K+] was associated with a prolongation of Tpe (110 ± 8 vs. 87 ± 5 ms, respectively, p = 0.03) and an increase in Tpe/QT ratio (0.28 ± 0.01 vs. 0.23 ± 0.01, respectively, p = 0.01). Analyses of serial data revealed [K+] as a predictor of Tpe in healthy participants (β = -0.54 ±0.05, p < 0.0001), in ESRD patients (β = -0.75 ± 0.06, p < 0.0001) and for all data pooled (β = -0.61 ± 0.04, p < 0.0001). The [K+] was also a predictor of Tpe/QT ratio in healthy participants and ESRD patients. Tpe and Tpe/QT ratio are predicted by [K+] during exercise. Low [K+] during recovery from exercise was associated with increased Tpe and Tpe/QT, indicating accentuated dispersion of ventricular repolarisation. The findings suggest that variations in [K+] with physical exertion may unmask electrophysiological vulnerabilities to arrhythmia.

Purpose of Review The risk of cardiac implantable electronic device (CIED) interference from cell phones was previously thought to be low based on older studies. Current generation of smartphones have incorporated more magnets for optimization of wireless charging, attachment of accessories, and convenience functionalities. These magnets have the potential to cause CIEDs to inadvertently revert into magnet mode. The purpose of this review is to summarize recent findings on smartphones and their accessories causing interference on CIEDs. Recent Findings Recent reports have demonstrated that the iPhone 12 series and accessories have the capability to cause CIED magnetic interference. Summary Current generation of smartphones, smartwatches, wireless headphones, and accessories have the potential to cause CIEDs to revert into magnet mode in both in vivo and ex vivo experiments. The risk of a clinically significant event is unlikely as long as the Food and Drug Administration (FDA) recommendations are followed; keeping smartphones and accessories at least six inches away from CIEDs.

