Quantification of Mechanical Characteristics of Conventional Steerable Ablation Catheters for Treatment of Atrial Fibrillation Using a Heart Phantom.

PURPOSE: Accurate and reliable catheter navigation is important in formation of adequate lesions during radiofrequency cardiac catheter ablation. To inform future device design efforts and to characterize the limitations of conventional devices, the focus of this study is to assess and quantify the mechanical performance of manual ablation catheters for pulmonary vein isolation procedures within a phantom heart model. METHODS: We measured three important metrics: accuracy of catheter tip navigation to target anatomical landmarks at the pulmonary veins (PVs), orientation of the catheter relative to the tissue at the targets, and the delivered force values and their stability and variations at those targets. A stereovision system was used for navigational guidance and to measure the catheter's tip position and orientation relative to the targets. To measure force, piezoelectric sensors were used which were integrated at the targets, whereby operators were instructed to stabilize the catheter to achieve a chosen reference force value. RESULTS: An overall positioning accuracy of 1.57 ± 1.71 mm was achieved for all targets. No statistical significance was observed in position accuracy between the right and left PVs (p = 0.5138). The orientation of the catheter relative to tissue surface was 41° ± 21° with no statistical significance between targets. The overall force stability was 41 ± 6 g with higher difficulty in force stabilization in the right compared to the left PV (40 ± 8 vs. 43 ± 2 g, p < 0.0001). CONCLUSION: Based on our results, future improvements to manual catheter navigation for ablation should focus on improving device performance in orientation control and improved force stability.

First reported case of a longevity overestimation error in the new Medtronic tablet-based device programmer.

With the advancement and miniaturization of mobile technologies, major device companies are replacing the traditional cardiac rhythm device programmers with smaller and more efficient tablet-based systems. As clinicians rely on data obtained from multitude of these systems, it is imperative that they provide consistent, reliable, and reproducible results. In this case report, we illustrate, for the first time, a major discrepancy between remote monitoring data, a conventional device programmer, and the new tablet-based Medtronic CareLink SmartSync Device Manager which erroneously overestimated the battery longevity in a pacemaker-dependent patient whose device had reached Recommended Replacement Time (RRT) status.

An Alarming Change: What Caused an Instance of Inappropriate Detection in a Wearable Cardioverter-defibrillator?

We describe the case of a patient who received cardiac resynchronization pacemaker therapy (CRT-P) incorporating bridge protection via a wearable cardioverter-defibrillator (WCD) while awaiting final evaluation for permanent placement of an implantable CRT device with defibrillation capabilities. In an attempt to mitigate symptoms of heart failure, reprogramming of the CRT-P with a V-V offset caused an unusual interaction and alarm from the WCD. This case highlights a unique interaction not previously reported and is clinically relevant to patients awaiting final evaluation for implantable defibrillator system placement.

Efficient approach to superior vena cava baffle stenosis following the Mustard procedure: Expanding the role of a mechanical rotating dilator sheath for lead extraction.

INTRODUCTION: In adult congenital patients with transposition of the great arteries originally treated with the Mustard (atrial switch) procedure, the most common reason for re-intervention is baffle stenosis. This may be exacerbated by permanent transvenous pacemaker lead placement across the baffle. CASE REPORT: A 47-year-old female status post Mustard procedure performed at 15 months old presented with a high-grade stenosis of the superior vena cava (SVC) baffle from the SVC to the left atrium, with a nonfunctional permanent pacemaker lead passing through the baffle. A mechanical rotating dilator sheath was used for attempted lead extraction, relieving the baffle stenosis almost completely as a secondary effect, before the placement of a 10 × 27 mm Visipro balloon-expandable stent in the SVC baffle. CONCLUSIONS: Use of the mechanical rotating dilator sheath is an evolving treatment strategy in adult congenital heart disease to minimize the risk of bleeding, trauma to surrounding structures, and death. Its ability to fully alleviate baffle stenosis even when full lead extraction is not feasible or is associated with significant procedural risk, further demonstrates its expanded role in this patient population. A multidisciplinary approach and great diligence must be employed to avoid potential complications.

What is the cost of non-response to cardiac resynchronization therapy? Hospitalizations and healthcare utilization in the CRT-D population.

