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(BQ) Part 2 book Atrial fibrillation - A multidisciplinary approach to improving patient outcomes presents the following contents: LAA excision, ligation and occlusion devices; atrial fibrillation - a surgical approach; anesthesia care for the atrial fibrillation patient; team approach to the care of the AF patient; shared decision making for patients with atrial fibrillation, patient preferences and ecisionaids,...
c h a pt e r Left Atrial Appendage Excision, Ligation, and Occlusion Devices Taral K Patel, MD, and Bradley P Knight, MD ATRIAL FIBRILLATION AND STROKE Atrial fibrillation (AF) currently affects up to million Americans and remains the most common arrhythmia encountered in clinical practice.1,2 With an aging population, the burden of AF is expected to rise 3-fold by 2050.3 Among the several downstream consequences of AF, the most feared is stroke due to thromboembolism The primary cause of thrombus formation is mechanical dysfunction in the atria, leading to impaired blood flow and stasis AF also promotes endothelial dysfunction, inflammation, platelet activation, and hypercoagulability, which further contribute to thrombus formation.4–6 Stroke remains the number one cause of major disability and the third leading cause of death in the United States.7 AF increases stroke risk 5-fold, leading to a 5% annual stroke rate for all-comers.7 Seen another way, the percentage of strokes attributable to AF ranges from 1.5% in those aged 50 to 59 years to an impressive 23.5% in those aged 80 to 89 years.7 While these statistics are dramatic, the influence of AF on stroke is almost certainly underestimated as AF is commonly silent and underdiagnosed.8 LEFT ATRIAL APPENDAGE Johnson and colleagues described the left atrial appendage (LAA) as “our most lethal human attachment.”9 Derived from the embryonic left atrium, the LAA forms a blind pouch to cm long and most commonly lies on the anterior surface of the heart Its narrow neck forms a natural obstacle to normal blood flow The LAA endocardial surface is highly irregular due to the presence of pectinate muscles This is in sharp contrast to the true left atrium, which is derived from venous tissue and has a smooth endocardial surface The LAA also has a variable number of lobes; an autopsy survey of 500 patients found that 20% had one lobe while 77% had two or three lobes.10 Atrial Fibrillation: A Multidisciplinary Approach to Improving Patient Outcomes © 2015 Joseph S Alpert, Lynne T Braun, Barbara J Fletcher, Gerald Fletcher, Editors-in-Chief, Cardiotext Publishing, ISBN: 978-1-935395-95-9 109 110 Se ct io n 1: At ria l Fib rilla t io n : Ba ckg ro u n d , Eva lu a t io n , a n d Ma n a g e m e n t The LAA, because of its complex anatomy, innumerable potential spaces, and low blood flow during AF, is particularly susceptible to thrombus formation Studies using magnetic resonance imaging (MRI) and transesophageal echocardiography (TEE) have suggested that larger LAA ostia, more lobes, and greater length all predict higher risk of stroke.11 An important review of 23 studies found that 17% of patients with nonrheumatic AF had left atrial thrombi, of which a striking 91% were located in the LAA.12 It is now well-accepted that the vast majority of strokes caused by AF represent thromboembolism originating from the LAA LIMITATIONS OF ORAL ANTICOAGULATION Stroke prevention is the foundation of AF management Currently, the standard of care is oral systemic anticoagulation by using the widely adopted CHADS2 stroke risk-assessment tool.13,14 The newer CHA2DS2-VASc score has helped further refine stroke risk in patients with otherwise low CHADS2 scores.15 These scoring systems balance the bleeding risk from anticoagulation with the thromboembolic risk from untreated AF Supported by decades of data, oral anticoagulation has been unequivocally effective in reducing stroke Warfarin, still the predominant anticoagulant, was demonstrated to reduce AF-related stroke by 64% in an extensive meta-analysis.16 However, the widespread use of systemic anticoagulation has highlighted several important limitations of this strategy Most importantly, systemic anticoagulation unavoidably increases bleeding risk Up to 40% of AF patients have relative or absolute contraindications to anticoagulation, usually owing to a history of pathologic bleeding or an elevated risk of falls.17,18 The HAS-BLED score has helped quantify the bleeding risk of warfarin in a manner analogous to the CHADS2 score for stroke risk It is notable that several components of the HASBLED score—hypertension, prior stroke, and advanced age—are also found in the CHADS2 score In other words, patients at high risk for stroke also happen to be patients at high risk for bleeding, illustrating the complexity in properly selecting patients for oral anticoagulation Aside from bleeding risk, warfarin use is further limited by the inconvenience of frequent blood testing and extensive interactions with food and other medications Often because of these limitations, warfarin is not utilized in up to 50% of eligible AF patients.19 Even when patients are treated with warfarin, they spend up to half of the treatment time outside the therapeutic range.20 Motivated by the challenges of using warfarin, the newer oral anticoagulants dabigatran (a direct thrombin inhibitor), rivaroxaban (a factor Xa inhibitor), and apixaban (a factor Xa inhibitor) were developed and are now in general clinical Chapte r 8 LAA Excisio n, Lig atio n, and Occlusio n De vice s use These novel agents are comparably effective to warfarin with equivalent or lower