Performance and acute procedural outcomes of the EnSite Precision™ cardiac mapping system for electrophysiology mapping and ablation procedures: results from the EnSite Precision™ observational study.

BACKGROUND: The EnSite Precision™ cardiac mapping system (Abbott) is a catheter navigation and mapping system capable of displaying the three-dimensional (3D) position of conventional and sensor-enabled electrophysiology catheters, as well as displaying cardiac electrical activity as waveform traces and dynamic 3D maps of cardiac chambers. The EnSite Precision™ Observational Study (NCT-03260244) was designed to quantify and characterize the use of the EnSite Precision™ cardiac mapping system for mapping and ablation of cardiac arrhythmias in a real-world environment and evaluate procedural outcomes. METHODS: A total of 1065 patients were enrolled at 38 centers in the USA and Canada between 2017 and 2018 and were followed for 12 months post procedure for arrhythmia recurrence, medication use, and quality-of-life changes. Eligible subjects were adults undergoing a cardiac electrophysiology mapping and radiofrequency ablation procedure using the EnSite Precision™ System. RESULTS: A final cohort of 925 patients (64.3 years of age, 30.2% female) were analyzed. The primary procedural indication was atrial flutter in 48.1% (445/925), atrial fibrillation in 46.5% (430/925), and other arrhythmias in 5% (50/925). Electroanatomic mapping was performed in 81.5% (754/925) of patients. Mapping was stable throughout 79.8% (738/925) of procedures with initial mapping time of 8.6 min (IQR 4.7-15.0). Average mapping efficiency created with AutoMap or TurboMap was 164.9 ± 365.7 used points per minute. Median number of mapping points collected and used was 1752.5 and 811.0, respectively. Only 335/925 (36.2%) required editing and 66.0% (221/335) of these patients required editing of less than 10 points. Fluoroscopy was utilized in most cases (n = 811/925, 87.4%) with fluoroscopy time of 11.0 min (IQR 6.0-18.0). Overall median procedure time was 101.0 min (IQR 59.0-152.0). Acute procedural success was high for both atrial fibrillation (n = 422/430, 98.1%) and atrial flutter (n = 434/445, 97.5%). CONCLUSION: In a real-world study analysis, use of the EnSite Precision™ mapping system was associated with high procedural stability, short mapping times, high point density requiring infrequent editing, low fluoroscopy time, and high prevalence of acute procedural success.

Achievement of optimal medical therapy goals for U.S. adults with coronary artery disease: results from the REGARDS Study (REasons for Geographic And Racial Differences in Stroke).

OBJECTIVES: In a nonclinical trial setting, we sought to determine the proportion of individuals with coronary artery disease (CAD) with optimal risk factor levels based on the COURAGE (Clinical Outcomes Utilizing Revascularization and Aggressive DruG Evaluation) trial. BACKGROUND: In the COURAGE trial, the addition of percutaneous coronary intervention (PCI) to optimal medical therapy did not reduce the risk of death or myocardial infarction in stable CAD patients but resulted in more revascularization procedures. METHODS: The REGARDS (REasons for Geographic And Racial Differences in Stroke) study is a national prospective cohort study of 30,239 African-American and white community-dwelling individuals older than 45 years of age who enrolled in 2003 through 2007. We calculated the proportion of 3,167 participants with self-reported CAD meeting 7 risk factor goals based on the COURAGE trial: 1) aspirin use; 2) systolic blood pressure <130 mm Hg and diastolic blood pressure <85 mm Hg (<80 mm Hg if diabetic); 3) low-density lipoprotein cholesterol <85 mg/dl, high-density lipoprotein cholesterol >40 mg/dl, and triglycerides <150 mg/dl; 4) fasting glucose <126 mg/dl; 5) nonsmoking status; 6) body mass index <25 kg/m(2); and 7) exercise ≥4 days per week. RESULTS: The mean age of participants was 69 ± 9 years; 33% were African American and 35% were female. Overall, the median number of goals met was 4. Less than one-fourth met ≥5 of the 7 goals, and 16% met all 3 goals for aspirin, blood pressure, and low-density lipoprotein cholesterol. Older age, white race, higher income, more education, and higher physical functioning were independently associated with meeting more goals. CONCLUSIONS: There is substantial room for improvement in risk factor reduction among U.S. individuals with CAD.

