Scott & White Memorial Hospital and Clinic Texas A&M University Health Science Center

1. Atrial Fibrillation Steven M. Costa, M.D. FACC Assistant Professor Department of Medicine Division of Cardiology Scott & White Memorial Hospital and Clinic Texas A&M University Health Science Center

3. Arrhythmia CLUES Width? (narrow complex)NCT vs (wide)WCT Regular? Irregular? Rate? P waves? No P waves Relation to QRS? Morphology (s) RP Interval

4. Case #1

5. Sinus Tachycardia General HR > 100 bpm Upper Limits: 220 – age Behavior: Warm up, Cool Down Etiology Hyperadrenergic States Hypovolemia Fever Pain Hyperthyroidism Treatment Correct underlying cause

6. Case #2 • You’ve Just admitted at patient • 68 y/o with cough, fever and leukocytosis with RLL infiltrate on CXR • h/o COPD • You tuck him away • Nurse calls you – they’re Tachycardic

8. MAT

9. Multifocal Atrial Tachycardia General Seen in Elderly, Critically Ill pts Etiologies Pulmonary Disease COPD, Hypoxia Theophylline Electrolytes – i K+, Mg+ Infxns Metabolic Disturbances Acidosis ECG Recognition 3 different P wave morphologies Rate: 100 – 180 bpm Treatment Treat the underlying cause!!!!

10. Case #3

11. Atrial Flutter • (Macro) Reentrant Circuit located in the RA • Typical Flutter = Cavotricuspid Isthmus Dependent • Atrial Rate: 250-350 bpm • Ventricular Rate: Depends on degree of conduction

12. Atrial Flutter (A-Flutter) • Rapid and regular form of atrial tachycardia • Usually paroxysmal • Sustained by a macro-reentrant circuit • Circuit is confined to the right atrium • Episodes can last from seconds to years • Chronic atrial flutter may progress to atrial fibrillation Morady F. N Engl J of Med. 1999;340:534-544.

13. Atrial flutter

14. RF Ablation of Atrial Flutter

15. Case #4 • 76 y/o WM • HPI: 3 hours history of “fluttering in chest” with SOB; never had this before; came on at rest • No chest pain or symptoms consistent with heart failure • PMHx: significant for HTN (not on meds), Obesity, and Anxiety • FHx positive for mother and two brothers with irregular heart rhythms • Exam unremarkable except for irregularly irregular rhythm and BMI of 31

16. ECG #4

17. AFIB ECG

18. A.Multiple-wavelet reentry Wavelets (indicated by arrows) randomly reenter tissue previously activated by them or by another wavelet. B. Focal activation. The initiating focus often lies within the region of the pulmonary veins.

19. What are the important issues in managing this gentleman? • Etiology/Risk Factors • Initial Rate control • Do we anti-coagulate? • Convert? • Should we do other test? • What medicines do we send him out on?

20. Background • Atrial fibrillation is the most common sustained arrhythmia • Affects 2 million Americans • 6% over the age of 65 experience it • Responsible for 15% strokes • Benjamin E: Epidemiology of Atrial Fibrillation. In Falk RH, Podrida PJ, eds:Atrial Fibrillation: Mechanisms and Management. 2nd Ed, Lippincott-Raven Press, New York 1997, pp.1-22.

21. Atrial Fibrillation Demographics by Age U.S. populationx 1000 Population with AFx 1000 Population withatrial fibrillation 30,000 20,000 10,000 0 500 400 300 200 100 0 U.S. population <5 5-9 10-14 15-19 20-24 25-29 30-34 35-39 40-44 45-49 50-54 55-59 60-64 65-69 70-74 75-79 80-84 85-89 90-94 >95 Age, yr Adapted from Feinberg WM. Arch Intern Med. 1995;155:469-473.

22. Clinical Manifestations • 3 factors affect hemodynamic function: • loss of synchronous atrial mechanical activity. • Irregularity of ventricular response. • Inappropriately rapid heart rate

23. Symptoms • Symptoms vary with the ventricular rate, underlying functional status, duration of AF, and individual patient perceptions. • Most patients with AF complain of palpitations, chest pain, dyspnea,fatigue, or light headedness/syncope. • Inappropriate heart rate response • Tachycardia induced cardiomyopathy • Irregular rate “fluttering” • Loss of atrial systolic function • CHF- reduced EF Lots of patient have no symptoms present with Thromboembolic event

24. Atrial Fibrillation: Causes • Cardiac • Non-cardiac • “Lone” atrial fibrillation

25. Pathophysiological Mechanisms The most frequent pathoanatomic changes in AF are atrial fibrosis and loss of atrial muscle mass. Fibrosis is triggered by atrial dilation which activates several molecular pathways, including the renin-angiotensin-aldosterone system (RAAS). Experimental studies show that ACE inhibition may prevent AF by reducing this fibrosis. ACC/AHA/ESC guidelines 2006

26. Other Factors Contributing to Atrial Fibrillation 1. Inflammation - In a case-control study, levels of C-reactive protein (CRP) were higher in patients with AF. 2. Oxidative stress - In the experimental model, tachycardia-related electrical remodeling was suppressed by pretreatment with simvastatin but not by the antioxidant vitamins C and E. 3. Autonomic nervous system - In animal models, parasympathetic stimulation shortens atrial and PV refractory periods, thus potentiating initiation and maintenance of AF. 4. LV diastolic dysfunction - There is a strong association between obstructive sleep apnea, hypertension and AF possibly by increasing pressure that affects stretch receptors in PV or other areas of the atrial myocardium. ACC/AHA/ESC guidelines 2006

