Percutaneous VDD leadless pacer implant post recent bioprosthetic tricuspid valve replacement for infective endocarditis.

In January 2020, the first Medtronic VDD leadless pacemaker Micra AV was approved by FDA to treat patients with advanced AV block, based on the encouraging results from the Micra Atrial tRacking using a Ventricular accELerometer 2 (MARVEL 2). There is reassuring data about safety and short-term outcomes of traditional leadless pacemaker implant after recent surgical tricuspid valve replacement, but only few cases are reported in literature. No data was found regarding AV Micra implant safety and outcomes in patients following bioprosthetic tricuspid valve replacement as of today. Our patient is a 44-year-old gentleman with history of IV drug use who recently underwent tricuspid replacement with bioprosthesis for infective endocarditis complicated by postsurgical heart block, acute kidney insufficiency requiring hemodialysis, persistent bacteremia and candidemia, and progressive failure of the epicardial pacing wires. Given the elevated infective risk, the decision of attempting leadless pacer implant through the bioprosthetic valve was taken and our patient underwent successful Micra AV implant on postoperative day 30. To our knowledge, this is the first AV Micra placement following bioprosthetic tricuspid valve replacement. The uneventful procedure and the encouraging short-term device follow-up results seem to confirm the relative safety of this device in treating advanced atrioventricular conduction disorders in patients at elevated infective risk.

Yield and cost-effectiveness of tilt table tests combined with video-EEG.

To study the outcomes of a series of consecutive tilt table tests combined with video-EEG (TTVE) at a single center, and assess their cost-effectiveness compared with other neurophysiological tests. We retrospectively reviewed medical records of patients who underwent TTVE studies between March 1st, 2013 to April 1st, 2018. Detailed clinical history, including patient demographics, reasons for referral, anti-seizure medications, and neurophysiological studies obtained prior to the TTVE studies were extracted from chart reviews. The fee for each neurophysiological test was identified from the Centers for Medicare & Medicaid Services. Fifty-two patients underwent TTVE studies. Thirteen patients (25%) were diagnosed with vasovagal syncope, two (3.8%) were diagnosed with postural orthostatic tachycardia syndrome, and three (5.8%) had psychogenic non-epileptic events during the test. Four out of 12 patients stopped anti-seizure medication(s) after the TTVE. Prior to referral for TTVE, an average of $3,748 per person was spent on neurophysiological tests, which were inconclusive. The average fee for one TTVE test was $535.32, and the fee per test affecting diagnosis or management (defined as the cost divided by the yield of the test) was $1,547. The TTVE test is cost-effective in evaluating refractory episodes of loss of consciousness, atypical of epileptic seizures. In addition to diagnosing syncope, TTVE can be valuable in identifying psychogenic events.

Outcomes of Acute Conduction Abnormalities Following Transcatheter Aortic Valve Implantation With a Balloon Expandable Valve and Predictors of Delayed Conduction System Abnormalities in Follow-up.

Transcatheter aortic valve implantation (TAVI) is an acceptable treatment for severe aortic stenosis in high or intermediate risk patients. Conduction abnormalities are a known complication of TAVI. Most abnormalities occur perioperatively but can develop later. The predictors of delayed conduction abnormalities are unknown. Patients who underwent TAVI at our institution were reviewed. Patients with a pre-existing pacemaker were excluded. Baseline, in-hospital, and 30-day follow-up ECGs were reviewed. Patient and procedural characteristics were analyzed to look for predictors of acute and delayed abnormalities. Ninety-eight patients were included. All valves implanted were balloon expandable, most commonly SAPIEN S3 (78%). Thirty-seven (37.7%) patients developed abnormalities before discharge. Of these patients, 20 (57.1%) had complete resolution at 30-day follow-up. No patients with new conduction abnormalities during hospitalization had additional abnormalities at 30-day follow-up. Five (5.1%) patients developed new conduction abnormalities following discharge. Overall, 22 (22.4%) patients had conduction abnormalities at 30-day follow-up which were not present at baseline. Predilatation (p = 0.003), higher ratios of balloon (p = 0.03) or valve (p = 0.05) size to left ventricular outflow tract, and previous myocardial infarction (p = 0.034) were predictive of acute conduction abnormalities. Baseline right bundle branch block (p = 0.002), longer baseline (p <0.001) and discharge (p = 0.004) QRS duration, moderate, or severe aortic insufficiency (p = 0.002) and atrial fibrillation (p = 0.031) were predictors of new conduction abnormalities after discharge. In conclusion, most new in-hospital conduction abnormalities resolve by 30-day follow-up. In-hospital conduction abnormalities are related to technical aspects of TAVI while delayed conduction abnormalities are related to baseline conduction system disease.