bleeding risk.21–23 They have the advantage of minimal food and drug interactions and also eliminate the need for INR monitoring, increasing the ease of use and compliance Unfortunately, they still suffer from the problem of elevated bleeding risk; this risk is further heightened because, unlike warfarin, the new drugs are not easily reversible with blood-product transfusion Finally, the new agents are more costly and, at present, it is unclear whether they are truly cost effective in comparison with warfarin Even with improved oral anticoagulation options, there remains a more fundamental issue Because AF-related stroke appears to be largely a focal problem— thromboembolism from the LAA—a focal approach would be preferable to the currently imprecise strategy of systemic anticoagulation Theoretically, a procedure to exclude the LAA (either by excision or by ligation or occlusion) should offer similar stroke prophylaxis while eliminating the disadvantages of systemic anticoagulation LAA exclusion would be especially appealing for patients with either intolerance or contraindications to anticoagulation In recent years, substantial progress has been made in developing techniques to exclude the LAA as a viable alternative for stroke prevention in AF LEFT ATRIAL APPENDAGE EXCLUSION: SURGICAL TECHNIQUES LAA exclusion was first reported in 1949, when the surgeon Madden 24 published a case series of patients who underwent LAA removal as a prophylaxis for recurrent arterial emboli The high morbidity and mortality of the procedure prevented its widespread adoption for decades, until interest was reignited in the 1990s by the development of the Cox-Maze III procedure, which included removal of the LAA.25 Surgical techniques have evolved along two lines: LAA exclusion (using various suture techniques) and LAA excision (via surgical stapler or removal with oversew) Data for LAA surgery consist primarily of case reports and retrospective case series Intepretation of the data is hampered by nonuniform surgical techniques and nonstandardized outcomes measurements The use of TEE, considered the gold standard for LAA visualization, is absent in many reports A large review of existing literature found that surgical success was highly dependent on both operator and technique; complete LAA closure rates ranged from 17% to 93%.26 Excision and oversew appeared to demonstrate the most durable results A recent pilot trial randomized 51 patients to surgical LAA closure versus oral anticoagulation and demonstrated comparable stroke rates during follow-up.27 The results 111 112 Se ct io n 1: At ria l Fib rilla t io n : Ba ckg ro u n d , Eva lu a t io n , a n d Ma n a g e m e n t pave the way for a larger trial to answer the critical question of whether surgical LAA exclusion effectively reduces stroke risk Current ACC/AHA guidelines limit surgical LAA exclusion as an adjunctive procedure during mitral valve or Maze surgery.13 However, two recently developed devices may rekindle interest in stand-alone surgical LAA exclusion The first, AtriClip LAA Exclusion System (Atricure, West Chester, OH), is approved in both the United States and Europe, although it is indicated only in conjunction with other open cardiac surgical procedures in the United States The device consists of a titanium ring covered by a woven polyester fabric Under direct visualization, the clip is secured around the base of the LAA using a special deployment tool In the largest trial to date, 70 patients undergoing open cardiac surgery in seven US centers had the AtriClip successfully placed.29 Of the 61 patients who underwent imaging at months, 60 achieved persistent LAA exclusion There were no device-specific adverse events reported Although this was a small study with short-term follow-up, it demonstrated that the device could be deployed safely during open cardiac surgery The second device involves a minimally invasive thoracoscopic approach After left lung deflation, an endoscopic cutter (Ethicon Endo-Surgery, Cincinnati, OH) is introduced via the left lateral thorax The cutter then simultaneously removes the LAA and staples its base closed The procedure eliminates the need for thoracotomy, although concerns remain about the risks of lung deflation and the potential for catastrophic bleeding into a closed chest Ohtsuka et al.30 published their experience with the technique in 30 patients with prior thromboembolism, achieving 100% procedural success and no major complications Anticoagulation was discontinued and no recurrence of thromboembolism occurred after 18 months of follow-up These preliminary data suggest that stand-alone surgical LAA exclusion may eventually have a place alongside the various transcatheter techniques LEFT ATRIAL APPENDAGE EXCLUSION: TRANSCATHETER TECHNIQUES In an effort to avoid the morbidity of open surgery for LAA exclusion, minimally invasive percutaneous techniques have rapidly developed over the past decade Of these, have been tested in humans and shown promise PLAATO Device Important for historical purposes, the Percutaneous LAA Transcatheter Occlusion (PLAATO) device (ev3 Endovascular, Plymouth, MN) became the first device of Chapte r 8 LAA Excisio n, Lig atio n, and Occlusio n De vice s 113 Fig u r e The PLAATO device, mounted on its delivery catheter Source: Reprinted with permission from Syed T, Halperin J Nat Rev Cardiol 2007:4;428–435 its kind deployed in humans in 2001 The device consisted of a self-expanding nitinol cage covered by a blood-impermeable polytetrafluoroethylene membrane (Figure 8.1) The device was deployed in the LAA via transseptal catheterization under fluoroscopic