IntroductionThe magnet-activated switch in implanted cardiac devices, including cardioverter-defibrillators and permanent pacemakers (PPM), is susceptible to interference from consumer devices with built-in magnets. For example, a recent case report showed that a patient's implanted cardioverter-defibrillator (ICD) magnet mode became activated owing to interaction with his e-cigarette.1Shea J.B. Aguilar M. Sauer W. Tedrow U. Unintentional magnet reversion of an implanted cardiac defibrillator by an electronic cigarette.HeartRhythm Case Rep. 2020; 6: 121-123Google Scholar While testing has shown that cellular phones and smart watches themselves have minimal interference with cardiac devices,2Lacour P. Parwani A.S. Schuessler F. et al.Are contemporary smartwatches and mobile phones safe for patients with cardiovascular implantable electronic devices?.JACC Clin Electrophysiol. 2020; 6: 1158-1166Google Scholar this has failed to account for the magnets used in the wristband of smart watches and fitness trackers. Fitness trackers are capable of tracking heart rate, step count, and other variables of interest to fitness-minded consumers. In 2019, the company Fitbit, manufacturer of several different devices, sold nearly 16 million units.3Tankovska H. Fitbit device unit sales worldwide 2010-2019.https://www.statista.com/statistics/472591/fitbit-devices-sold/Date accessed: October 8, 2020Google Scholar The popular Apple Watch also features these capabilities, with Garmin and Samsung producing models as well. These products are lightweight and low-profile and sometimes sold with a built-in magnet-clasped wristband. Though this magnet is small, most manufacturers have adopted the magnetic element neodymium, which is known to interfere with device functions.4Wolber T. Ryf S. Binggeli C. et al.Potential interference of small neodymium magnets with cardiac pacemakers and implantable cardioverter-defibrillators.Heart Rhythm. 2007; 4: 1-4Google Scholar We investigated whether these magnetic wristbands had clinically relevant effects on ICD function through ex vivo testing.Key Teaching Points•Magnets used in the wristbands of fitness trackers and smart watches can interfere with implanted cardiac devices; however, this is not widely appreciated by manufacturers of the watches or the cardiac devices.•Possible complications include implanted cardioverter-defibrillator deactivation and permanent pacemaker mode switch.•Patients should be counseled on this risk and advised to keep their wristbands at least 6 inches away from their cardiac devices, and not to wear them to sleep.Case reportA 55-year-old woman with history of sustained ventricular tachycardia secondary to arrhythmogenic right ventricular dysplasia was treated with a dual-chamber ICD for secondary prevention. She was recommended to avoid strenuous exercise to reduce arrhythmic risk. She subsequently purchased an Apple Watch with fitness tracking capabilities to monitor her heart rate, which she wore sometimes overnight. While asleep one night, she was awoken by several beeps emanating from her implanted cardiac device. Subsequent interrogation of the device showed no alerts or abnormal parameters. Upon further investigation, it was found that the device had reverted to magnet mode, owing to magnetic interference from the fitness watch's wristband. No other possible sources of interference were identified. This was replicated in the office, where interrogation of the ICD confirmed magnetic reversion when placed in proximity to the wristband. The watch itself did not have magnetic interference.Methods and materialsThe Medtronic Visia AF MRI S DF-1 single-chamber ICD (Medtronic, Minneapolis, MN) was used for testing. In the electrophysiology lab, sheets of commercial printer paper were stacked to create distance on top of the device that could be easily quantified, and the maximum distance where different magnets could deactivate the ICD was measured. This distance was then confirmed without any paper stacked on the device (Figure 1). Paper and air were chosen as the contact media as they are very weakly diamagnetic and thus do not significantly attenuate the magnetic field of the tested wristbands. This is similar to human tissue itself.5Di Luzio S. Obletter G. Comani S. Del Gratta C. Romani G.L. Magnetic mapping of DC fields related to tissue susceptibility in the human body.in: Williamson S.J. Hoke M. Stroink G. Kotani M. Advances in Biomagnetism. Springer, Boston, MA1989Google ScholarFitbit and Apple Watch wristbands (similar to the patient's in the described case) were used for testing. The results were compared against 2 clinical magnets: a donut magnet and a Medtronic programming head (Medtronic, Minneapolis, MN). The fitness trackers were oriented in the fashion in which they would come up against the ICD in real life, as if the volar aspect of a patient's wrist with the magnet clasped came into contact with their chest.ResultsThe Fitbit and Apple Watch wristband magnets could deactivate the ICD up to distances of 2.4 and 2.0 centimeters, respectively. Meanwhile, the clinical magnets in the donut and programming head could