Rate Versus Rhythm Control in Patients with Normal to Mild Left Atrial Enlargement: Insights from the AFFIRM Trial.

BACKGROUND: Atrial fibrillation is the most commonly encountered sustained arrhythmia and is associated with significant morbidity and mortality. Several trials have demonstrated that no mortality benefit exists when choosing a rhythm-control strategy over a rate-control strategy, with some trials suggesting an increase in mortality. Using the AFFIRM trial database we sought to determine the effect of rhythm control strategy in patients with normal or mild atrial enlargement. METHODS: AFFIRM Trial database was used to evaluate the effect of rhythm-control strategy compared to rate-control strategy in a subgroup of patients with normal to mild left atrial (LA) enlargement. The primary outcome measures of this study were all-cause mortality, cardiovascular mortality, non-cardiovascular mortality, and hospitalization/ED visit. RESULTS: We identified a subgroup of subjects from the AFFIRM trial with normal or mild LA enlargement (n=2022 of 4060 total subjects). Subjects in the rhythm-control group(n= 1022) had an increased risk of all-cause mortality by 34% (RR 1.34, 95% CI 1.08-1.67; P=0.007) and hospitalization/ED visits by 10% (RR 1.10, 95% CI 1.05-2.16; P=<0.001) compared to rate control group(n= 1000). CONCLUSION: This study demonstrated that rhythm-control strategy increases the risk of mortality and hospitalization in a subgroup of patients with normal to mild atrial enlargement compared to rate-control strategy. Amiodarone use in this subgroup of patients likely drove these findings.

Selective autonomic stimulation of the AV node fat pad to control rapid post-operative atrial arrhythmias.

Junctional ectopic tachycardia (JET) and atrial fibrillation (AF) occur in patients recovering from open-heart surgery (OHS). Pharmacologic treatment is used for the control of post-operative atrial arrhythmias (POAA), but is associated with side effects. There is a need for a reversible, modulated solution to rate control. We propose a non-pharmacologic technique that can modulate AV nodal conduction in a selective fashion. Ten mongrel dogs underwent OHS. Stimulation of the anterior right (AR) and inferior right (IR) fat pad (FP) was done using a 7-pole electrode. The IR was more effective in slowing the ventricular rate (VR) to AF (52 +/- 20 vs. 15 +/- 10%, p = 0.003) and JET (12 +/- 7 vs. 0 +/- 0%, p = 0.02). Selective site stimulation within a FP region could augment the effect of stimulation during AF (57 +/- 20% (maximum effect) vs. 0 +/- 0% (minimum effect), p<0.001). FP stimulation at increasing stimulation voltage (SV) demonstrated a voltage-dependent effect (8 +/- 14% (low V) vs. 63 +/- 17 (high V) %, p<0.001). In summary, AV node fat pad stimulation had a selective effect on the AV node by decreasing AV nodal conduction, with little effect on atrial activity.

Autofluorescence hyperspectral imaging of radiofrequency ablation lesions in porcine cardiac tissue.

Radiofrequency ablation (RFA) is a widely used treatment for atrial fibrillation, the most common cardiac arrhythmia. Here, we explore autofluorescence hyperspectral imaging (aHSI) as a method to visualize RFA lesions and interlesional gaps in the highly collagenous left atrium. RFA lesions made on the endocardial surface of freshly excised porcine left atrial tissue were illuminated by UV light (365 nm), and hyperspectral datacubes were acquired over the visible range (420-720 nm). Linear unmixing was used to delineate RFA lesions from surrounding tissue, and lesion diameters derived from unmixed component images were quantitatively compared to gross pathology. RFA caused two consistent changes in the autofluorescence emission profile: a decrease at wavelengths below 490 nm (ascribed to a loss of endogenous NADH) and an increase at wavelengths above 490 nm (ascribed to increased scattering). These spectral changes enabled high resolution, in situ delineation of RFA lesion boundaries without the need for additional staining or exogenous markers. Our results confirm the feasibility of using aHSI to visualize RFA lesions at clinically relevant locations. If integrated into a percutaneous visualization catheter, aHSI would enable widefield optical surgical guidance during RFA procedures and could improve patient outcome by reducing atrial fibrillation recurrence.