27. Atrial Fibrillation: Cardiac Causes • Hypertensive heart disease • Ischemic heart disease • Valvular heart disease • Rheumatic: mitral stenosis • Non-rheumatic: aortic stenosis, mitral regurgitation • Pericarditis • Cardiac tumors: atrial myxoma • Sick sinus syndrome • Cardiomyopathy • Hypertrophic • Idiopathic dilated (? cause vs. effect) • Post-coronary bypass surgery • Familial Variety

28. Atrial Fibrillation: Non-Cardiac Causes • Pulmonary • COPD • Pneumonia • Pulmonary embolism • Metabolic • Thyroid disease: hyperthyroidism • Electrolyte disorder • Toxic: alcohol (‘holiday heart’ syndrome)

29. “Lone” Atrial Fibrillation • Absence of identifiable cardiovascular, pulmonary, or associated systemicdisease • Approximately 0.8 - 2.0% of patients with atrial fibrillation (Framingham Study)1 • In one series of patients undergoing electrical cardioversion, 10% had lone AF.2 • These patients have a favorable prognosis with respect to thromboembolism and mortality. 1 Brand FN. JAMA. 1985;254(24):3449-3453.2 Van Gelder IC. Am J Cardiol. 1991;68:41-46.

30. Management • Three basic goals: • Rate control (meds or DCCV) • Anticoagulate- Prevention of Thromboembolism • Treatment- Correction of rhythm disturbance

31. Recommendations for Rate Control • Class I • Rate control using pharmacologic agents (BB, CCB) • IV Beta Blocker or Non-Dihydro Ca Channel Blocker for rapid afib • IV digoxin, amiodarone for rate control if no accessory pathway • Stress testing if symptoms during exercise • Digoxin for rest rate control in LV dysfxn, HF, sedentary pts • Class IIa • Dig + (BB or CCB) for rate control at rest/exercise • IV amio if other measures ineffective • When DCCV is not necessary in AFIB-accessory pathway consider Procainamide/ibutilide ACC/AHA/ESC guidelines 2006

32. Recommendations for Rate Control • Class IIb • Oral amio if others ineffective • Ablation if rate can not be controlled medically, or if tachy-mediated CM suspected • Class III • Dig alone in paroxysmal AFib • AV node Catheter ablation without prior trial of medications • IV NDCCB with decompensated HF and AFib • IV dig or CCB for preexcitation syndrome ACC/AHA/ESC guidelines 2006

33. RATE CONTROL • Beta-blockers and nondihydropyridine CCBS are the first line of therapy • Digoxin is NOT the first line of therapy • Rare patient can’t be controlled with meds - AV node ablation and pacing • Tachycardia mediated cardiomyopathy • Chicken or Egg

34. RATE CONTROL

35. Metoprolol/Lopressor 2.5 to 5 mg IV bolus/2 min; up to 3 doses Diltiazem 0.25 mg/kg IV over 2 min then dose 5-15 mg/h IV

37. New Onset AFib Work Up Work Up ECG - Telemetry CBC, TSH Electrolytes, Magnesium Echo – TTE vs TEE Ingestion History – EtOH, Cocaine PE Work up (if indicated)

38. Other tests • Echo • Left atrial enlargement • LV function • RV function • Pulmonary HTN • Valvular Heart disease • Shunt – ie ASD is young • “Smoke” (TEE) • Poorly contractile LA appendage (TEE) • Pericardial Disease

39. Immediate Treatment • Significant symptoms • Restore NSR +/- Antiarrhthymics • Minimal symptoms • Strongly Consider rate control • AFFIRM Trial

42. Afib Management Unstable Stable < 48 Hrs > 48 Hrs DCCV/Shock! Rate/Anticoag Rate/Anticoag Asymptomatic Symptomatic 3-4 wks Symptomatic Rate/Anticoag CCV/DCCV TEE DCCV

43. Unstable=Shock

44. Heart Site

45. Heart 1999;82:726-730 doi:10.1136/hrt.82.6.726

46. Cardioversion (electrical or pharmacological) of AF 48 Hours* Duration of Atrial Fibrillation 0 TIME Class I Anticoagulation recommended ≥ 3 weeks before and ≥ 4 weeks after (INR 2-3) Administer heparin concomitantly if urgent cardioversion required Class IIa TEE can negate anticoagulation before cardioversion (use heparin during and keep INR 2-3 for ≥ 4 weeks after) Treat Atrial Flutter similarly Class IIa Anticoagulation before and after may be based on patient risk * Unknown duration is equivalent to > 48 hours

47. Guidelines: Definitions

49. Therapeutic Approaches to Atrial Fibrillation • Control of Ventricular Response • Pharmacologic • Catheter modification or ablation of the AV node • Anticoagulation • ASA, ASA+Clopidogrel, Warfarin, and Dabigatran • Antiarrhythmic Suppression • Curative Procedures • Catheter based ablation • Surgery • Cox-Maze III • Pulmonary Vein Isolation - “Mini-Maze”

50. Benefit of Warfarin Absolute Risk of Stroke • Age < 65 years and no risk factors, “lone AF”: 1%/yr. • All others: lowered to ~1.5%/yr by warfarin The Atrial Fibrillation Investigators Arch Intern Med 1994;154:1449