Idiopathic premature ventricular contractions arising from the intraventricular septum adjacent to the his bundle.

A 57-year-old woman with idiopathic premature ventricular contractions (PVCs) exhibiting a left bundle branch block and left inferior axis QRS morphology underwent electrophysiological testing. Mapping revealed that the earliest ventricular activation times during the PVCs recorded on either side of the interventricular septum were the same and no excellent pace maps were reproduced at these sites. Successful radiofrequency catheter ablation was achieved in the right ventricular septum adjacent to the recording site of the His bundle electrogram. These findings suggested that the origin of this PVC was located in the intraventricular septum rather than the endocardial surface.

Effect of chest compressions on ventricular activation.

External mechanical forces can cause ventricular capture and fibrillation (i.e., commotio cordis). In animals, we showed that chest compressions (CCs) can also cause the phenomenon. The aim of the present study was to determine whether ventricular capture by CCs occurs in humans. Electronic rhythm strips were analyzed in 31 cases of out-of-hospital cardiac arrest. The timing of the CCs was identified from the changes in thoracic impedance between the defibrillator pads. Ventricular capture was defined as QRS complexes of similar morphology occurring intermittently but synchronized with the CC artifact and impedance waveform. Only intermittent ventricular capture was identified to avoid misclassifying constant motion artifacts or intrinsic rhythm as ventricular capture. Of the 29 patients who received CCs for ≥1 minute, minimal or stable motion artifact was present in 24. Intermittent ventricular capture was found in 7 of the 24 patients. In the patients with ventricular capture, the number of ventricular activations (from ventricular capture and native beats) was greater during the CCs than when the CCs was not being performed (18 ± 8.9 vs 9.7 ± 4.0 activations in 15 seconds, p = 0.01). However, in patients without ventricular capture, they were similar (6.8 ± 8.2 vs 7.2 ± 8.8 activations in 15 seconds, p = 0.47). Refibrillation occurred in 22 patients; it began during the CCs in 16 and closely following their initiation in 3. In conclusion, CCs during cardiopulmonary resuscitation can electrically stimulate the heart. Additional studies evaluating the effect of ventricular capture on cardiopulmonary resuscitation outcomes, its relation to refibrillation, and methods to prevent or time ventricular capture by CCs are warranted.

Processes of care associated with acute stroke outcomes.

BACKGROUND: Many processes of care have been proposed as metrics to evaluate stroke care. We sought to identify processes of stroke care that are associated with improved patient outcomes after adjustment for both patient characteristics and other process measures. METHODS: This retrospective cohort study included patients 18 years or older with an ischemic stroke or transient ischemic attack (TIA) onset no more than 2 days before admission and a neurologic deficit on admission. Patients were excluded if they resided in a skilled nursing facility, were already admitted to the hospital at stroke onset, or were transferred from another acute-care facility. The combined outcome included in-hospital mortality, discharge to hospice, or discharge to a skilled nursing facility. Seven processes of stroke care were evaluated: fever management, hypoxia management, blood pressure management, neurologic evaluation, swallowing evaluation, deep vein thrombosis (DVT) prophylaxis, and early mobilization. Risk adjustment included age, comorbidity (medical history), concomitant medical illness present at admission, preadmission symptom course, prestroke functional status, code status, stroke severity, nonneurologic status, modified APACHE (Acute Physiology and Chronic Health Evaluation) III score, and admission brain imaging findings. RESULTS: Among 1487 patients, the outcome was observed in 239 (16%). Three processes of care were independently associated with an improvement in the outcome after adjustment: swallowing evaluation (adjusted odds ratio [OR], 0.64; 95% confidence interval [CI], 0.43-0.94); DVT prophylaxis (adjusted OR, 0.60; 95% CI, 0.37-0.96); and treating all episodes of hypoxia with supplemental oxygen (adjusted OR, 0.26; 95% CI, 0.09-0.73). CONCLUSION: Outcomes among patients with ischemic stroke or TIA can be improved by attention to swallowing function, DVT prophylaxis, and treatment of hypoxia.