and TEE guidance Clinical experience with PLAATO was reported in small studies Sievert et al.31 implanted the device in 15 patients with 100% procedural success and one incident of hemopericardium A larger international registry of 111 patients reported a 97% implant success rate and a 6% adverse event rate, including one death.32 The 10-month stroke rate of 2.2% compared favorably with the CHADS2-predicted rate of 6.3% A North American registry of 64 patients reported 100% procedural success.33 After years of follow-up, the stroke rate was 3.8%, a relative risk reduction of 42% from the expected stroke rate of 6.6% Despite this promising clinical experience, the PLAATO device was withdrawn from development in 2006 However, its design became the inspiration for the subsequently developed WATCHMAN device WATCHMAN Device The WATCHMAN device (Boston Scientific, Natick, MA) was first implanted in 2002 It also consists of a self-expanding nitinol frame, but is open-ended and has a permeable polyethylene membrane that only covers the part of the device exposed to the left atrium (Figure 8.2) The WATCHMAN device is also delivered via a transseptal system (Figure 8.3) Initial protocols required at least weeks 114 Se ct io n 1: At ria l Fib rilla t io n : Ba ckg ro u n d , Eva lu a t io n , a n d Ma n a g e m e n t A B Fig u r e (A) The WATCHMAN device consists of a nitinol frame and permeable membrane (B) Illustration of the device properly deployed in the left atrial appendage Source: Used with permission of Boston Scientific Corporation Chapte r 8 LAA Excisio n, Lig atio n, and Occlusio n De vice s 115 Fig u r e Fluoroscopic image of the WATCHMAN device (arrow) deployed in the left atrial appendage of warfarin post-implant to prevent thrombus formation prior to device endothelialization Warfarin was discontinued once a follow-up TEE demonstrated no flow into the LAA, signifying complete endothelialization Subsequently, a strategy of substituting dual antiplatelet therapy for warfarin was evaluated in 150 warfarin-ineligible patients who underwent WATCHMAN implantation.34 After 14 months of follow-up, the actual ischemic stroke rate was 1.7% compared with the CHADS2-predicted rate of 7.3%, demonstrating that WATCHMAN implantation without a warfarin transition was a viable alternative for patients with contraindications to anticoagulation Following several feasibility studies, the WATCHMAN device underwent a head-to-head trial against warfarin in the landmark PROTECT-AF trial.35 116 Se ct io n 1: At ria l Fib rilla t io n : Ba ckg ro u n d , Eva lu a t io n , a n d Ma n a g e m e n t To date, this study represents the only randomized trial comparing LAA exclusion with anticoagulation In PROTECT-AF, 707 patients from 59 centers in the United States and Europe were randomized 2:1 to WATCHMAN versus warfarin therapy Patients had relatively low stroke risk (68% had a CHADS2 score of or 2) and no contraindications to warfarin Overall implant success rate was 91% and at months, 92% of patients in the WATCHMAN arm had discontinued anticoagulation The trial was designed to test noninferiority of WATCHMAN to standard warfarin therapy After 1065 patient-years, the primary efficacy end point (stroke, systemic embolism, or cardiovascular or unexplained death) was superior in the WATCHMAN arm versus the warfarin arm (3.0% vs 4.9% per 100 patientyears), fulfilling the criteria for noninferiority However, the primary safety end point (excessive bleeding or procedure-related complications) was worse in the WATCHMAN group (7.4% vs 4.4%) Procedure-related complications included 22 pericardial effusions, air emboli, and device embolizations On the other hand, the warfarin group had higher rates of major bleeding (4.1% vs 3.5%) and hemorrhagic stroke (2.5% vs 0.2%) In 2013, the 2.3-year results of PROTECT-AF were published, highlighting the durability of the initial results.36 After 1588 patient-years, the primary efficacy end point occurred in 3.0% of WATCHMAN patients and 4.3% of warfarin patients, again meeting criteria for noninferiority With respect to the safety event rate, the WATCHMAN group continued to fare worse (5.5% vs 3.6%), although the gap had narrowed As expected, the adverse events in the WATCHMAN group were driven by early procedure-related complications, with relatively few events occurring in follow-up On the other hand, adverse events continued to gradually acrue in the warfarin arm, driven primarily by warfarin-related bleeding Despite the generally positive reception for PROTECT-AF, concerns still remain regarding periprocedural complications and thrombus formation on the device prior to endothelialization (Figure 8.4) Of note, procedure-related complications were greater in the first half of PROTECT-AF than in the second half, underscoring the learning curve involved with device implantation; adverse events continued to remain low in the Continued Access Protocol (CAP) registry of 460 patients.37 A second randomized trial of WATCHMAN versus warfarin, called PREVAIL, sought to address concerns about the high adverse-event rate from WATCHMAN implantation The preliminary data appear promising and are currently under peer review Another registry (Continued Access to PREVAIL) has also been created to generate more safety and efficacy data In late 2013, the accumulated WATCHMAN data was compelling enough for an FDA advisory panel to vote strongly in favor of the device when asked if its benefits outweigh its risks, likely paving the way for eventual FDA approval Chapte r 8 LAA Excisio n, Lig atio n, and Occlusio n De vice s Fig u r e Transesophageal echocardiographic