deactivate up to 8.0 and 7.0 centimeters, respectively (Table 1).Table 1Maximum distances, in centimeters, at which various magnets could deactivate the implanted cardioverter-defibrillatorMagnet typeDistance at which ICD deactivates (cm)Fitbit wristband2.4Apple Watch wristband2.0Donut magnet8.0Programming head7.0ICD = implanted cardioverter-defibrillator. Open table in a new tab DiscussionThe fitness tracker wristband magnets were considerably weaker than clinical-grade magnets; however, the magnetic field strength was still capable of deactivating the ICD at clinically relevant distances, as most devices are implanted subcutaneously. The implantable devices produced by all major manufacturers are potentially susceptible to this interference, as most of the devices utilize a magnet sensor. Older devices relied on a Reed switch, whereas newer devices may be equipped with alternative sensors including Hall-effect sensors or magnetosensitive resistors. Subcutaneous ICD devices may be also vulnerable, as their location of implantation allows closer interaction with the left wrist of the patient.While magnets could deactivate the ICD tachy-therapies, resulting in untreated sustained ventricular arrhythmia, the most feared complication on PPM devices is a switch to asynchronous pacing modes (DOO/VOO).6Jacob S. Panaich S.S. Maheshwari R. Hadded J.W. Padanilam B.J. John S.K. Clinical applications of magnets on cardiac rhythm management devices.Europace. 2011; 14: 1222-1230Google Scholar Such a switch could cause an R-on-T event, especially for those with intrinsic native rhythms, triggering a malignant arrhythmia.The manufacturers of these wristbands as well as the cardiac devices should include appropriate warnings in their user manuals and online resources. Some fitness tracker creators have issued appropriate warnings alongside their products. The Apple Watch user guide acknowledges that the wristband as well as charging apparatus are capable of interfering with ICDs and PPMs.7AppleApple Watch: User Guide. 2020..https://support.apple.com/guide/watch/important-safety-information-apdcf2ff54e9/watchosDate accessed: November 2, 2020Google ScholarConclusionWearable fitness tracker accessories can contain powerful magnets capable of interfering with ICD or PPM functions. Patients should be counseled on this and recommended to take appropriate precautions, such as choosing a nonmagnetic wristband, keeping magnetic wristbands at least 6 inches from the implanted device, and removing magnetic wristbands before going to bed. IntroductionThe magnet-activated switch in implanted cardiac devices, including cardioverter-defibrillators and permanent pacemakers (PPM), is susceptible to interference from consumer devices with built-in magnets. For example, a recent case report showed that a patient's implanted cardioverter-defibrillator (ICD) magnet mode became activated owing to interaction with his e-cigarette.1Shea J.B. Aguilar M. Sauer W. Tedrow U. Unintentional magnet reversion of an implanted cardiac defibrillator by an electronic cigarette.HeartRhythm Case Rep. 2020; 6: 121-123Google Scholar While testing has shown that cellular phones and smart watches themselves have minimal interference with cardiac devices,2Lacour P. Parwani A.S. Schuessler F. et al.Are contemporary smartwatches and mobile phones safe for patients with cardiovascular implantable electronic devices?.JACC Clin Electrophysiol. 2020; 6: 1158-1166Google Scholar this has failed to account for the magnets used in the wristband of smart watches and fitness trackers. Fitness trackers are capable of tracking heart rate, step count, and other variables of interest to fitness-minded consumers. In 2019, the company Fitbit, manufacturer of several different devices, sold nearly 16 million units.3Tankovska H. Fitbit device unit sales worldwide 2010-2019.https://www.statista.com/statistics/472591/fitbit-devices-sold/Date accessed: October 8, 2020Google Scholar The popular Apple Watch also features these capabilities, with Garmin and Samsung producing models as well. These products are lightweight and low-profile and sometimes sold with a built-in magnet-clasped wristband. Though this magnet is small, most manufacturers have adopted the magnetic element neodymium, which is known to interfere with device functions.4Wolber T. Ryf S. Binggeli C. et al.Potential interference of small neodymium magnets with cardiac pacemakers and implantable cardioverter-defibrillators.Heart Rhythm. 2007; 4: 1-4Google Scholar We investigated whether these magnetic wristbands had clinically relevant effects on ICD function through ex vivo testing.Key Teaching Points•Magnets used in the wristbands of fitness trackers and smart watches can interfere with implanted cardiac devices; however, this is not widely appreciated by manufacturers of the watches or the cardiac devices.•Possible complications include implanted cardioverter-defibrillator deactivation and permanent pacemaker mode switch.•Patients should be counseled on this risk and advised to keep their wristbands at least 6 inches away from their cardiac devices, and not to wear them to sleep.

