Prevalence and incidence of patients with paroxysmal supraventricular tachycardia in the United States.

BACKGROUND: Paroxysmal supraventricular tachycardia (PSVT) encompasses a range of heart rhythm disorders leading to rapid heart rates. By virtue of its episodic nature, diagnosing PSVT is difficult and estimating incidence and prevalence on a population level is challenging. The objective of this study was to estimate the incidence and prevalence of PSVT in the United States (US) in contemporary practice. METHODS AND RESULTS: An observational retrospective longitudinal study using claims, enrollment, and demographic data from the IBM MarketScan® Commercial Research database (age < 65) and the Medicare Limited Data Set (age ≥ 65) from 2008 to 2016. Patients with a PSVT diagnosis code (ICD-9: 427.0; ICD-10: I47.1) on ≥2 outpatient, ≥1 emergency room, or ≥1 inpatient visit were considered as having PSVT. Patients with atrial fibrillation/atrial flutter (AF/AFL) were excluded from the initial analysis given the potential for misclassification. Incidence was estimated by assessing diagnoses made during year 5 of continuous enrollment. Finally, a sensitivity analysis was performed by including patients with both PSVT and AF/AFL diagnoses. Period prevalence and incidence rate were estimated to be 332.9 (323.2-342.9) and 57.8 (52.8-63.3) per 100 000 individuals, respectively, when excluding patients with AF/AFL. Projected to the 2018 US Census, prevalence and incidence are 1.26 million (1.21-1.30 million) and 188,981 (172,891-206,943), respectively. Including patients with AF/AFL, the prevalence may increase to 479.7 (467.9-491.8) with an incidence of 93.4 (86.9-100.5) per 100 000 individuals or a prevalence of 2.06 million (2.01-2.12 million). CONCLUSIONS: Approximately 1 in 300 people in the US had PSVT with the highest rates in older and female patients.

Outcomes following cardioversion for patients with cardiac amyloidosis and atrial fibrillation or atrial flutter.

Atrial arrhythmias commonly occur in patients with cardiac amyloidosis (CA), but there is limited data on safety or efficacy of cardioversion (DCCV) for management of these rhythms in CA. We identified 25 patients with CA (20 with transthyretin (TTR) and 5 with light-chain (AL) amyloidosis) at Duke University who underwent DCCV for atrial arrhythmias and documented procedural success, complications, and long-term morbidity and mortality. While DCCV successfully restored sinus rhythm in 96% of patients, 36% of patients experienced immediate procedural complications (primarily bradycardia and hypotension), 80% had recurrence of atrial arrhythmias at 1 year, and 52% died at 3 years, highlighting short-term safety concerns, long-term inefficacy, and poor prognosis associated with symptomatic atrial arrhythmias requiring DCCV in CA.

A care pathway for the cardiovascular complications of COVID-19: Insights from an institutional response.

The infection caused by severe acute respiratory syndrome coronavirus-2, or COVID-19, can result in myocardial injury, heart failure, and arrhythmias. In addition to the viral infection itself, investigational therapies for the infection can interact with the cardiovascular system. As cardiologists and cardiovascular service lines will be heavily involved in the care of patients with COVID-19, our division organized an approach to manage these complications, attempting to balance resource utilization and risk to personnel with optimal cardiovascular care. The model presented can provide a framework for other institutions to organize their own approaches and can be adapted to local constraints, resource availability, and emerging knowledge.

Implantable cardioverter-defibrillator lead revision following left ventricular assist device implantation.

INTRODUCTION: Lead dysfunction can lead to serious consequences including failure to treat ventricular tachycardia or fibrillation (VT/VF). The incidence and mechanisms of lead dysfunction following left ventricular assist device (LVAD) implantation are not well-described. We sought to determine the incidence, mechanisms, timing, and complications of right ventricular lead dysfunction requiring revision following LVAD implantation. METHODS: Retrospective observational chart review of all LVAD recipients with pre-existing implantable cardioverter-defibrillator (ICD) from 2009 to 2018 was performed including device interrogation reports, laboratory and imaging data, procedural reports, and clinical outcomes. RESULTS: Among 583 patients with an ICD in situ undergoing LVAD implant, the median (interquartile range) age was 62.5 (15.7) years, 21% were female, and the types of LVADs included HeartWare HVAD (26%), HeartMate II (52%), and HeartMate III (22%). Right ventricular lead revision was performed in 38 patients (6.5%) at a median (25th, 75th) of 16.4 (3.6, 29.2) months following LVAD. Mechanisms of lead dysfunction included macrodislodgement (n = 4), surgical lead injury (n = 4), recall (n = 3), insulation failure (n = 8) or conductor fracture (n = 7), and alterations in the lead-myocardial interface (n = 12). Undersensing requiring revision occurred in 22 (58%) cases. Clinical sequelae of undersensing included failure to detect VT/VF (n = 4) and pacing-induced torsade de pointes (n = 1). Oversensing occurred in 12 (32%) and sequelae included inappropriate antitachycardia pacing ([ATP], n = 8), inappropriate ICD shock (n = 6), and ATP-induced VT (n = 1). CONCLUSION: The incidence of right ventricular lead dysfunction following LVAD implantation is significant and has important clinical sequelae. Physicians should remain vigilant for lead dysfunction after LVAD surgery and test lead function before discharge.