image of a thrombus (arrow) on a WATCHMAN device several months after anticoagulation was discontinued At present, the WATCHMAN device is the only LAA exclusion device with demonstrated noninferiority to warfarin for stroke prevention There is also evidence that patients achieve improvement in quality-of-life measures after WATCHMAN implantation, likely due to discontinuation of daily warfarin, reduction in bleeding complications, and elimination of dietary and drug interactions.38 117 118 Se ct io n 1: At ria l Fib rilla t io n : Ba ckg ro u n d , Eva lu a t io n , a n d Ma n a g e m e n t AMPLATZER Cardiac Plug After the success of the AMPLATZER Septal Occluder (St Jude Medical, Plymouth, MN) for patent foramen ovale and atrial septal defect closure, the product was redesigned specifically for the LAA and named the AMPLATZER Cardiac Plug (ACP; St Jude Medical) (Figure 8.5) This device consists of a self-expanding nitinol mesh constructed in two parts: a distal lobe designed to prevent device migration and a proximal disk designed to occlude the LAA ostium The lobe and disk are joined by an articulating waist that accommodates anatomic variation The ACP is also delivered transseptally to the LAA Three published registries summarize the worldwide data on the ACP The initial human experience in Europe demonstrated a 96% implant success rate in 137 patients, with serious complications in 10 patients (including ischemic strokes, pericardial effusions, and device embolizations).39 The Asian-Pacific experience, although consisting of only 20 patients, provided one-year follow-up data demonstrating no incidence of stroke or death.40 Finally, a Canadian registry of 52 patients achieved procedural success in all but one patient.41 Of note, the Canadian patients all had contraindications to anticoagulation Two serious complications occurred (one device embolization and one cardiac tamponade) TEE at months showed a disappointing 16% rate of peri-device leak, but 20-month follow-up demonstrated no incidence of device-related death or thromboembolism Importantly, ACP implantation protocols have generally not involved periprocedural anticoagulation, instead employing dual antiplatelet therapy for one month followed by aspirin monothereapy Concerns remain about the incidence of persistent leaks following device implantation While achieving CE mark approval in Europe, the ACP is still in Phase I clinical trials in the United States LARIAT Suture Delivery System Receiving FDA approval in 2009 for soft tissue approximation, the LARIAT suture delivery system (SentreHEART, Palo Alto, CA) is the newest LAA exclusion device This hybrid system involves both epicardial and transseptal access Epicardial and endocardial magnet-tipped guidewires meet at the tip of the LAA, forming a single rail for the delivery of an epicardial snare with a pre-tied suture loop A balloon catheter serves as a marker for the LAA base and stabilizes the epicardial snare (Figure 8.6) Under fluoroscopic and TEE guidance, the suture is tightened around the LAA base and released from the snare Importantly, LAA closure can be evaluated in real-time with TEE or left atrial angiography If closure is not satisfactory, the snare can be repositioned prior to irreversible suture release (Figure 8.7) 262 Se ct io n 3: Ca se St u d ie s Ta b le Percent Risk of Stroke Based on CHA2DS2VASc Number of Points Risk of Stroke 0% 1.3% 2.2% 3.2% 4.0% 6.7% 9.8% 9.6% 6.7% 15.2% CASE DISCUSSION Our patient had persistence of symptomatic AF despite attempt at rate control He had been on metoprolol XL 25 mg daily and digoxin 0.125 mcg daily We were unable to increase metoprolol XL doses because of a low blood pressure His digoxin dose was at a standard dose and digoxin levels were within the therapeutic range, so it would have been inappropriate to increase the dose of digoxin Because of our patient’s reduced LV function and tenuous cardiac Ta b le HAS-BLED Scoring System Risk Points H: Hypertension (Systolic > 160) A: Abnormal renal or liver function Renal (chronic dialysis, transplant patient or creatinine > 2.3 mg/dL) Hepatic (chronic hepatitis, or Bilirubin 2× normal with AST/ALT 3× normal) or (renal point, hepatic point) S: History of Stroke B: History of Bleeding L: Labile INRs E: Elderly > 65 or frail D: Drugs or Alcohol (1 point each), i.e., antiplatelet agents, antiinflammatory or Chapte r 17 Case Study: Pe rmane nt Atrial Fibrillatio n Ta b le Risk of Bleeding Based on HAS-BLED Number of Points Risk of Stroke 1.13% 1.02% 1.88% 3.74% 8.7% 12.5% status, nondihydropyridine calcium channel blockers were appropriately avoided because of their negative inotropic effect and risk of exacerbating CHF A single IV bolus of 150 mg and then 200 mg daily of oral amiodarone for rate control would have been a reasonable option with a very low risk of conversion to SR in our patient who had a 5-cm severely dilated left atrium We chose to avoid amiodarone because of its pulmonary side effects, particularly in our patient who has had lung cancer, a right upper lobectomy and radiation therapy (Figure 17.5) As mentioned before, our patient had a CRT device with only 30% effective BiV pacing At this point in time, given that our patient had symptomatic AF and was not benefiting from his CRT device, we felt that the next step would be an AV node ablation We performed the procedure successfully and programmed his device to pace at 75 bpm for month This strategy ensures that CRT is delivered, without fusion or pseudo-fusion It also regularizes the patient’s rhythm and eliminates the risk of uncontrolled ventricular rates, which could be