Limited response to cardiac resynchronization therapy in patients with concomitant right ventricular dysfunction.

INTRODUCTION: Patients with left ventricular dysfunction (LVD) and LV dyssynchrony may respond to cardiac resynchronization therapy (CRT). However, right ventricular dysfunction (RVD) is a predictor of decreased survival in patients with LVD, and its influence on clinical response to CRT is unknown. The purpose of this study was to examine the effect of RVD on the clinical response to CRT. METHODS AND RESULTS: A retrospective cohort of consecutive patients who underwent implantation of a CRT implantable cardioverter-defibrillator (ICD) were included and deemed to have RVD based on a RV ejection fraction <0.40. A lack of response to CRT was defined as: death, heart transplantation, implantation of an LV assist device, absent improvement in NYHA functional class at 6 months or hospice care. Among 130 patients included (mean age 58 +/- 11 years, 68.5% male, 87.7% Caucasian, 51.5% nonischemic cardiomyopathy), 77 (59.2%) had no response to CRT as defined above. Of the nonresponders, 43 (56%) had RVD and 34 (44%) did not have RVD (P = 0.02). After adjustment for age, race, gender, cardiomyopathy type, atrial fibrillation, serum sodium, and severe mitral regurgitation, RVD (adjusted OR = 0.34, 95%CI 0.14-0.82), female gender (adjusted OR = 0.36, 95%CI 0.14-0.95), and serum creatinine (adjusted OR = 0.25, 95%CI 0.09-0.71) were independently associated with decreased odds of response to CRT. There was a significant difference in survival of patients with and without RVD after CRT (log rank P = 0.01). CONCLUSION: RVD represents a strong predictor of lack of clinical response to CRT in patients with CHF due to LVD and should be considered when prescribing CRT.

Successful catheter ablation of epicardial ventricular tachycardia worsened by cardiac resynchronization therapy.

Soon after an upgrade from a single-chamber implantable cardioverter-defibrillator (ICD) to cardiac resynchronization therapy (CRT) with an ICD, a 64-year-old man with non-ischaemic cardiomyopathy began to have increasingly frequent ICD shocks for slow ventricular tachycardia (VT). At electrophysiological study, no clinical VT was induced by endocardial right ventricular pacing, but was easily induced by epicardial left ventricular (LV) pacing via a subxiphoid pericardial approach. The VT was successfully ablated on the LV epicardial surface. This case suggests that epicardial catheter ablation may be an alternative for managing CRT-induced proarrhythmias without the inactivation of LV pacing.

Epicardial macro-reentrant ventricular tachycardia exhibiting an endocardial centrifugal activation pattern in a case with arrhythmogenic right ventricular cardiomyopathy.

Macro-Reentrant ARVC epi-VT with a Focal Endo-Activation. A 55-year-old man with arrhythmogenic right ventricular cardiomyopathy underwent catheter ablation of ventricular tachycardia (VT) with left bundle branch block and left superior axis QRS morphology with an early precordial transition. Endocardial mapping during the VT revealed a focal activation pattern from a small region of low voltage in the left ventricular (LV) septum. Despite earliest endocardial activation in the LV septum, epicardial mapping demonstrated a macro-reentrant circuit with successful catheter ablation at an inferior peritricuspid annular site. Activation from the reentrant circuit propagated through the scar area in the epicardial right ventricle to the remote endocardial LV breakout site.

Increased cycle length during long-duration ventricular fibrillation is caused by decreased upstroke velocity as well as prolonged refractoriness.