Catheter ablation of atrial fibrillation in cardiac amyloidosis.

BACKGROUND: Cardiac amyloidosis is a progressive infiltrative disease involving deposition of amyloid fibrils in the myocardium and cardiac conduction system that frequently manifests with heart failure (HF) and arrhythmias, most frequently atrial fibrillation (AF), atrial flutter (AFL), and atrial tachycardia (AT). METHODS: We performed an observational retrospective study of patients with a diagnosis of cardiac amyloid who underwent catheter ablation at our institution between January 1, 2011 and December 1, 2018. Patient demographics, procedural characteristics, and outcomes were determined by manual chart review. RESULTS: A total of 13 catheter ablations were performed over the study period in patients with cardiac amyloidosis, including 10 AT/AF/AFL ablations and three atrioventricular nodal ablations. Left ventricular ejection fraction was lower at the time of AV node ablation than catheter ablation of AT/AF/AFL (23% vs 40%, P = .003). Cardiac amyloid was diagnosed based on the results of preablation cardiac MRI results in the majority of patients (n = 7, 70%). The HV interval was prolonged at 60 ± 15 ms and did not differ significantly between AV nodal ablation patients and AT/AF/AFL ablation patients (69 ± 18 ms vs 57 ± 14 ms, P = .36). The majority of patients undergoing AT/AF/AFL ablation had persistent AF (n = 7, 70%) and NYHA class II (n = 5, 50%) or III (n = 5, 50%) HF symptoms, whereas patients undergoing AV node ablation were more likely to have class IV HF (n = 2, 66%, P = .014). Arrhythmia-free survival in CA patients after catheter ablation of AT/AF/AFL was 40% at 1 year and 20% at 2 years. CONCLUSIONS: Catheter ablation of AT/AF/AFL may be a feasible strategy for appropriately selected patients with early to mid-stage CA, whereas AV node ablation may be more appropriate in patients with advanced-stage CA.

Electrical storm in patients with left ventricular assist devices: Risk factors, incidence, and impact on survival.

BACKGROUND: Ventricular arrhythmias (VAs) and electrical storm (ES) are recognized complications following left ventricular assist device (LVAD) implantation; however, their association with long term-outcomes remains poorly understood. OBJECTIVE: The purpose of this study was to describe the clinical impact of ES in a population of patients undergoing LVAD implantation at a quaternary care center in the United States. METHODS: This was an observational retrospective study of patients undergoing LVAD implantation from 2009 to 2020 at Duke University Hospital. The incidence of ES (≥3 sustained VA episodes over a 24-hour period without an identifiable reversible cause) was determined from patient records. Risk factors for ES were identified using multivariable Cox proportional hazards modeling. RESULTS: Among 730 patients undergoing LVAD implant, 78 (10.7%) developed ES at a median of 269 (interquartile range [IQR] 7-766) days following surgery. Twenty-seven patients (34.6%) developed ES within 30 days, while 51 (65.4%) presented with ES at a median 639 (IQR 281-1017) days after implant. Following ES, 41% of patients died within 1 year. Patients who developed ES were more likely to have a history of VAs, ventricular tachycardia ablation, antiarrhythmic drug use, and perioperative mechanical circulatory support around the time of LVAD implant than patients without ES. CONCLUSION: ES occurs in 1 in 10 patients after LVAD and is associated with higher mortality. Risk factors for ES include a history of VAs, VT ablation, antiarrhythmic drug use, and perioperative mechanical circulatory support. Optimal management of ES surrounding LVAD implant, including escalation of medical therapy, catheter ablation, or adjunctive sympatholytic therapies, remains uncertain.

Cardiac Implantable Electronic Devices: A Window Into the Evolution of Conduction Disease in Cardiac Amyloidosis.