responsible for our patient’s symptoms All of these factors are particularly beneficial in our patient with AF and CHF who can now take advantage of the decreased morbidity and mortality associated with effective CRT therapy One can argue that our patient should have had an AV node ablation at the time of CRT placement One study compared the efficacy of CRT in patients with AF who underwent AV node ablation and patients in whom rate control was achieved pharmacologically This study showed that patients who underwent AV node ablation with CRT achieved significantly better symptomatic relief with improvement in their LV function, a benefit that was maintained for up to years.43 With regards to anticoagulation, our patient had a CHA2DS2-VASc score of 4, putting him at a 4% yearly risk of stroke Given his history of lung cancer, he may be at an even higher risk of thromboembolism, which is not accounted for in our current scoring systems His HAS-BLED score was because of age, so it was appropriate to continue him on warfarin with a goal INR of to His INRs had 263 264 Se ct io n 3: Ca se St u d ie s Fig u r e Chest x-ray (CXR) of our patient This is a posteroanterior CXR There is evidence of scarring and fibrosis of the right upper lung field at the site of prior right upper lobectomy with deviation of the trachea to the right A CRT-D device is seen on the left-hand side with a right atrial lead, a right ventricular dual coil lead, and a left ventricular lead sitting the middle cardiac vein been stable on warfarin, eliminating the need to consider a novel anticoagulant At 1-month follow-up, we saw our patient in clinic; he was doing very well, with improvement to a NYHA functional class II We programmed his CRT to pace at VVIR 60 CONCLUSION Patients with AF and CHF are more susceptible to increased morbidity and mortality and poor outcomes The goals of therapy in these patients should be directed at prolonging life and most importantly improving quality of life through symptom management and thromboembolism prophylaxis These patients need regular and frequent outpatient monitoring, which does not always require physician participation Nurse practitioners have an important role in follow up and Chapte r 17 Case Study: Pe rmane nt Atrial Fibrillatio n monitoring of patients with CHF and AF Educating patients about their condition is essential to achieve symptom control and avoid hospitalizations With regards to CHF, patients should be counseled carefully about maintaining euvolemia This is achieved by guidance on salt and water intake, following daily weights, and careful adjustment of diuretic dose based on changes in weight With regard to AF, patients must be educated about AF triggers that should be avoided, including alcohol They need to be instructed about maintenance of a consistent diet and avoidance of certain vitamin K-rich foods, which may dramatically affect their INR Patients on warfarin also need consistent follow-up of their INRs and warfarin adjustment accordingly More recently, home INR kits have further decreased the need for frequent office visits This does, however, increase the importance of having a nurse practitioner to be available to answer phone calls, attend to patient concerns, and advise patients appropriately With the emergence of quality measures, including 30-day rehospitalization for CHF, effective communication and counseling are crucial The nurse practitioner is a valuable bridge between physician and patient, and this role will become more involved as health care evolves to meet certain standards, cut costs, and better serve our patients REFERENCES January CT, Wann LS, Alpert JS, et al 2014 AHA/ACC/HRS Guideline for the 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al Four-year efficacy of cardiac resynchronization therapy on exercise tolerance and disease progression: The importance of performing atrioventricular junction ablation in patients with atrial fibrillation J Am Coll Cardiol 2006;48:734–743 267 Index Page numbers followed by f, t, refer to figures, tables A ablation See also catheter ablation; surgical ablation atrial fibrillation, 151–156 endocardial and epicardial, 98–100, 100t, 136 hybrid, 100, 101t, 102–105, 102f ACC See American College of Cardiology acetylsalicylic acid (ASA), 30 ACT See anesthesia care team ACUTE See Assessment of Cardioversion Using Transesophageal Echocardiography Investigators AF See atrial fibrillation AF-CHF See atrial fibrillation and congestive heart failure AFFIRM See Atrial Fibrillation Follow-up Investigation of Rhythm Management AFIB Innovation Program, 43 age, as a risk factor, AHA See American Heart Association alcohol consumption, 31, 32 ambulatory care pharmacists, 167–168 American College of Cardiology/American Heart Association (ACC/AHA) classification, 3–4, 253–254 guidelines for rate control, 259t indications for ablation, 129–130 American Heart Association, 43, 165 See also American College of Cardiology/ American Heart Association (ACC/AHA) American Society for Anesthesiology (ASA), 144, 147t, 154t, 155–156 American Society of Health-System Pharmacists, 167 amiodarone, 29, 62, 65, 66t, 69t, 71–72, 80–81, 192, 234–235, 234t, 258 AMPLATZER Cardiac Plug, 118, 119f AMPLATZER Septal Occluder, 118 anesthesia airway and esophageal intubation, 155 atrial fibrillation ablation, 151–156 cardioversion, electrical (direct-current), 149–151 classification of physical status, 147t dosing agents for conscious and deep sedation, 153t dosing agents for general, 153t hemodynamic monitoring, 155–156 intubation aids, 144–145, 146f–147f, 155 levels of sedation, 148t patient history, 141–143 