John Windle MD October 18, 2013 Professor and Chief of Cardiology University of Nebraska Medical Center.
Download ReportTranscript John Windle MD October 18, 2013 Professor and Chief of Cardiology University of Nebraska Medical Center.
John Windle MD October 18, 2013 Professor and Chief of Cardiology University of Nebraska Medical Center “Ha ha ha, Biff. Guess what? After we go to the drugstore and the post office, I’m going to the vet’s to get tutored.” Conflict of Interest I have no relevant conflicts. Just lots of opinions Atrial Fibrillation in the Era of the Accountable Care Organization A Quick Review of the Basics The importance of Definitions The importance of atrial transport The clinical trials that drive the guidelines Filling in the Gaps Rate Control versus Rhythm Control issues Perspectives on bleeding versus stroke but not discussing new therapies. Musings on how this might work in an ACO model Atrial Fibrillation Most common sustained symptomatic tachyarrhythmia. Over 3,000,000 Americans suffer from atrial fibrillation. Incidence with age and presence of structural heart disease Slightly more common in men than women 15%(75,000 per year) of all strokes occur in AF patients One of the top causes of hospitalizations and extension of stays in Hospitals Bialy et al. Journal of the American College of Cardiology 1992; 19(3):41A. Prystowsky et al. Circulation. 1996; 93(6):1262-1277. Wolf et al. Archives of Internal Medicine. 1987; 147(9):1561-1564. Incidence of Atrial Fibrillation (Framingham Study) Chronic AF 14- Paroxysmal AF 1412.9 12.7 6- 5.4 4.8 42.2 2- - - 30-39 64.8 4- 1.5 0.7 0 Women 8- 2- 0.9 - 0- 0.5 40-49 50-59 60-69 70-79 Age Kannel et al. American Heart Journal. 1983;106(2):389-396. 9.2 0- 0.5 0 0 30-39 0.4 1.9 0.6 0.5 - 6.7 Men - Women 8- 10- - Men - 10- 2-yr Incidence (per 1000) 12- - 2-yr Incidence (per 1000) 12- 40-49 50-59 60-69 70-79 Age Consequences of Atrial Fibrillation Arrhythmia-associated symptoms, look at exertional symptoms of shortness of breath, exertional dyspnea and decreased exercise tolerance. LV function: Impact of atrial transport and diastolic function. Tachycardia-mediated cardiomyopathy (heart rates over 130 b/m) 2-fold in cardiac mortality 5-fold in risk of stroke “Why do I feel like crap?” Myocardial and Hemodynamic Consequences of Atrial fibrillation Loss of atrial contraction decreases cardiac output 9% drop in C.O. in canine model 15% drop in C.O. in irregular response vs. same average rate pacing. Decrease in coronary blood flow with irregular ventricular rhythm. Tachycardia-induced cardiomyopathy (heart rate >130 for several weeks). LVH (diastolic dysfunction) accentuates the importance atrial contraction. The impact of atrial contribution by cardiac doppler Atrial Fibrillation-The 3 Ps Paroxysmal-Self-limited, often occurring in structurally normal hearts Persistent-Requiring intervention, either chemical (antiarrhythmic drugs) or electrical to restore sinus rhythm Long-standing persist-a term created by cardiac electrophysiologists to “not give up”. Permanent-”Uncardiovertable” Atrial Fibrillation Guidelines Paroxysmal Atrial Fibrillation Vasovagal-nocturnal, triggered by stress, meals or alcohol Self-limited but shortened duration with propafenone or flecainide Often have pulmonary vein foci Amenable to Ablative therapy Persistent Atrial Fibrillation Need an intervention to restore sinus rhythm More likely to involve structural heart disease: Cardiac effects of hypertension and LVH, prior myocardial damage such as MI Try to figure out the symptom trigger: Rate, regularity or Atrial synchrony and atrial transport. Permanent Atrial Fibrillation Un-cardiovertable atrial fibrillation Duration Left atrial size Comorbidities Absence of Symptoms Decision Points for Atrial Fibrillation Prevention of Thromboembolism