BACKGROUND: Cardiac resynchronization therapy (CRT) is an effective treatment for heart failure (HF) with left ventricular systolic dysfunction and prolonged QRS interval. However, one third of patients do not benefit from treatment. This study compares the heart failure hospitalization (HFH) rates and corresponding costs between responders and non-responders to CRT. METHODS: At a single center in New Jersey, we enrolled patients with de novo CRT-D implants between January 2011 and July 2013. Medical history at implant and all subsequent hospitalizations were collected. A retrospective chart review of the cardiology visit at or closest to 12 months post-CRT implant was performed, and patients were classified into responders and non-responders. Universal billing records (UB-04), ICD-9-CM diagnoses, and procedure codes were used to determine whether each hospitalization was due to HF. For each heart failure hospitalization (HFH), an MS-DRG-based US national average Medicare reimbursement was determined. HFH rates and associated payor costs were compared between responders and non-responders using negative binomial regression and non-parametric bootstrapping (×10,000), respectively. RESULTS: CRT response was determined in 135 patients (n = 103 responders, n = 32 non-responders, average follow-up 1.4 years). Demographics, pre-implant HF characteristics, NYHA Class, QRS duration, ejection fraction (EF), left bundle branch block (LBBB) status, and co-morbidities were not statistically different between the two groups. The HFH rate was significantly lower in responders (0.43/patient year) compared to non-responders (0.96/patient year, IRR = 0.45, 95 % CI (0.23 0.90), P = 0.0197). Average US national Medicare reimbursement for the responder group (US$7205/patient year) was 48 % lower than that for the non-responder group (US$13,861/patient year, P = 0.035). CONCLUSION: In this single-center retrospective study, responders to CRT had significantly lower rates of post-implant heart failure hospitalization rate and reduced associated payor costs compared to non-responders. Therapies that increase CRT response rates can substantially reduce healthcare utilization.

Less with More: Hospitalization Cost and Event Rates with Quadripolar versus Bipolar CRT-D System.

BACKGROUND: This is a comparative effectiveness study for cardiac resynchronization therapy defibrillator (CRT-D) therapy enabled by quadripolar (QUAD) versus bipolar (BIP) left ventricular (LV) leads.  Heart failure (HF) hospitalization (HFH) rates, associated costs, and 30-day readmissions after index HFH were compared. METHODS: Patients with de novo LV leads implanted as part of a CRT-D system between January 2011 and August 2013 with ≥1-year follow-up were included. Medical history, dates, and locations of HFH were collected thereafter. Patients were divided based on LV lead model: QUAD or BIP. Universal billing records (UB-04) for each HFH and ICD-9-CM (International Classification of Diseases, Ninth Revision, Clinical Modification) diagnoses/procedure codes were used to classify hospitalizations as HF or non-HF and calculate concurrent U.S. national-average medicare reimbursement. Rates, associated payer costs, and 30-day readmissions were then compared using nonparametric bootstrapping. RESULTS: Baseline characteristics (N = 69 QUAD and N = 56 BIP) were similar. The inpatient HFH for the QUAD group (0.20/patient-year) was lower than the BIP group (0.31/patient-year, incidence rate ratio [IRR] = 0.62, P = 0.036). The overall HFH rate for the inpatient or outpatient setting for QUAD (0.29/patient-year) was lower than the BIP group (0.42/patient-year, IRR = 0.69, P = 0.055). Average cost of HFH in QUAD ($4,428/patient-year) was lower than BIP ($7,354/patient-year), a 39.8% cost reduction (P = 0.026). The 30-day readmission rate was also lower in QUAD compared to BIP (19% vs 28%, IRR = 0.68, P = 0.18). CONCLUSION: This U.S. economic comparative study demonstrated that QUAD exhibited lower postimplant inpatient HFH rates and reduced healthcare utilization compared to BIP systems.

Cardiac positron emission tomography enhances prognostic assessments of patients with suspected cardiac sarcoidosis.

OBJECTIVES: This study sought to relate imaging findings on positron emission tomography (PET) to adverse cardiac events in patients referred for evaluation of known or suspected cardiac sarcoidosis. BACKGROUND: Although cardiac PET is commonly used to evaluate patients with suspected cardiac sarcoidosis, the relationship between PET findings and clinical outcomes has not been reported. METHODS: We studied 118 consecutive patients with no history of coronary artery disease, who were referred for PET, using [(18)F]fluorodeoxyglucose (FDG) to assess for inflammation and rubidium-82 to evaluate for perfusion defects (PD), following a high-fat/low-carbohydrate diet to suppress normal myocardial glucose uptake. Blind readings of PET data categorized cardiac findings as normal, positive PD or FDG, positive PD and FDG. Images were also used to identify whether findings of extra-cardiac sarcoidosis were present. Adverse events (AE)-death or sustained ventricular tachycardia (VT)-were ascertained by electronic medical records, defibrillator interrogation, patient questionnaires, and telephone interviews. RESULTS: Among the 118 patients (age 52 ± 11 years; 57% males; mean ejection fraction: 47 ± 16%), 47 (40%) had normal and 71 (60%) had abnormal cardiac PET findings. Over a median follow-up of 1.5 years, there were 31 (26%) adverse events (27 VT and 8 deaths). Cardiac PET findings were predictive of AE, and the presence of both a PD and abnormal FDG (29% of patients) was associated with hazard ratio of 3.9 (p < 0.01) and remained significant after adjusting for left ventricular ejection fraction (LVEF) and clinical criteria. Extra-cardiac FDG uptake (26% of patients) was not associated with AE. CONCLUSIONS: The presence of focal PD and FDG uptake on cardiac PET identifies patients at higher risk of death or VT. These findings offer prognostic value beyond Japanese Ministry of Health and Welfare clinical criteria, the presence of extra-cardiac sarcoidosis and LVEF.