Seeing the Invisible: Revealing Atrial Ablation Lesions Using Hyperspectral Imaging Approach.

BACKGROUND: Currently, there are limited means for high-resolution monitoring of tissue injury during radiofrequency ablation procedures. OBJECTIVE: To develop the next generation of visualization catheters that can reveal irreversible atrial muscle damage caused by ablation and identify viability gaps between the lesions. METHODS: Radiofrequency lesions were placed on the endocardial surfaces of excised human and bovine atria and left ventricles of blood perfused rat hearts. Tissue was illuminated with 365nm light and a series of images were acquired from individual spectral bands within 420-720nm range. By extracting spectral profiles of individual pixels and spectral unmixing, the relative contribution of ablated and unablated spectra to each pixel was then displayed. Results of spectral unmixing were compared to lesion pathology. RESULTS: RF ablation caused significant changes in the tissue autofluorescence profile. The magnitude of these spectral changes in human left atrium was relatively small (< 10% of peak fluorescence value), yet highly significant. Spectral unmixing of hyperspectral datasets enabled high spatial resolution, in-situ delineation of radiofrequency lesion boundaries without the need for exogenous markers. Lesion dimensions derived from hyperspectral imaging approach strongly correlated with histological outcomes. Presence of blood within the myocardium decreased the amplitude of the autofluorescence spectra while having minimal effect on their overall shapes. As a result, the ability of hyperspectral imaging to delineate ablation lesions in vivo was not affected. CONCLUSIONS: Hyperspectral imaging greatly increases the contrast between ablated and unablated tissue enabling visualization of viability gaps at clinically relevant locations. Data supports the possibility for developing percutaneous hyperspectral catheters for high-resolution ablation guidance.

Visualization of epicardial cryoablation lesions using endogenous tissue fluorescence.

BACKGROUND: Percutaneous cryoballoon ablation is a commonly used procedure to treat atrial fibrillation. One of the major limitations of the procedure is the inability to directly visualize tissue damage and functional gaps between the lesions. We seek to develop an approach that will enable real-time visualization of tissue necrosis during cryo- or radiofrequency ablation procedures. METHODS AND RESULTS: Cryoablation of either blood-perfused or saline-perfused hearts was associated with a marked decrease in nicotinamide adenine dinucleotide (NADH) fluorescence, leading to a 60% to 70% loss of signal intensity at the lesion site. The total lesion area observed on the NADH channel exhibited a strong correlation with the area identified by triphenyl tetrazolium staining (r=0.89, P<0.001). At physiological temperatures, loss of NADH became visually apparent within 26±8 s after detachment of the cryoprobe from the epicardial surface and plateaued within minutes after which the boundaries of the lesions remained stable for several hours. The loss of electrical activity within the cryoablation site exhibited a close spatial correlation with the loss of NADH (r=0.84±0.06, P<0.001). Cryoablation led to a decrease in diffuse reflectance across the entire visible spectrum, which was in stark contrast to radiofrequency ablation that markedly increased the intensity of reflected light at the lesion sites. CONCLUSIONS: We confirmed the feasibility of using endogenous NADH fluorescence for the real-time visualization of cryoablation lesions in blood-perfused cardiac muscle preparations and revealed similarities and differences between imaging cryo- and radiofrequency ablation lesions when using ultraviolet and visible light illumination.

Nonpharmacologic control of postoperative supraventricular arrhythmias using AV nodal fat pad stimulation in a young animal open heart surgical model.