Background Magnet wireless charging is being utilized increasingly in current generation smartphones. Apple's MagSafe is a proprietary wireless charging technology with an array of magnets that has the capacity to generate magnet fieldstrength >50 gauss (G). We hypothesize that there is clinically significant magnet interference caused by Apple's MagSafe technology on cardiac implantable electronic devices (CIED). Methods and Results This study has an in vivo and an ex vivo component. The in vivo component consists of consecutive patients who presented to the electrophysiology laboratory with previously implanted CIEDs. The iPhone 12 Pro Max was directly placed on the skin over the pocket of these patients and the effect was studied by device interrogation. For the ex vivo component of the study, CIEDs from major device companies were tested for magnetic interference caused by iPhone 12 Pro Max through unopened packages. We found that iPhone 12 Pro Max resulted in clinically identifiable magnet interference in 3/3 (100%) participants in vivo and in 8/11 (72.7%) devices ex vivo. Conclusions Apple's iPhone 12 Pro Max MagSafe technology can cause magnet interference on CIEDs and has the potential to inhibit lifesaving therapy.

BACKGROUND Lyme disease is a tick-borne illness caused by bacteria of the Borrelia genus, endemic to the northeastern region of the United States. It typically presents with fevers, myalgias, and erythema migrans, but it can result in disseminated symptoms if left untreated. Lyme carditis is a rare, but potentially fatal complication of Lyme disease, occurring in up to 4-10% of untreated cases. Typically, it presents with atrioventricular conduction abnormalities, which resolve with intravenous antibiotics and temporary pacing if indicated. Diverse cardiac pathology, however, has been associated with Lyme carditis, which may be underrecognized in practice. CASE REPORT A 34-year-old woman with no significant medical history presented with fatigue, dizziness, and shortness of breath, 2 weeks after camping in Rhode Island. Her presenting electrocardiogram demonstrated third-degree heart block. She was noted to have targetoid rashes on her left shoulder and breast on physical examination. On laboratory work-up, she was found to have positive Lyme total antibody enzyme immunoassay and positive Lyme western immunoblot. The findings were diagnostic for Lyme carditis. The patient's cardiac rhythm subsequently converted to slow atrial flutter with variable ventricular response unresponsive to antibiotic therapy. Given evidence suggesting that atrioventricular conduction was preserved, synchronized electrical cardioversion was pursued and was ultimately successful in rhythm conversion to normal sinus rhythm. CONCLUSIONS Although Lyme carditis is rare, this diagnosis should be of high clinical consideration in presentations of cardiac conduction abnormalities with acute onset and without other obvious cause, particularly in Lyme-endemic regions such as the northeastern United States.

Background and Aims: Cigarette Smoke (CS) is causally linked to the development of atherosclerosis. Tobacco harm reduction, by substituting cigarettes with less harmful products, is a complementary approach to the current strategies for smokers who would otherwise continue to smoke. The Tobacco Heating System (THS) is a novel tobacco product that heats tobacco instead of burning it, never allowing a higher temperature than 350°C, thereby preventing combustion and producing lower levels of toxicants.

Introduction: Over the past 10-15 years, there has been an increasing amount of evidence that frequent premature ventricular contractions (PVCs) are associated with the development of a reversible cardiomyopathy.Areas covered: This review considers current evidence of the association between PVCs and the development of cardiomyopathy, risk factors, and available treatment modalities based on available published literature.Expert commentary: The field is rapidly evolving, although evidence is based primarily on observational studies. Pharmacological therapy may suppress PVCs and lead to resolution of cardiomyopathy in many patients. In addition, catheter ablation has emerged as an effective treatment modality that has compared favorably to pharmacological antiarrhythmic therapy. The excellent outcome in successfully treated patients should prompt physicians to consider whether frequent PVCs may be a contributing factor in patients with heart failure.

Disturbances in plasma potassium concentration (pK) are well known risk factors for the development of cardiac arrhythmia. The aims of the present study were to evaluate the effect of hemodialysis on exercise pK dynamics and QT hysteresis, and whether QT hysteresis is associated with the pK decrease following exercise. Twenty-two end-stage renal disease patients exercised on a cycle ergometer with incremental work load before and after hemodialysis. ECG was recorded and pK was measured during exercise and recovery. During exercise, pK increased from 5.1 ± 0.2 to 6.1 ± 0.2 mM (mean ± SE; P < 0.0001) before hemodialysis and from 3.8 ± 0.1 to 5.1 ± 0.1 mM (P < 0.0001) after hemodialysis. After 2 min of recovery, pK had decreased to 5.0 ± 0.2 mM and 4.1 ± 0.1 mM (P < 0.0001) before and after hemodialysis, respectively. pK increase during exercise was accentuated after hemodialysis. The pK increase was negatively linearly correlated with pK before exercise (β = -0.21, R(2) = 0.23, P = 0.001). QT hysteresis was negatively linearly correlated with the decrease in pK during recovery (β = -28 ms/mM, R(2) = 0.36, P = 0.006). Thus, during recovery, low pK was associated with relatively longer QT interval. In conclusion, new major findings are an accentuated increase in pK during exercise after hemodialysis, an attenuated increase in pK in hyperkalemia, and an association between pK and QT interval adaptation during recovery. The acute pK shift after exercise may modulate QT interval adaptation and trigger cardiac arrhythmias.