Contemporary approaches to persistent atrial fibrillation.

Atrial fibrillation (AF) is currently the most commonly treated cardiac arrhythmia. It is generally a progressive disease, often more difficult to control as electromechanical remodeling alters the underlying substrate. Patients typically evolve from infrequent, self-terminating episodes, to more frequent and sustained events. In addition, atrial remodeling may make sinus rhythm more challenging to achieve. Although an ablation strategy limited to pulmonary vein isolation may be curative in those with paroxysmal AF, a more extensive approach is often required in those with persistent AF. This article discusses the current approaches and most recent advances in the ablation of persistent and long-standing persistent AF.

The use of ω-3 poly-unsaturated fatty acids in heart failure: a preferential role in patients with diabetes.

PURPOSE: To review the evidence for a beneficial effect of ω-3 PUFAs in heart failure (HF) and its co-morbidities, their possible preferential effect in diabetes and the potential mechanism for their benefit. METHODS: We summarize the clinical studies which investigated the use of ω-3 PUFAs in patients with HF with an emphasis on diabetes. We briefly summarize the evidence for an effect of ω-3 PUFAs in patients with coronary artery disease (CAD), atrial fibrillation (AF) and ventricular arrhythmias. We also discuss the proposed mechanisms of ω-3 PUFA action in cardiovascular diseases. RESULTS: While there is emerging evidence for a beneficial effect of ω-3 PUFA supplementation in patients with HF, the evidence for other indications have been variable and conflicting. In HF patients with diabetes, ω-3 PUFAs may have a preferential therapeutic benefit. Randomized controlled trials did not show considerable beneficial effects of ω-3 PUFAs in other conditions such as CAD and AF. In a diabetic and insulin-resistant state, ω-3 PUFAs bind to the G-protein coupled receptor, GPR120, resulting in reduced cytokine production from inflammatory macrophages and improved signaling in adipocytes, leading to a reduction in insulin resistance. CONCLUSIONS: There is promising evidence showing that use of ω-3 PUFA supplementation improves clinical outcomes of HF patients with diabetes. Further clinical trials are needed in this regard.

Atrial fibrillation and heart failure in the elderly.

Atrial fibrillation (AF) is a common clinical problem in elderly patients and especially in those with heart failure (HF). It is a major risk factor for serious cardiovascular events, such as stroke, HF and premature death. Both the prevalence and incidence of AF increase with age and its prevalence in the United States are estimated at more than 2.2 million, with nearly 75% of patients aged >65 years. Aging-related atrial remodeling with fibrosis, dilation and mitochondrial DNA mutations predispose elderly patients to AF. Current management options for AF, including rate control and anticoagulation therapy, can be successfully applied to the elderly population. New antiarrhythmic and anticoagulation medications such as dronedarone and dabigatran, respectively, can impact the approach to therapy in the elderly. Non-pharmacological options such as catheter-based ablation have also gained prominence and have been incorporated into the guidelines for management of AF. However, more trials in the elderly and very elderly segments are needed to clarify the safety and long-term efficacy of the new treatment options.

A novel mutation in the RYR2 gene leading to catecholaminergic polymorphic ventricular tachycardia and paroxysmal atrial fibrillation: dose-dependent arrhythmia-event suppression by ß-blocker therapy.

Catecholaminergic polymorphic ventricular tachycardia (CPVT) is a genetic condition that presents with exercise-induced polymorphic arrhythmias. We describe a case report of a 25-year-old woman who had a cardiac arrest due to ventricular fibrillation. Genetic analysis revealed a novel missense mutation in exon 90 of the ryanodine receptor (RyR2) gene resulting in substitution of arginine for serine at residue 4153 (S4153R). The patient received an implantable cardioverter-defibrillator and low-dose ß-blocker therapy. She had recurrent polymorphic ventricular arrhythmias treated with appropriate cardioverter-defibrillator shocks and paroxysmal atrial fibrillation. Titration of ß-blocker to a much higher dose suppressed further episodes of ventricular arrhythmia and paroxysmal atrial fibrillation, resulting in reduction in device therapies.

