Atrial fibrillation...rx

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ATRIAL FIBRILLATION THE GRANDFATHER OF ARRHYTHMIAS..

Atrial fibrillation...rx

  1. 1. ATRIAL FIBRILLATION<br />Dr. Nagula Praveen<br />
  2. 2. Management<br />GOALS:<br /><ul><li>Prevention of stroke
  3. 3. Prevention of tachycardia induced cardiomyopathy
  4. 4. Symptom relief
  5. 5. Improved survival
  6. 6. Primary prevention</li></li></ul><li>Three strategies<br /><ul><li>Rate control – in all patients with AF
  7. 7. Rhythm control – in selected patients with AF
  8. 8. Prevention of thrombo embolism</li></li></ul><li>Management<br /><ul><li>MEDICAL
  9. 9. 1.ANTIARRHYTHMIC DRUGS
  10. 10. 2.AV NODAL BLOCKING DRUGS
  11. 11. 3.ACEI
  12. 12. 4.ARBS
  13. 13. 5.STATINS
  14. 14. 6.FATTY ACIDS
  15. 15. 7.STEROIDS
  16. 16. SURGICAL —MAZE PROCEDURE
  17. 17. ABLATION
  18. 18. PACEMAKER
  19. 19. ANTI THROMBOTIC TREATMENT</li></li></ul><li>Anticoagulation<br /><ul><li>Risk stratification
  20. 20. Pericardioversion</li></li></ul><li>RISK FACTORS<br />Highest risk of stroke >6% /yr<br /><ul><li>Valvular
  21. 21. 15- 20 times the nonvalvular
  22. 22. Prosthetic valves 2.5-3.5
  23. 23. MVR – 2.0- 3.0
  24. 24. previous h/o TIA/stroke</li></ul>Intermediate risk factors ---3—5 % /yr<br /><ul><li>CHA2DS2VASc score</li></ul>One intermediate risk factor present<br /><ul><li>HTN
  25. 25. Diabetes
  26. 26. Age
  27. 27. Lone AF lowest risk < 2% yr</li></li></ul><li>FRAMINGHAM RISK SCORE<br />
  28. 28. CHA2DS2VASc SCORE<br />
  29. 29. THERAPY ACCORDING TO RISK FACTORS<br />
  30. 30. Pericardioversion<br /><ul><li>AF ---- mechanical stasis in atria, atrial appendage.---pro inflammatory state--- pro thrombotic state.
  31. 31. Unstable thrombus – dislodge on contraction.
  32. 32. Atrial mechanical function lags behind electrical function.
  33. 33. Atrial mechanical stunning --- 4 weeks JACC 1989
  34. 34. If not risk of event – 5%</li></li></ul><li><ul><li>If > 48 hrs
  35. 35. Empiric anticoagulation for 3 weeks.
  36. 36. Short term anticoagulation : TEE guided
  37. 37. Why 3 weeks – organisation of thrombus
  38. 38. Warfarin?--- target 2.5
  39. 39. Do weekly INR before cardioversion.
  40. 40. Low INR more events JACC;2002;40(5)
  41. 41. Heparin followed by TEE – thrombus present --- warfarin for three weeks .
  42. 42. Post cardioversion for 4 weeks.
  43. 43. Then based on risk factors assess the risk</li></li></ul><li><ul><li>Most occur in < 72 hrs.
  44. 44. Not needed in < 48 hrs.
  45. 45. Symptoms are unreliable--- ECG documentation needed…otherwise assume > 48 hrs..</li></li></ul><li>Newer agents <br /><ul><li>Why?
  46. 46. Disadvantage of OAC
  47. 47. Inter individual variation
  48. 48. Drug /food interactions
  49. 49. Regular INR check up needed--- monthly.
  50. 50. DABIGATRAN (pradaxa)--- direct thrombin inhibitor
  51. 51. REL –Y trial --- same as warfarin in stroke prevention
  52. 52. Higher dose more effective but with risk of bleeding.
  53. 53. No INR monitoring,150-220 mg daily
  54. 54. FDA approved------- NEJM 2009 361(2);1139-51
  55. 55. RIVAROXABAN (xaretto)--- factor X a inhibitor
  56. 56. Related to linezolid,mitochondrial toxicity
  57. 57. ROCKET AF trial </li></li></ul><li>Other ways <br />LAA occlusion<br /><ul><li>Most common source of embolism
  58. 58. WATCHMAN device
  59. 59. PROTECT AF trial
  60. 60. Periprocedural complications more
  61. 61. Used when OAC contraindicated
  62. 62. lancet 2009 ;374;534--40</li></li></ul><li>RATE VS RHYTHM CONTROL<br /><ul><li>Theoretically rhythm control > rate control