patient monitoring and delivery of, 149–151, 150f, 152–154, 154t patient positioning, 154–156 physical examination, 143–145, 144f plan, formulation of, 148–149 postprocedure, 156–159 preanesthesia evaluation, 141–149, 142t procedural, 149–156 recovery from, 157, 158t, 159 review of diagnostics, 145, 148 anesthesia care team (ACT), 141, 154, 157–158 angiotensin converting enzyme inhibitors, 9, 258, 259 antiarrhythmic agents, 29 See also name of case study of paroxysmal atrial fibrillation, 233–235, 234t case study of persistent atrial fibrillation, 245–246, 245f dosing and safety, 164–165 efficacy and safety of, 66t–67t for rate control, 80–81 for rhythm control, 65, 66t–67t, 67–74, 69t, 191–192 Atrial Fibrillation: A Multidisciplinary Approach to Improving Patient Outcomes © 2015 Joseph S Alpert, Lynne T Braun, Barbara J Fletcher, Gerald Fletcher, Editors-in-Chief, Cardiotext Publishing, ISBN: 978-1-935395-95-9 269 270 role of, 61–62 to suppress atrial fibrillation recurrences, 69t, 135, 135f anticoagulation (anticoagulants) See also name of description of, 51–52, 62, 189–190 limitations of, 110–111 management of, 91, 179–180 novel oral, 91, 189–190, 237–239 pharmacist-run services, 165, 167–168 primary care physician, role of, 179–180 target-specific, 91 anticoagulation (anticoagulants), case study of paroxysmal atrial fibrillation, 235–239 of persistent atrial fibrillation, 243–251 apixaban, 62, 110–111, 189, 190, 238 AQI (Anesthesia Quality Institute) quality indicators, 158t ARIC See Atherosclerosis Risk in Communities ASA See acetylsalicylic acid; American Society for Anesthesiology Assessment of Cardioversion Using Transesophageal Echocardiography Investigators (ACUTE) trial, 231 ATAs See atrial tachyarrhythmias atenolol, 234t Atherosclerosis Risk in Communities (ARIC), 6, atrial fibrillation (AF) ablation, 151–156 classification, 3–4, 185 complications and costs, diagnosing, 183–185 epidemiology, 4, 5f, longitudinal history, pathophysiology, 9–12 risk factors, 6–7, 11f risk prediction, 7–8, 8f, 185–187 atrial fibrillation, case study of paroxysmal antiarrhythmic agents, 233–235, 234t anticoagulation, 235–239 background information, 229, 230f cardioversion, need for, 230–231 case discussion, 240 initial evaluation, 229–230 management goals, 229, 255f rate control, 231–233, 234t rhythm- or rate-control strategy, 233–235, 235f, 236f atrial fibrillation, case study of permanent atrioventricular node ablation and pacing, 83, 260 Inde x background information, 253, 254f cardiac resynchronization therapy, 259–260 case discussion, 262–264, 264f heart failure, 255–259, 256f, 259t management goals, 253–254, 255f rate control, 256–258 stroke prevention, 261 upstream therapy and prevention, 258–259 atrial fibrillation, case study of persistent antiarrhytmic agents, 245–246, 245f background information, 243, 244f case discussion, 250–251 early management of, 243–245 effects when anticoagulation has been discontinued, 249–250 efficacy of ablation techniques, 246f, 248–249 management goals, 255f pulmonary vein isolation, 246, 247f stroke, risk of, 246–248 atrial fibrillation and congestive heart failure (AF-CHF), 50, 51t, 52t, 54, 56, 213t, 255–259, 256f, 259t, Atrial Fibrillation Follow-up Investigation of Rhythm Management (AFFIRM), 51–52, 51t, 52t, 54, 56, 79, 80, 81, 213t, 233, 256–257 atrial structural abnormalities, as a risk factor, 6, 9–10 atrial tachyarrhythmias (ATAs), 133–134, 135–136, 135f ATRIA score, 248 AtriClip LAA Exclusion System, 112, 214 atrioventricular (AV) junction ablation, 28–29, 48 atrioventricular node ablation and pacing, 83, 260 AV See atrioventricular B benzodiazepine, 151 β-blockers, 28, 61, 234t See also name of for rate control, 80, 82, 258 bisoprolol, 234t BMI See body mass index body mass index (BMI), as a risk factor, 6, C CABANA trial, 56 caffeine consumption, 31 calcium channel blockers, 28, 61–62, 234t Inde x See also name of for rate control, 80, 62, 258 Canadian Cardiovascular Society (CCS), Severity of Atrial Fibrillation scale, 29 Cardiac Arrhythmia Suppression Trial (CAST), 234 cardiac resynchronization therapy (CRT), 83–84, 84f, 259–260 cardioversion, electrical (direct-current) See also antiarrhythmic agents anticoagulants, 62 atrial fibrillation recurrence after, 64–65 case study of paroxysmal atrial fibrillation, 230–231 complications from, 64 description of method, 62–64, 149–151 development of, 62 implantable cardioverter-defibrillators and, 64 role of, 29, 49, 61–62, 191 carvedilol, 234t, 258 CAST See Cardiac Arrhythmia Suppression Trial catheter ablation, 29, 49, 50 anticoagulation, management of, 91 complications, 88, 88t modalities used to perform, 89t outcomes, 91–93, 93f patient selection, 87–88 rate- versus rhythm-control strategy and, 56 rhythm control and, 87–93, 88t, 89f, 89t, 90t, 92t, 93f, 193–193 sites for, 90t techniques, 88–91, 89f tools to improve pulmonary vein isolation, 92t CCS See Canadian Cardiovascular Society CFAEs See complex fractionated atrial electrograms CHADS2 index, 29–30, 110, 130, 175, 186, 214, 221 CHA2DS2 - VASc index, 29–30, 110, 145, 175, 175t, 176t, 186, 186t, 214, 221, 261, 261t, 262t CHARGE-AF See Cohorts for Heart and Aging Research in Genomic Epidemiology-AF CHF See congestive heart failure clinical evaluation assessment checklist, 22, 23t–27t background questions, 23t diagnostic, 30 guidelines for, 31–32 history taking, 23t–26t lifestyle recommendations, 31 271 physical examination, 26t–27t predictive stroke-risk score, 29–30 rate- versus rhythm-control strategy, 28–29 software programs for data, 22, 28, 33–42 systematic, protocol-based approach to, 21–22 tests, 26t, 27t