Ventricular Rate Control Conversion to NSR Maintenance of NSR Short Term NSR = normal sinus rhythm Time Long Term Rate Control Therapy A-V Nodal Agents (slow ventricular response) Digoxin-increases vagal tone, reduces resting heart rate but not exercise rate Beta Blockers-underutilized but most effective Calcium Channel Agents Diltiazem and verapamil not nifedipine Adenosine A-V Node Ablation with pacemaker placement Single versus Bi-V device Rhythm Control Therapy Atrial Muscle Agents (restoration and maintenance of sinus rhythm) Procainamide and Quinidine-What we learned about in School but of limited use and availability now Propafenone, Flecainide-Good for acute conversion and normal hearts (Pill-in-the Pocket) Disopyramide-Still in good option for some, decreases vagal tone Sotalol and Dofetilide-Torsades de Pointes but otherwise great agents Dronederone-very limited use. Amiodarone* *The Vaughn-Williams Classification system is easy but wrong. The Affirmed Trial The Affirmed Trial-Rate Control versus Rhythm Control in Patients with Atrial Fibrillation Critical Study: Randomized Control Trial Rhythm Control no better than Rate Control Rate control less costly The Affirmed Trial: Part II Short follow-up on “elderly”, asymptomatic patients Based on an “intention to treat” “Failure” based on first recurrence versus time spent in desired rhythm Very high overlap in assigned patients in their actual rhythm (sinus rhythm versus atrial fibrillation). Not a comparison of atrial fibrillation versus sinus rhythm (The sinus rhythm patients did significantly better) Atrial Fibrillation; now what?! No significant improvement in quality of life with “rhythm control” strategy in multiple trials above. STAF and HOT CAFÉ showed increase in exercise tolerance. It’s just AF; it won’t KILL ME. Excess mortality in AF patients compared to matched (non-AF). Framingham Heart Study (1983); The Regional Heart Study Whitehall Study Manitoba Study (1995) HF promotes AF, AF exacerbates HF, and patients with either who develop the other, share a poor prognosis. Stroke in AF averages 5% per year! 1.5% annual in 50-59y to 23% annual in 80-89 yrs. Framingham Data. My Take Home Messages: Yep-Sinus rhythm and rate controlled atrial fibrillation equivalent in asymptomatic, elderly patients followed over 3-5 years. Yep-Lower utilization of resources with rate control strategy But, Didn’t answer sinus versus rate control Most of my patients are not truly asymptomatic Atrial fibrillation causes a 5-10% drop in EF in most patients, what do you think will happen over time? Anticoagulation Anticoagulation is recommended for ALL patients with atrial fibrillation, except those with “LONE AF” or contraindications. Anticoagulation with a vitamin K antagonist is recommended for patients with more than 1 moderate risk factor Aspirin 81-325 mg for low-risk patients, or those with CI to oral anticoagulation Anticoagulation for atrial flutter is recommended as per AF. Long term anticoagulation with vitamin K antagonist is NOT recommended for primary strike prevention in patients <60 yrs of age without heart disease. CHADS2 Score EF <35% Circulation. 2006;114:e257-e357. Why anticoagulation to a target of 2.0 to 3.0? Warfarin vs. Aspirin Why not everyone with AF? Atrial Fibrillation: Interventions Cardioversion: Medical versus Electrical Dual Chamber Pacing (Bradycardic-dependent arrhythmias) AV Node Ablation and Ventricular Pacing EF <45% Pacing over 40% Pulmonary Vein Isolation Ablation Surgical MAZE Procedure Dilbert Dilbert All roads lead to catheter ablation! Catheter Ablation for AF Rationale: Triggers within the pulmonary veins and other sites (SVC, LM, CS, CT) Isolation of the pulmonary veins eliminates AF in many patients with PAF. Alteration of substrate in Persistent AF patients dramatically reduces