BACKGROUND: Cycle length (CL) increases as ventricular fibrillation (VF) progresses. OBJECTIVE: The purpose of this study was to test the hypotheses that increased CL is due to increased diastolic interval (DI), not increased action potential duration (APD), and that the DI increase is not solely due to increased postrepolarization refractoriness. METHODS: In 10 swine, VF was recorded for 20 minutes using a floating microelectrode through a hole in a 504-electrode epicardial plaque. Mean APD, DI, action potential amplitude (APA), maximum change in voltage during the AP upstroke (V(max)), and CL were calculated from the floating microelectrode recordings each minute of VF. The refractory period was estimated from the minimum DI (DI(min)). In two animals, rapid pacing was performed to gauge refractoriness. RESULTS: As VF progressed, CL, DI, and DI(min) increased (P <.05), whereas APD, V(max), and APA decreased (P <.05). At 20 minutes, DI(min) was not different from mean DI at VF onset. Pacing captured, but 53% of paced wavefronts blocked within the plaque. CONCLUSION: Increasing CL in VF is due to increased DI and not APD, which shortens. The increase in DI(min) over time is much less than the increase in mean DI, indicating that the myocardium is excitable during much of the DI. This finding, along with the ability to pace at a CL shorter than the native VF CL and the poor paced wavefront propagation, suggests that the increase in DI is due not only to increased postrepolarization refractoriness but also to poor wavefront propagation because of decreased APA and V(max) secondary to global ischemia caused by VF.

Mechanisms of VF maintenance: wandering wavelets, mother rotors, or foci.

Ventricular fibrillation (VF), despite its declining incidence as a cause of sudden cardiac death, is still a major health problem. The underlying mechanisms for the maintenance of VF are still disputed. Studies suggest that VF is unlikely one static mechanism but rather a dynamic process of electrical derangement that changes with duration. The 2 principal proposed mechanisms of VF are multiple wavelets and mother rotors. Most studies of these proposed mechanisms for VF maintenance have been during the first minute of VF. However, the time to external defibrillation in the community and pre-hospital settings, where the majority of sudden cardiac death occurs, ranges from 4 to 10 min and the time to defibrillation seems crucial because the odds of survival worsen with delay. Recent studies during the first 10 min of VF suggest that Purkinje fibers are important in maintaining VF after the first 1 to 2 min, either as a part of a reentrant circuit or as a source of focal activations.

Transseptal catheterization in the catheter ablation of atrial fibrillation in a patient with cor triatriatum sinister.

A 66-year-old man with cor triatriatum sinister underwent pulmonary vein (PV) isolation (PVI) for atrial fibrillation (AF) twice because of AF recurrence. Different transseptal approaches into the anterior chamber receiving the left atrial appendage and posterior chamber receiving the PVs, were achieved in two sessions. PVI of the left PVs and right superior PV was challenging via the anterior chamber, whereas PVI of the right inferior PV was challenging via the posterior chamber because of the disturbance of the membrane. Therefore, an intentional transseptal catheterization into the more appropriate chamber may be necessary for PVI in a cor triatriatum sinister.

Successful catheter ablation of a ventricular tachycardia storm originating from the left ventricular posterior papillary muscle involved with a remote myocardial infarction.

A 61-year-old man with a remote posterior myocardial infarction underwent electrophysiological testing for a ventricular tachycardia (VT) storm. Repeated cardioversions terminated the VT with immediate resumption after one sinus beat. Pacing neither terminated the VT nor demonstrated transient entrainment. Echocardiographically guided electroanatomic mapping revealed a centrifugal activation from the septal mid-apical region of the left ventricle on the septal portion of the posterior papillary muscle where a high frequency potential was observed within the local ventricular electrogram. Irrigated radiofrequency current at this site eliminated the VT. This case suggested that papillary muscles may be a target for catheter ablation of electrical storms after myocardial infarctions.

QRS alternans with 2:1 atrioventricular conduction block: what is the mechanism?

An 81-year-old woman was admitted for symptomatic bradycardia. On admission, the ECG exhibited QRS alternans, narrow QRS complex and left bundle branch block with 2:1 AV block. The patient soon had complete AV block and underwent a pacemaker implantation. An appropriate mechanism for explaining those ECG findings might be 4:1 conduction over the left bundle branch and 2:1 conduction over the right bundle branch. An ECG pattern exhibiting QRS alternans with a narrow QRS complex and bundle branch block with 2:1 AV block may suggest the coexistence of both bundle branch blocks and a high risk of complete AV block.

Hospital admissions for stroke among the very old in the USA.