treatment plan, 27t CM See Cox-Maze Cohorts for Heart and Aging Research in Genomic Epidemiology-AF (CHARGE-AF) prediction model, 7–8, 7f, 10 community pharmacists, 168–170 complex fractionated atrial electrograms (CFAEs), 98 complications, congestive heart failure (CHF) See also atrial fibrillation and congestive heart failure rate- versus rhythm-control strategy and worsening, 52–53, 53f costs, rate- versus rhythm-control strategy and, 54–55, 55f Cox-Maze (CM) procedures, 98–99, 111, 127, 128–136, 129f, 130f, 132f, 133f CRT See cardiac resynchronization therapy cryoablation, 98, 129, 131–132, 133 D dabigatran, 62, 110–111, 189, 190, 237–238 death rates, rate- versus rhythm-control strategy, 50–51, 51t decision making aids, 215–218, 216t–218t, 219f choices to consider, 212–215 ethics and, 211–212 models, 202–204 patient, role of, 201 shared, 207–211, 209f, 219–221 types of, 204–207, 205t diabetes, 6, 7, 143 diagnostic evaluations, 30 digoxin, 28, 62, 80, 82, 234t, 258 dilation, left atrial, 10 diltiazem, 80, 82, 234t, 258 direct current cardioversion See cardioversion, electrical disopyramide, 65, 66t, 67 dofetilide, 29, 65, 66t, 69–70, 69t, 164, 191, 192, 234, 235 dronedarone, 29, 65, 67t, 69t, 72, 192 272 E ECAS See European Cardiac Arrhythmia Society educational interventions/counseling, 31, 32, 43 EHRA See European Heart Rhythm Association electrical cardioversion See cardioversion, electrical electrophysiology studies, endocardial and epicardial surgical ablation, 98–100, 100t, 136 endoscopic cutter, 112 epidemiology, 4, 5f, ESC See European Society of Cardiology esmolol, 80, 234t esophageal intubation, 155 ethics, decision making and, 211–212 ethnic/racial differences, 6, etomidate, 62 European Cardiac Arrhythmia Society (ECAS), 97, 129–130 European Heart Rhythm Association (EHRA), 97, 129–130 European/Euro Heart Survey, 8, 21 European Society of Cardiology (ESC) classification, 3–4, 253–254 guidelines for rate control, 259t evaluation See clinical evaluation exercise, 31 F fentanyl, 151 fibrosis, 10 flecainide, 29, 65, 66t, 68, 69t, 192, 234 Framingham Heart Study, 6, 7, 8, 50, 184 FRI See Functional Recovery Index Functional Recovery Index (FRI), 157, 159 G gender differences, gene expression, alterations in, genetics, role of, 6–7 Global Burden of Disease (2010) study, 6, H HARMONY trial (a study to evaluate the effect of ranolazine and dronedarone when given alone and in combination in patients with paroxysmal atrial fibrillation), 74 HAS-BLED score, 110, 176, 176t, 177t, 186, 187t, 214, 221, 248, 261, 262t, 263t HCAHPS See Hospital Consumer Assessment of Healthcare Providers and Systems Inde x healthcare team members, role of, 10, 11f, 12 Heart and Stroke Foundation of Canada, 43 heart failure, as a risk factor, 6, 7, heart rate control See rate control Heart Rhythm Society (HRS), 97 classification, 3–4 indications for ablation, 129–130 resources from, 43 heparin, unfractionated or low molecular weight, 62, 190 Hospital Consumer Assessment of Healthcare Providers and Systems (HCAHPS) scores, 166 HRS See Heart Rhythm Society hybrid ablation, 100, 101t, 102–105, 102f hypertension, 6, 7, 8, 30, 32 hyperthyroidism, 6, 30 hypotension, 64 I ibutilide, 65, 67t, 72–73, 191 ICDs See implantable cardioverter-defibrillators implantable cardioverter-defibrillators (ICDs), cardioversion and, 64 inflammation, 10 inpatient/institutional pharmacists, 163–167 interdisciplinary healthcare team members, role of, 10, 11f, 12 International Patient Decision Aids Standards (IPDAS), 215–216, 219f intubation aids, 144–145, 146f–147f, 155 IPDAS See International Patient Decision Aids Standards K ketamine, 151 L LAA See left atrial appendage LARIAT suture deliver system, 118, 120f, 121, 190, 214 left atrial appendage (LAA) exclusion, surgical techniques, 111–112 exclusion, transcatheter techniques, 112–121 stroke and, 109–110 lifestyle recommendations, 31 longitudinal history, M Mallampati test, 143–144 medication(s) Inde x See also name of errors, 165 patient acquisition of, and role of pharmacists, 169–170 reconciliation, 166–167, 168, 169 Metabolic Efficiency with Ranolazine for Less Ischemia in Non-ST elevation acute coronary syndromes, 74 MERLIN See Metabolic Efficiency with Ranolazine for Less Ischemia in Non-ST elevation acute coronary syndromes trial methohexital, 151 metoprolol, 80, 234t, 258 midazolam, 151 mitral valve disease, as a risk factor, myocardial infarction, as a risk factor, 6, myocardial ischemia, test for, 20 N nadolol, 234t NOACs See novel oral anticoagulants novel oral anticoagulants (NOACs), 91, 189–190, 237–239 nurse practitioners, role of, 193–195 O OACs See oral anticoagulants obesity, as a risk factor, 10, 32 oral anticoagulants (OACs), 30 Ottawa Decision-Making Model, 202–203 P pacemaker implantation, with atrioventricular junction ablation, 28–29, 40 PACU See postanesthesia care unit paroxysmal atrial fibrillation See also atrial fibrillation, case study of paroxysmal defined, Patient Centered Medical Home, 178 Patient Centered Medical Home Neighborhood, 178 patient evaluation See clinical evaluation Percutaneous LAA Transcatheter Occlusion (PLAATO), 112–113, 113f permanent atrial fibrillation See also atrial fibrillation, case study of permanent defined, persistent atrial fibrillation 273 See also atrial fibrillation, case study of persistent defined, pharmacists ambulatory care, 167–168 anticoagulation services, 165, 167–168 antiarrhythmic dosing and safety, 164–165 community, 168–170 inpatient/institutional, 163–167 medication errors and role of, 165 medication reconciliation, 166–167, 168, 169 as part of the patient care team, 165 patient