BACKGROUND: Supraventricular arrhythmias (junctional ectopic tachycardia [JET] and atrial tachyarrhythmias) frequently complicate recovery from open heart surgery in children and can be difficult to manage. Medical treatment of JET can result in significant morbidity. Our goal was to develop a nonpharmacological approach using autonomic stimulation of selective fat pad (FP) regions of the heart in a young canine model of open heart surgery to control 2 common postoperative supraventricular arrhythmias. METHODS AND RESULTS: Eight mongrel dogs, varying in age from 5 to 8 months and weighting 22±4 kg, underwent open heart surgery replicating a nontransannular approach to tetralogy of Fallot repair. Neural stimulation of the right inferior FP was used to control the ventricular response to supraventricular arrhythmias. Right inferior FP stimulation decreased baseline AV nodal conduction without altering sinus cycle length. AV node Wenckebach cycle length prolonged from 270±33 to 352±89 ms, P=0.02. Atrial fibrillation occurred in 7 animals, simulating a rapid atrial tachyarrhythmias. FP stimulation slowed the ventricular response rate from 166±58 to 63±29 beats per minute, P<0.001. Postoperative JET occurred in 7 dogs. FP stimulation slowed the ventricular rate during postoperative JET from 148±31 to 106±32 beats per minute, P<0.001, and restored sinus rhythm in 7/7 dogs. CONCLUSIONS: Right inferior FP stimulation had a selective effect on the AV node, and slowed the ventricular rate during postoperative JET and atrial tachyarrhythmias in our young canine open heart surgery model. FP stimulation may be a useful new technique for managing children with JET and atrial tachyarrhythmias.

Newly created animal model of human postoperative junctional ectopic tachycardia.

OBJECTIVE: Junctional ectopic tachycardia complicates the postoperative recovery from open heart surgery in children. The reported risk factors include younger age, prolonged cardiopulmonary bypass times, and administration of inotropic agents. Junctional ectopic tachycardia occurs early after open heart surgery, in the setting of relative postoperative sinus node dysfunction, and exhibits QRS morphology consistent with an origin from the atrioventricular node or proximal conduction system. Our goal was to develop a reproducible animal model for postoperative junctional ectopic tachycardia. METHODS: Eleven pigs, aged 2 to 4 months, underwent open heart surgery after induction of general anesthesia. Electrodes were sewn to the left atrium and right ventricle. RESULTS: Sinus node dysfunction was created using clamp crushing without or with radiofrequency ablation (successful in 1 of 5 pigs) or sinus node removal (successful in 4 of 4). After prolonged cardiopulmonary bypass (>120 minutes) alone and with isoproterenol infusion, no spontaneous junctional ectopic tachycardia developed. Junctional ectopic tachycardia or fascicular tachycardia could be initiated after either slow atrioventricular nodal pathway ablation and/or digoxin administration. Junctional ectopic tachycardia occurred in 8 of 9 pigs (mean ventricular rate, 171 ± 32 bpm), and fascicular tachycardia occurred in 9 of 9 pigs (mean ventricular rate, 187 ± 39 bpm). His and right bundle recordings confirmed the conduction system origin. CONCLUSIONS: Experimental junctional ectopic tachycardia or fascicular tachycardia can occur in the intraoperative setting of sinus node dysfunction, prolonged cardiopulmonary bypass, and enhanced conduction system automaticity. Conduction system automaticity occurred after either physical injury (ablation or tricuspid valve stretch) or measures to augment the transient inward current of the conduction system (isoproterenol and digoxin). This animal model can serve as the basis to assess new treatments of postoperative junctional ectopic tachycardia.

Use of endogenous NADH fluorescence for real-time in situ visualization of epicardial radiofrequency ablation lesions and gaps.

Radiofrequency ablation (RFA) aims to produce lesions that interrupt reentrant circuits or block the spread of electrical activation from sites of abnormal activity. Today, there are limited means for real-time visualization of cardiac muscle tissue injury during RFA procedures. We hypothesized that the fluorescence of endogenous NADH could be used as a marker of cardiac muscle injury during epicardial RFA procedures. Studies were conducted in blood-free and blood-perfused hearts from healthy adult Sprague-Dawley rats and New Zealand rabbits. Radiofrequency was applied to the epicardial surface of the heart using a 4-mm standard blazer ablation catheter. A dual camera optical mapping system was used to monitor NADH fluorescence upon ultraviolet illumination of the epicardial surface and to record optical action potentials using the voltage-sensitive probe RH237. Epicardial lesions were seen as areas of low NADH fluorescence. The lesions appeared immediately after ablation and remained stable for several hours. Real-time monitoring of NADH fluorescence allowed visualization of viable tissue between the RFA lesions. Dual recordings of NADH and epicardial electrical activity linked the gaps between lesions to postablation reentries. We found that the fluorescence of endogenous NADH aids the visualization of injured epicardial tissue caused by RFA. This was true for both blood-free and blood-perfused preparations. Gaps between NADH-negative regions revealed unablated tissue, which may promote postablation reentry or provide pathways for the conduction of abnormal electrical activity.