BACKGROUND: We sought to describe the proportion of acute ischemic stroke admissions for very old patients (> or =85 years), compare the characteristics of very old versus younger patients and identify factors among very old patients associated with adverse outcomes. METHODS: The 2000 Healthcare Cost and Utilization Project data included acute ischemic stroke hospitalizations for patients > or =45 years. The combined outcome was in-hospital mortality or discharge to a long-term care facility. RESULTS: Among 15,020 stroke hospitalizations, 20.4% were for very old patients. The outcome rate was higher in hospitalizations for very old patients (2,176/3,058, 71.2%; versus 5,748/11,962, 48%; p < 0.0001). More hospitalizations for very old patients were for women (73.5 versus 55.1%; p < 0.0001), fewer for Blacks (6.1 versus 12.3%; p < 0.0001) and fewer at teaching hospitals (30.4 versus 36.2%; p < 0.0001). Among very old patients, factors that were independently associated with the outcome included: age [years; adjusted OR = 1.02 (95% CI = 1.000-1.05)], female gender [1.4 (1.18-1.68)], atrial fibrillation [1.37 (1.15-1.63)], acute myocardial infarction [1.68 (1.20-2.35)], respiratory failure [3.59 (1.60-8.05)] and teaching hospital admission [0.82 (0.69-0.98)]. Similar results were observed in the hospitalizations for younger patients. The adjusted OR for the outcome displayed geographic disparities in both age groups, but the pattern of the geographic variation was not similar between the two age groups. CONCLUSIONS: The very old constitute a substantial proportion of stroke hospitalizations. Hospitalizations for very old patients are more likely to end in death or discharge to a long-term care facility than hospitalizations for younger patients. The pattern of geographic disparity in poststroke adverse outcomes differs between younger and very old patients.

Chemical ablation of the Purkinje system causes early termination and activation rate slowing of long-duration ventricular fibrillation in dogs.

Endocardial mapping has suggested that Purkinje fibers may play a role in the maintenance of long-duration ventricular fibrillation (LDVF). To determine the influence of Purkinje fibers on LDVF, we chemically ablated the Purkinje system with Lugol solution and recorded endocardial and transmural activation during LDVF. Dog hearts were isolated and perfused, and the ventricular endocardium was exposed and treated with Lugol solution (n = 6) or normal Tyrode solution as a control (n = 6). The left anterior papillary muscle endocardium was mapped with a 504-electrode (21 x 24) plaque with electrodes spaced 1 mm apart. Transmural activation was recorded with a six-electrode plunge needle on each side of the plaque. Ventricular fibrillation (VF) was induced, and perfusion was halted. LDVF spontaneously terminated sooner in Lugol-ablated hearts than in control hearts (4.9 +/- 1.5 vs. 9.2 +/- 3.2 min, P = 0.01). After termination of VF, both the control and Lugol hearts were typically excitable, but only short episodes of VF could be reinduced. Endocardial activation rates were similar during the first 2 min of LDVF for Lugol-ablated and control hearts but were significantly slower in Lugol hearts by 3 min. In control hearts, the endocardium activated more rapidly than the epicardium after 4 min of LDVF with wave fronts propagating most often from the endocardium to epicardium. No difference in transmural activation rate or wave front direction was observed in Lugol hearts. Ablation of the subendocardium hastens VF spontaneous termination and alters VF activation sequences, suggesting that Purkinje fibers are important in the maintenance of LDVF.

Serial evaluations of myocardial infarct size after alcohol septal ablation in hypertrophic cardiomyopathy and effects of the changes on clinical status and left ventricular outflow pressure gradients.

Alcohol septal ablation (ASA) as a treatment for obstructive hypertrophic cardiomyopathy produces septal infarction. There is a concern that such infarcts could be detrimental. Changes in the size of these infarcts by serial perfusion testing have not been studied. We performed resting serial-gated single-photon emission computed tomographic myocardial perfusion imaging in 30 patients (age 51+/-17 years, 57% were women) who had ASA between September 2003 and March 2007 before, 2+/-0.8 days (early), and 8.4+/-6.9 months (late) after ASA. Patients were also followed clinically and with serial 2-dimensional echocardiography. New York Heart Association class decreased from 3.50+/-0.51 before to 1.14+/-0.36 (p<0.0001) 3 months after ASA. The left ventricular (LV) outflow gradient (by Doppler echocardiography) decreased from 63+/-32 mm Hg before to 28+/-23 mm Hg after ASA (p<0.005). None of the patients had perfusion defects at rest before ASA. After ASA, perfusion defect size, involving the basal septum, decreased from 9.4+/-5.8% early to 5.2+/-4.2% of LV myocardium late after ASA (p<0.001). There were no changes in LV size and ejection fraction after ASA. In conclusion, ASA produces small basal ventricular septal infarcts (resting perfusion abnormality) involving<10% of the LV myocardium (including ventricular septum). There is a significant reduction in the perfusion abnormality late after ASA without an increase in LV outflow obstruction or recurrence of symptoms.