Vascular matrix remodeling in patients with bicuspid aortic valve malformations: implications for aortic dilatation.

BACKGROUND: Patients with bicuspid aortic valve malformations are at an increased risk of aortic dilatation, aneurysm formation, and dissection. Vascular tissues with deficient fibrillin-1 microfibrils release matrix metalloproteinases, enzymes that weaken the vessel wall by degrading elastic matrix components. In bicuspid aortic valve disease a deficiency of fibrillin-1 and increased matrix metalloproteinase matrix degradation might result in aortic degeneration and dilatation. METHODS: Samples of the pulmonary artery and aorta were obtained from surgical patients with bicuspid aortic valves (n = 21) and tricuspid aortic valves (n = 16). RESULTS: Fibrillin-1 content was reduced in bicuspid aortic valve aortas compared with that seen in tricuspid aortic valve aortas (P =.001), whereas the associated matrix components, elastin and collagen, were unchanged (P =.51 and P =.21). Reductions of aortic fibrillin-1 content were independent of valve function and patient age. Compared with tricuspid aortic valve aorta, matrix metalloproteinase 2 activity was increased more than 2-fold in bicuspid aortic valve aortas (P =.04) and correlated positively with aortic diameter (r = 0.74, P =.05). Matrix metalloproteinase 9 activity was not significantly different. Fibrillin-1 content was also reduced in the pulmonary arteries of patients with bicuspid aortic valves (P =.06), suggesting a systemic deficiency of fibrillin-1. Promatrix metalloproteinase 2 was increased (P =.04), reflecting an increased production of matrix metalloproteinase 2 in these fibrillin-1-deficient tissues, whereas active matrix metalloproteinase 2 and matrix metalloproteinase 9 species were unchanged, and correspondingly, the pulmonary arteries were not dilated. CONCLUSIONS: Deficient fibrillin-1 content in the vasculature of patients with bicuspid aortic valves might trigger matrix metalloproteinase production, leading to matrix disruption and dilatation. This process of vascular matrix remodeling in patients with bicuspid aortic valves offers novel therapeutic targets to prevent the aortic degeneration and dilatation characteristic of this disease.

Fibroblast growth factor 2 regulation of mitral valve interstitial cell repair in vitro.

OBJECTIVE: Because elongated mitral valve interstitial cells have features of myofibroblasts, it is likely that these cells are essential for the repair of injured valve leaflets. We characterized the cellular morphology and pattern of repair of these interstitial cells in wounds produced in vitro and tested the hypothesis that fibroblast growth factor 2 enhances interstitial cell repair. METHODS: Mitral valve interstitial cells were plated onto glass coverslips, reached confluence after 1 week, and were wounded by passage of a spatula along the center of a monolayer, which created a linear wound with two edges. The wounds were observed from 0 to 96 hours by phase-contrast microscopy. Wounds were also fixed at 0, 2, and 24 hours and stained for fibroblast growth factor 2 and fibroblast growth factor receptor 1 by means of immunofluorescence and laser confocal microscopy. RESULTS: Cells in confluent monolayers and in the monolayer behind the wound edge formed a multilayered orthogonal pattern of elongated cells similar to fibroblasts. Cells along the wound edge migrated into the wound after 4 hours, and at 24 hours single cells with prominent lamellipodia and tails were present within the wound. There was overlapping of cells as well, similar to smooth muscle cells. Fibroblast growth factor 2 and fibroblast growth factor receptor 1 were present in the cells of the undisturbed confluent monolayer. They were upwardly regulated relative to the unwounded monolayer in the cells along the wound edge at 2 hours and in the monolayer behind the wound edge at 24 hours. In single cells that migrated into the wound, fibroblast growth factor 2 and fibroblast growth factor receptor 1 were prominent. Fibroblast growth factor 2 showed a 6-fold increase in concentration relative to unwounded cultures in conditioned medium from wounded cultures at 2 hours after wounding. Addition of a neutralizing antibody to fibroblast growth factor 2 significantly delayed wound closure at 24 to 96 hours. Addition of exogenous fibroblast growth factor 2 to cultures at the time of wounding did not enhance wound repair. CONCLUSION: Mitral valve interstitial cells have the ability to repair wounds, and fibroblast growth factor 2 is a modulator of these repair processes.