Severe tricuspid valve stenosis secondary to pacemaker leads presenting as ascites and liver dysfunction: a complex problem requiring a multidisciplinary therapeutic approach.

Tricuspid stenosis secondary to ventricular pacemaker leads is uncommon. We present a unique case of iatrogenic tricuspid stenosis secondary to fusion of the valve leaflets to transvenous implanted pacing leads. This occurred in an adult with childhood repaired Tetralogy of Fallot and high grade surgical heart block following multiple pacemaker procedures. The case was complicated by superior vena cava (SVC) and innominate vein stenosis secondary to implanted pacing leads, severe tricuspid valve (TV) stenosis, perforation of the heart by one of the implanted transvenous ventricular pacing leads, prolapse of the transvenous atrial pacing lead into the right ventricle, and unusual coronary sinus anatomy. We describe a multidisciplinary approach to management.

Internet diagnosis of digitalis toxicity.

A 65-year-old male with an ischaemic cardiomyopathy and an implantable cardioverter defibrillator got a shock at home. A web-based monitoring system was used to check his device, and the interrogation showed that he had had several episodes of ventricular fibrillation and new onset of complete heart block that required back-up pacing by his defibrillator. The combination of enhanced automaticity (frequent premature ventricular complexes and ventricular arrhythmias) and impaired conduction (heart block) are the hallmarks of digitalis toxicity. Paramedics were called and the patient was brought to the emergency room where he was confirmed to have digitalis toxicity and was quickly treated with digoxin-specific Fab antibody fragments. Web-based monitoring systems helped in the diagnosis of this potentially lethal drug toxicity.

Assessing the direct costs of treating nonvalvular atrial fibrillation in the United States.

OBJECTIVE: To determine the health-care resource use and costs attributable to treating atrial fibrillation (AF) in the United States. METHODS: Retrospective analyses of three federally funded US databases (2001 data): 1) hospital inpatient stays (the Healthcare Cost and Utilization Project [HCUP]); 2) physician office visits (the National Ambulatory Medical Care Survey [NAMCS]); and 3) emergency department (ED) and hospital outpatient department visits (OPD) (the National Hospital Ambulatory Medical Care Survey [NHAMCS]). Identification of AF medical encounters was based on occurrence of AF-specific International Classification of Diseases (9th Edition)--Clinical Modification (ICD-9-CM) diagnosis code 427.31 (principal discharge diagnosis for inpatient setting; any diagnosis field for other settings). For the 10 most common principal discharge diagnoses in the inpatient setting, case-control comparison analyses were performed to estimate annual incremental costs of AF as a comorbid discharge diagnosis for hospital stays. Regression models were used to assess the impact of AF on hospitalization costs. Costs were estimated in year 2005 US dollars. RESULTS: Approximately 350,000 hospitalizations, 5.0 million office visits, 276,000 ED visits, and 234,000 OPD were attributable to AF annually within the United States. Total annual costs for treatment of AF were estimated at $6.65 billion, including $2.93 billion (44%) for hospitalizations with a principal discharge diagnosis of AF, $1.95 billion (29%) for the incremental inpatient cost of AF as a comorbid diagnosis, $1.53 billion (23%) for outpatient treatment of AF, and $235 million (4%) for prescription drugs. In all regressions, AF was a significant contributor to hospital cost. CONCLUSIONS: Treatment of AF represents a significant health-care burden with the costs of treating AF in the inpatient setting outweighing the costs of treating AF in the office, emergency room or hospital outpatient settings. Further research is needed to fully capture the costs of treating AF.