In a swine model, chest compressions cause ventricular capture and, by means of a long-short sequence, ventricular fibrillation.

BACKGROUND: During resuscitation, fibrillation often recurs. In swine, we studied refibrillation after long-duration ventricular fibrillation, investigating an association with chest compressions (CCs). METHODS AND RESULTS: In protocol A, 47 episodes of long-duration ventricular fibrillation lasting at least 2.5 minutes were induced in 8 animals. After defibrillation, CCs were required for 35 episodes and delivered with a pneumatic device (Lucas cardiopulmonary resuscitation). In 9 episodes, refibrillation occurred within 2 seconds of CC initiation (group 1) and in 26 episodes, CCs were delivered without refibrillation (group 2). From the ECG and intracardiac electrodes, the RR interval preceding CCs, the shortest cycle length during the first 2 CCs (short), and the preceding cycle length (long) were measured. A similar study was conducted in 3 more animals without intracardiac catheters (protocol B). In protocol A, the mean RR before CC was 665+/-292 ms in group 1 and 769+/-316 in group 2. CCs stimulated ventricular beats in all 35 episodes. The short and long intervals were shorter in group 1 (215+/-31 and 552+/-210 ms) than in group 2 (402+/-153 and 699+/-147 ms) (P=0.009 and P=0.04, respectively). The prematurity index (short/RR) was lower in group 1 than in group 2 (0.35+/-0.09 vs 0.58+/-0.21; P<0.01). A short interval <231 ms predicted refibrillation with 88% sensitivity and 91% specificity. In protocol B, CCs were required in 11 episodes, causing ventricular stimulation in all of them and ventricular fibrillation within the first 2 CCs in 3. CONCLUSIONS: Under some conditions, CC during resuscitation can stimulate the ventricles and initiate ventricular fibrillation by a long-short sequence.

Activation patterns of Purkinje fibers during long-duration ventricular fibrillation in an isolated canine heart model.

BACKGROUND: The roles of Purkinje fibers (PFs) and focal wave fronts, if any, in the maintenance of ventricular fibrillation (VF) are unknown. If PFs are involved in VF maintenance, it should be possible to map wave fronts propagating from PFs into the working ventricular myocardium during VF. If wave fronts ever arise focally during VF, it should be possible to map them appearing de novo. METHODS AND RESULTS: Six canine hearts were isolated, and the left main coronary artery was cannulated and perfused. The left ventricular cavity was exposed, which allowed direct endocardial mapping of the anterior papillary muscle insertion. Nonperfused VF was induced, and 6 segments of data, each 5 seconds long, were analyzed during 10 minutes of VF. During 36 segments of data that were analyzed, 1018 PF or focal wave fronts of activation were identified. In 534 wave fronts, activation was mapped propagating from working ventricular myocardium to PF. In 142 wave fronts, activation was mapped propagating from PF to working ventricular myocardium. In 342 wave fronts, activation was mapped arising focally. More than 1 of these 3 patterns could occur in the same wave front. CONCLUSIONS: PFs are highly active throughout the first 10 minutes of VF. In addition to retrograde propagation from the working ventricular myocardium to PFs, antegrade propagation occurs from PFs to working ventricular myocardium, which suggests PFs are important in VF maintenance. Prior plunge needle recordings in dogs indicate activation propagates from the endocardium toward the epicardium after 1 minute of VF, which suggests that focal sites on the endocardium may represent foci and not breakthrough. If so, in addition to reentry, abnormal automaticity or triggered activity may also occur during VF.