OBJECTIVES: This study characterized the relationship between conduction disease and cardiac amyloidosis (CA) through longitudinal analysis of cardiac implantable electronic device (CIED) data. BACKGROUND: Bradyarrhythmias and tachyarrhythmias are commonly reported in CA and may precede a CA diagnosis, although the natural history of conduction disease in CA is not well-described. METHODS: Patients with CA (transthyretin amyloidosis cardiomyopathy [ATTR-CM] and light-chain amyloidosis [AL-CA]) and a CIED were identified within the Duke University Health System. Patient characteristics at the time of implantation, including demographics and data relevant to CA diagnosis, cardiac imaging, and CIED were recorded. CIED interrogations were analyzed for pacing and atrial fibrillation (AF) burden, activity level, lead parameters, and ventricular arrhythmia incidence and/or therapy. RESULTS: Thirty-four patients with CA (7 with AL-CA, 27 with ATTR-CM [78% with wild-type]; 82% men) with median age of 75 years and a mean ejection fraction of 42 ± 13% had a CIED implanted for bradycardia (65%) or prevention of sudden cardiac death (35%). CIED implantation preceded CA diagnosis in 14 patients (41%). Over a mean follow-up of 3.1 ± 4.0 years, right ventricular sensing amplitudes decreased but did not result in device malfunction; lead impedances and capture thresholds remained stable. Between post-implantation years 1 and 5, mean ventricular pacing increased from 56 ± 9% to 96 ± 1% (p = 0.003) and AF burden increased from 2 ± 1.3 to 17 ± 3 h/day (p = 0.0002). Ventricular arrhythmias were common (mean episodes per patient per year: 6.7 ± 2.3 [ATTR-CM] and 5.1 ± 3.2 [AL-CA]) but predominately nonsustained; only 1 patient with AL-CA required implantable cardioverter-defibrillator therapy. CONCLUSIONS: Longitudinal analysis of CIED data in patients with CA revealed progressive conduction disease, with high AF burden and eventual dependence on ventricular pacing, although lead parameters remained stable. Ventricular arrhythmias were common but predominantly nonsustained, particularly in ATTR-CM.

Cardiac Arrest in the Setting of Diffuse Coronary Ectasia: Perspectives on a Unique Ischemic Insult.

A 69-year-old man with a history of coronary artery ectasia, potentially resulting from an underlying heritable connective tissue disorder, presented with ventricular fibrillation. Despite medical management of ischemia, he developed recurrent ventricular tachycardia with poor neurological recovery. We highlight challenges in the management of coronary artery ectasia. (Level of Difficulty: Beginner.).

Cardiovascular Implantable Electronic Device Surgery Following Left Ventricular Assist Device Implantation.

OBJECTIVES: This study sought to determine the indications, characteristics, and outcomes of cardiovascular implantable electronic device (CIED) surgery in patients with LVAD. BACKGROUND: Many patients with a left ventricular assist device (LVAD) will require implantable cardioverter-defibrillator generator change or device revision or are candidates for de novo implantable cardioverter-defibrillator implantation following LVAD implantation. METHODS: We performed an observational retrospective study of all LVAD recipients who subsequently underwent CIED surgery at Duke University Hospital from 2009 to 2019. RESULTS: A total of 159 patients underwent CIED surgery following LVAD implantation, including generator change (n = 93), device revision (n = 38), and de novo implant (n = 28). The median (interquartile range) time from LVAD implantation to CIED surgery was 18.1 months (5.5 to 35.1 months). Pre-operative risk for infection was elevated in the overall cohort with a median (interquartile range) Prevention of Arrhythmia Device Infection Trial (PADIT) score of 7.0 (5.0 to 9.0). Pocket hematoma occurred in 21 patients (13.2%) following CIED surgery. Antimicrobial envelops were used in 43 patients (27%). Device infection due to CIED surgery occurred in 5 (3.1%) patients and occurred only in patients who developed post-operative pocket hematoma (p < 0.001). Mortality at 1 year following CIED surgery was 20% (n = 32). CONCLUSIONS: CIED surgery following LVAD implantation is associated with an increased risk for pocket hematoma and CIED infection. Further studies are needed to determine the risk-benefit ratio of CIED surgery in patients with LVADs.

The passive properties of muscle fibers are velocity dependent.

The passive properties of skeletal muscle play an important role in muscle function. While the passive quasi-static elastic properties of muscle fibers have been well characterized, the dynamic visco-elastic passive behavior of fibers has garnered less attention. In particular, it is unclear how the visco-elastic properties are influenced by lengthening velocity, in particular for the range of physiologically relevant velocities. The goals of this work were to: (i) measure the effects of lengthening velocity on the peak stresses within single muscle fibers to determine how passive behavior changes over a range of physiologically relevant lengthening rates (0.1-10Lo/s), and (ii) develop a mathematical model of fiber viscoelasticity based on these measurements. We found that passive properties depend on strain rate, in particular at the low loading rates (0.1-3Lo/s), and that the measured behavior can be predicted across a range of loading rates and time histories with a quasi-linear viscoelastic model. In the future, these results can be used to determine the impact of viscoelastic behavior on intramuscular stresses and forces during a variety of dynamic movements.