acquisition of medications and role of, 169–170 role of, 163 as a source for patient and provider education, 165–166, 169 pharmacological cardioversion See antiarrhythmic agents PLAATO See Percutaneous LAA Transcatheter Occlusion postanesthesia care unit (PACU), 158 PREVAIL See Prospective Randomized Evaluation of the WATCHMAN™LAA Closure Device in Patients With Atrial Fibrillation versus Long-Term Warfarin Therapy primary care physician, role of anticoagulation management and, 179–180 initial management and, 173–174 interaction with specialists, 178–179 subsequent management with cardiologist and, 174–177 procainamide, 65, 66t, 67 propafenone, 29, 65, 66t, 68–69, 69t, 80, 192, 234 propofol, 62, 151 propranolol, 80, 234t Prospective Randomized Evaluation of the WATCHMAN LAA Closure Device in Patients With Atrial Fibrillation versus Long-Term Warfarin Therapy (PREVAIL) trial, 115–116 PROTECT-AF pulmonary edema See WATCHMAN Left Atrial Appendage System for Embolic Protection in Patients with Atrial Fibrillation pulmonary vein isolation, 9, 97–98, 131 tools to improve, 92t Q QoR9 See Quality of Recovery Score 274 quality of life, rate- versus rhythm-control strategy, 53–54 Quality of Recovery Score (QoR9), 157 quinidine, 65, 66t, 67 R RACE See Rate Control versus Electrical Cardioversion for Persistent Atrial Fibrillation Study RAFT-AF See Rhythm Control Catheter Ablation With Medical Therapy and/ or Atrio-ventricular Junction Ablation and Pacemaker Treatment for Atrial Fibrillation trial Randomized Evaluation of Long Term Anticoagulation Therapy (RE-LY) trial, 237 ranolazine, 74 rate control atrioventricular node ablation and pacing, 83 β-blockers, calcium channel blockers, and antiarrhythmic agents, 79–81 cardiac resynchronization therapy, 83–84, 84f case study of paroxysmal AF, 231–233, 234t defined, 47–48 goals of, 81–82, 188 mortality rates, 213t reasons for using, 57t rhythm-control strategy versus, 28–29, 49–55 ventricular preexcitation, 82–83, 82f Rate Control versus Electrical Cardioversion for Persistent Atrial Fibrillation Study (RACE), 50, 51t, 52t, 81, 213t, 232, 257, 257f relief of symptoms, rate- versus rhythm-control strategy, 53–54 RE-LY See Randomized Evaluation of Long Term Anticoagulation Therapy renin-angiotensin-aldosterone inhibition, 9, 258, 259 Reykjavik Study, rheumatic heart disease, as a risk factor, rhythm control antiarrhythmic agents, 29, 61–62, 65, 66t–67t, 67–74, 69t, 191–192 cardioversion, electrical, 29, 49, 62–65, 191 case study of paroxysmal AF, 233–235, 235f, 236f catheter ablation, 87–93, 88t, 89f, 89t, 90t, 92t, 93f, 192–193 defined, 48–49 mortality rates, 213t rate-control versus, 28–29, 49–55 Inde x reasons for using, 57t, 190–193 Rhythm Control Catheter Ablation With Medical Therapy and/or Atrio-ventricular Junction Ablation and Pacemaker Treatment for Atrial Fibrillation (RAFT-AF) trial, 56, 260 right atrial lesion set, 131–132, 132f right minithoracotomy (RMT), 130–131, 135 risk factors, 6–7, 11f risk prediction, 7–8, 8f rivaroxaban, 62, 110–111, 189, 190, 238 RMT See right minithoracotomy Rotterdam Study, 6, S SAF See Severity of Atrial Fibrillation scale SAFIRE-D (symptomatic atrial fibrillation investigative research on dofetilide) trial, 191 Severity of Atrial Fibrillation (SAF) scale, 29 sick sinus syndrome, 64 sinus rhythm See rhythm control skin burns, 64 sleep apnea, 30, 32, 143 smoking, as a risk factor, 6, 7, 32 Society of Thoracic Surgeons, 129–130 software programs for patient data, 22, 28, 33–42 SOLVD (Studies of Left Ventricular Dysfunction) trial, 259 sotalol, 29, 65, 66t, 69t, 70–71, 80, 164, 192, 234 STAF See Strategies for Treatment of Atrial Fibrillation St Michael’s Hospital–Cardiac Arrhythmia Service, 43 Strategies for Treatment of Atrial Fibrillation (STAF) trial, 257 stress, 31 stroke left atrial appendage and, 109–110 prevention, 261 risk of, 246–248 stroke-risk score, predictive, 29–30 stroke/systemic embolus, rate- versus rhythmcontrol strategy, 51–52, 52t surgical ablation Cox-Maze procedures, 98–99, 111, 127, 128– 136, 129f, 130f, 132f, 133f history of, 127–128 patient selection, 129–130 recovery and complications, 133–134 results, 134–136, 135f techniques, 130–133 Inde x symptoms, rate- versus rhythm-control strategy and relief of, 53–54 T TEE See transesophageal echocardiogram thromboembolism, 64, 109, 128 TRACE (Trandolapril Cardiac Evaluation) study, 259 transesophageal echocardiogram (TEE), 63, 145, 148, 155, 231 V valvular heart disease, as a risk factor, 6, VAMCs See Veterans Affairs Medical Centers ventricular preexcitation, 82–83, 82f verapamil, 80, 82, 234t, 258 275 vernakalent, 67t, 73–74 Veterans Affairs Medical Centers (VAMCs), 167–168 W warfarin, 62, 91, 99, 110, 134, 189 WATCHMAN, 113, 114f, 115–117, 115f, 117f, 190, 214 WATCHMAN Left Atrial Appendage System for Embolic Protection in Patients with Atrial Fibrillation (PROTECT-AF) pulmonary edema, 64, 115–116 websites, 43 Wolff-Parkinson-White (WFW) syndrome, 187, 232–233 WFW See Wolff-Parkinson-White syndrome ... 18 19 20 21 22 23 24 25 26 27 28 29 30 with atrial fibrillation Ann Thorac Surg 1996;61 (2) :755–759 January CT, Wann LS, Alpert JS, et al 20 14 AHA/ACC/HRS guideline for the management of patients... heart survey on atrial fibrillation Chest 20 10;137 (2) :26 3? ?27 2 Hart RG, Pearce LA, Aguilar MI Meta-analysis: Antithrombotic therapy to prevent stroke in patients who have nonvalvular atrial fibrillation. .. Warfarin use among ambulatory patients with nonvalvular atrial fibrillation: The anticoagulation and risk factors in atrial fibrillation (ATRIA) study Ann Intern Med 1999;131( 12) : 927 –934 Walker AM, Bennett