K-depleted and control rats were anesthetized and infused with terbutalin. In controls, plasma K concentration (pK) decreased by 0.7 mM (P = 0.01). In moderate hypokalemia terbutalin-induced decrease in pK was reduced by 0.3 mM for each 1 mM decrease in pK (n = 8, R-2 = 0.82, P = 0.002) and by 0.2 mM for each 10 mmol/g wet wt. decrease in muscle K content (n = 8, R-2 = 0.66, P = 0.01). Hence, for baseline pK of 4, 3 and 2 mM, decrease in pK was 0.7, 0.4 and 0.1 mM, respectively. In severe hypokalemia (1.7 mM), terbutain induced no further reduction in pK. The combined infusion of insulin and terbutalin showed no additive effect. Normalization of pK by KCl infusion in severe hypokalemia immediately abolished protection against terbutalin induced further pK reduction. Hence, terbutalin clamped pK at around 4 mM, whereas it continued to increase to around 5 mM without terbutalin infusion. Major new findings are: Protection against terbutalin induced further reduction in pK in severe pre-existing hypokalemia (< 2 mM) and blunted but nevertheless severe further reduction in pK in more moderate preexisting hypokalemia; immediate abolishment of protection by normalization of pK; protection against additive reduction in pK by terbutalin and insulin in severe hypokalemia. It may be advisable to avoid hypokalemia when using beta adrenoceptor agonists and to maintain pK in the upper normal range if at the risk of arrhythmia.

Background: Postoperative atrial fibrillation is a common complication to cardiac surgery. Na,K-ATPase is of major importance for the resting membrane potential and action potential. The purpose of the present study was to evaluate the importance of Na,K-ATPase concentrations in human atrial biopsies and plasma potassium concentrations for the development of atrial fibrillation. Methods: Atrial myocardial biopsies were obtained from 67 patients undergoing open chest cardiac surgery. Na,K-ATPase was quantified using vanadate-facilitated 3H-ouabain binding. Plasma potassium concentration was measured with ion-selective electrode. Results: In patients with preoperative sinus rhythm, 3H-ouabain-binding site concentration was 16% higher in patients developing postoperative atrial fibrillation compared to patients maintaining sinus rhythm [302 ± 15 pmol/g wet weight (n = 20) vs. 261 ± 11 mmol/g wet weight (n = 33), p = 0.03]. Also with multivariable analysis, 3H-ouabain-binding site concentration was significantly associated with the development of atrial fibrillation. High increase in plasma potassium concentration during the perioperative period and surgery was associated with postoperative atrial fibrillation. Conclusions: The present study supports the increasing evidence of dysregulation of the potassium homeostasis as an important factor in the development of cardiac arrhythmias. High atrial Na,K-ATPase and sudden plasma potassium concentration increase may contribute to precipitate atrial fibrillation.

Summary Mannan-binding lectin (MBL) is a collectin plasma protein activating the lectin pathway of the complement system, enhancing opsonophagocytosis and modulating the cytokine response to inflammation. Deficiency of MBL, caused by structural mutations or promoter polymorphisms in the MBL2 gene, has been associated with increased susceptibility to infection and autoimmune disease. Thus, as infective endocarditis remains a severe disease requiring intensive and long-term treatment with antibiotics, we examined whether there was an association between MBL and clinical outcome in 39 well-characterized patients with infective endocarditis. Five patients (13%) had MBL concentrations < 100 µg/l and were considered MBL-deficient. This proportion was similar to that in a healthy control group of blood donors. Mortality 3 months after diagnosis was 20% in patients with MBL-deficiency and 9% in patients with normal MBL. The 5-year mortality was 80% and 25%, respectively. MBL-deficiency was on univariate survival statistics associated with significantly higher mortality on follow-up (P = 0·03). In conclusion, this is the first report of an association between MBL-deficiency and survival in infective endocarditis. The present observation is important, as replacement therapy in MBL-deficient patients is possible. For certain high-risk subgroups, it opens new perspectives for improvement of treatment and outcome in infective endocarditis.