Computational models predict larger muscle tissue strains at faster sprinting speeds.

INTRODUCTION: Proximal biceps femoris musculotendon strain injury has been well established as a common injury among athletes participating in sports that require sprinting near or at maximum speed; however, little is known about the mechanisms that make this muscle tissue more susceptible to injury at faster speeds. PURPOSE: This study aimed to quantify localized tissue strain during sprinting at a range of speeds. METHODS: Biceps femoris long head (BFlh) musculotendon dimensions of 14 athletes were measured on magnetic resonance (MR) images and used to generate a finite-element computational model. The model was first validated through comparison with previous dynamic MR experiments. After validation, muscle activation and muscle-tendon unit length change were derived from forward dynamic simulations of sprinting at 70%, 85%, and 100% maximum speed and used as input to the computational model simulations. Simulations ran from midswing to foot contact. RESULTS: The model predictions of local muscle tissue strain magnitude compared favorably with in vivo tissue strain measurements determined from dynamic MR experiments of the BFlh. For simulations of sprinting, local fiber strain was nonuniform at all speeds, with the highest muscle tissue strain where injury is often observed (proximal myotendinous junction). At faster sprinting speeds, increases were observed in fiber strain nonuniformity and peak local fiber strain (0.56, 0.67, and 0.72 for sprinting at 70%, 85%, and 100% maximum speed). A histogram of local fiber strains showed that more of the BFlh reached larger local fiber strains at faster speeds. CONCLUSIONS: At faster sprinting speeds, peak local fiber strain, fiber strain nonuniformity, and the amount of muscle undergoing larger strains are predicted to increase, likely contributing to the BFlh muscle's higher injury susceptibility at faster speeds.

The effects of aponeurosis geometry on strain injury susceptibility explored with a 3D muscle model.

In the musculoskeletal system, some muscles are injured more frequently than others. For example, the biceps femoris longhead (BFLH) is the most commonly injured hamstring muscle. It is thought that acute injuries result from large strains within the muscle tissue, but the mechanism behind this type of strain injury is still poorly understood. The purpose of this study was to build computational models to analyze the stretch distributions within the BFLH muscle and to explore the effects of aponeurosis geometry on the magnitude and location of peak stretches within the model. We created a three-dimensional finite element (FE) model of the BFLH based on magnetic resonance (MR) images. We also created a series of simplified models with a similar geometry to the MR-based model. We analyzed the stretches predicted by the MR-based model during lengthening contractions to determine the region of peak local fiber stretch. The peak along-fiber stretch was 1.64 and was located adjacent to the proximal myotendinous junction (MTJ). In contrast, the average along-fiber stretch across all the muscle tissue was 0.95. By analyzing the simple models, we found that varying the dimensions of the aponeuroses (width, length, and thickness) had a substantial impact on the location and magnitude of peak stretches within the muscle. Specifically, the difference in widths between the proximal and distal aponeurosis in the BFLH contributed most to the location and magnitude of peak stretch, as decreasing the proximal aponeurosis width by 80% increased peak average stretches along the proximal MTJ by greater than 60% while slightly decreasing stretches along the distal MTJ. These results suggest that the aponeurosis morphology of the BFLH plays a significant role in determining stretch distributions throughout the muscle. Furthermore, this study introduces the new hypothesis that aponeurosis widths may be important in determining muscle injury susceptibility.

Perivascular cells along venules upregulate NG2 expression during microvascular remodeling.

OBJECTIVE: Recently the authors have shown that neuron-glial antigen 2 (NG2) is expressed by perivascular cells along arterioles and capillaries, but not along venules in quiescent rat mesenteric microvascular networks. To investigate how the spatial distribution of this proteoglycan changes during microvascular remodeling, the objective of this study was to characterize the expression of NG2 in adult rat mesenteric microvascular networks undergoing active remodeling. METHODS: The distribution of NG2 expression was evaluated in adult rat mesenteric microvascular networks. Tissues were harvested from 250 g, female, Sprague-Dawley rats at 1, 3, and 5 days poststimulation and double immunolabeled for NG2 and CD31 (endothelial cell marker). RESULTS: After 1 day, NG2 expression was observed along 27 +/- 11% of network draining venules (14-55 microm) and after 3 days, 59 +/- 10% of draining venules (13-59 microm) stained positive for the proteoglycan. By 5 days poststimulation, the percentage of network draining venules (18-59 microm) staining positive for NG2 returned to 18 +/- 7%, indicating a downregulation of the proteoglycan toward quiescent levels along larger-sized venules. CONCLUSIONS: The results suggest that NG2 proteoglycan expression is transiently upregulated along venules during microvascular remodeling, implicating NG2 as a marker of activated venules.