symptoms of AF, and frequently reduces or eliminates the need for antiarrhythmic medications to control the rhythm. History of AF Ablation Initial procedure mimicked the surgical maze procedure. Success rate was 40-50% and complication rate high. (Prior to 1998). Automaticity within the pulmonary veins was then the target… Pulmonary Vein Isolation ~95% of the triggers for AF are suspected to be in the pulmonary veins. Additional triggers at sites of “Complex Fractionated Atrial Electrograms” (CFAEs) In PAROXYSMAL atrial fibrillation, pulmonary vein isolation is effective in 80-85% of cases at “CURING” atrial fibrillation. Currently, “Symptomatic atrial fibrillation refractory to or intolerant of medical therapy” is the primary indication for PVAI. Ultrasound Reconstruction of The Left Atrium with CartoSound/ICE WHAT FOR: Mapping veins, appendage Mitral annulus/valve Velocities, evaluate for PFO Map coronary arteries CONTINUOUSLY EVALUATE FOR PERICARDIAL EFFUSION CT scan merged with ultrasound image (right). Pulmonary vein isolation for paroxysmal AF Atrial fibrillation persists within the RSPV, but sinus rhythm is present elsewhere What about “Non-Paroxysmal” AF? More complex disease entity from an ablation standpoint. PVAI is not sufficient for elimination of atrial fibrillation in many patients. Additional lesions include approximation of the maze lesion set with ablation at the roof, mitral annulus, cavotricuspid isthmus, and svc. The addition of CFAE ablation is of unclear benefit and remains controversial. Complications: Perforation with pericardial tamponade ~1% of cases of PVAI (up to 5% depending on series) Usually self-limiting, requiring a drain Rarely can require surgical drainage/repair. Cerebrovascular accidents 0.5 to 2.5% of cases Dramatically reduced with higher ACT Phrenic Nerve Injury 0.1 to 0.48% of cases Recovery in 66% of cases, can be permanent Radiation related Fluoroscopy times can be prolonged. Pulmonary vein stenosis 1 to 2% with current techniques (15-20% historically) Atrio-Esophageal fistula New Ablation Tools and Techniques CryoBalloon (Arctic Front) Ablation Frontiers Catheter High-Intensity Focused Ultrasound Laser ablation And more…. Just around the corner. Where Do We Go From Here? 3,000,000 patients how do we divide up the work? Base-rate theory: EP>Cardiology>Primary Care Team-based Care Decision-making Rate versus rhythm control Antithrombotic Care Where do we go from here: the ACO In my “perfect-world” EP physicians would consult (either actual or virtually) on all patients at presentation of their atrial fibrillation The EP physician, the primary care provider and the patient would develop a consensus treatment plan with all three holding accountability for the outcome. If anti-thrombotic therapy was initiated it would be managed by a non-physician team member under protocol. Cardiologists would be involved in atrial fibrillation management. Questions? New Drugs Dronedarone: a non-iodinated amiodarone analog. Trials have compared the medication to placebo and amiodarone. Euridis and Adonis (European and American) trials showed efficacy relative to placebo. ANDROMEDA study showed higher death rate in NYHA Class IV patients. ATHENA trial demonstrated stroke risk reduction. Currently, approval is for “treatment of patients with a history of, or recurrent atrial fibrillation to reduce their risk of cardiovascular hospitalization due to this condition.” Azmilide Not yet approved Potassium blocker similar to dofetilide or sotalol, but blocks both iKr and iKs. Does not perform as a beta-blocker. LONG HALF-LIFE of up to 4 days. In a trial to assess its efficacy in MI patients with EF 1535%, (ALIVE), a higher proportion of patients in the treatment arm were in sinus rhythm at the end of the study… Placebo-controlled trial is in the works.