  63. 63. But complications anti arrhythmic drugs.</li></li></ul><li>CHOICE OF STRATEGY<br />
  64. 64. Rate control drugs<br />Atrioventricluar blocking agents<br /><ul><li>Calcium channel blockers
  65. 65. Beta blockers
  66. 66. Amiodarone
  67. 67. Digoxin</li></ul>ABCD<br />
  68. 68. Rate control<br />Bblockers , CCBs , digoxin are effective for rate control.<br />Do not convert AF into NSR.<br />C/I in pre excitation<br />Amiodarone for both rate and rhythm control.<br />Several side effects limits its use as first line drug.<br />Choice of drugs depends upon the clinical presentation<br />
  69. 69. Normal systolic function:<br /><ul><li>IV CCBs non dihydropyridine group
  70. 70. IV BBs --- class I recommendation</li></ul>LVD or HF :<br /><ul><li>IV digoxin or IV amiodarone –class I recommendation
  71. 71. In case of AV nodal blocking agents C/I </li></li></ul><li>DILTIAZEM:<br /><ul><li>Chemical defibrillator
  72. 72. 0.25 mg /kg (15-20 mg ) given IV over 2 minutes.
  73. 73. Monitor HR and BP
  74. 74. Rapid onset of action –within 10 min
  75. 75. 0.35 mg /kg (20-25 mg )IV over 4 min
  76. 76. HR < 100bpm ---maintenance dose 5-15 mg /hr is infused
  77. 77. t1/2 3-4 hrs
  78. 78. Oral dose within 3 hrs of IV dose.
  79. 79. 1.5 * total IV dose
  80. 80. 120-360 mg three to four divided doses
  81. 81. SR prepartion is useful in case of OD</li></li></ul><li>VERAPAMIL:<br /><ul><li>0.075-0.15 mg /kg (5-10mg) given IV over 2 min
  82. 82. Same if needed after 15 to 30 min
  83. 83. T ½ -- 4-12 hrs.
  84. 84. No need of continuous maintenance infusion
  85. 85. More hypotensive and more negatively inotropic than diltiazem.
  86. 86. Hypotension responds to IV calcium gluconate 1 gm.
  87. 87. Oral maintenance does is 120-360 mg in divided doses. </li></li></ul><li>Beta blockers<br /><ul><li>In myocardial ischemia
  88. 88. Thyrotoxicosis
  89. 89. Class I recommendation
  90. 90. Metoprolol:
  91. 91. Selective B1 blocker
  92. 92. 2.5 -5 mg IV over 2 min .. Up to three doses ( max 15 mg)
  93. 93. Oral maintenance dose of 25-100mg (50 mg) bid
  94. 94. Atenolol– use in hypertension 5mg IV—50 mg od
  95. 95. Propanolol – 0.15 mg /kg -- 80 -240 mg /day
  96. 96. Esmolol--- 0.5mg/kg over I min 60- 200mcg /min</li></li></ul><li>digoxin<br /><ul><li>Not used when LV function is preserved.
  97. 97. In hypotension
  98. 98. In COPD
  99. 99. LVD
  100. 100. Class 1 recommendation
  101. 101. Not effective as monotherapy.
  102. 102. Not useful in exercise and thyrotoxicosis</li></li></ul><li>amiodarone<br /><ul><li>Class II a recommendation in case of preserved LV Function
  103. 103. Class II b recommendation when rate control is not achieved by other agents.</li></li></ul><li>Patients with LVD<br /><ul><li>Digoxin:
  104. 104. 0.25 mg IV over 2 min every 2 hours.
  105. 105. Not to exceed 1.5 mg IV over 24 hrs
  106. 106. Maintenance dose is 0.125-0.375 mg daily IV or orally.
  107. 107. Orally 0.5 mg daily for 2-4 days— 0.125– 0.375 mg daily
  108. 108. Slow onset of action
  109. 109. Effective in controlling heart rates at rest as well as in individuals who are sedentary
  110. 110. But not so in adrenergic stress,hyperthyroidism,copd?</li></li></ul><li>Amiodarone:<br /><ul><li>Acute setting
  111. 111. 150 mg IV over 10 min
  112. 112. maintenance infusion of 1 mg/ min IV over 6 hrs ,</li></ul> 0.5 mg /min IV over 18 hrs..<br /><ul><li>Orally ,late onset of action – not in acute setting
  113. 113. Oral dose is 800 mg /day in divided doses /week
  114. 114. Oral maintenance dose 200mg daily.
  115. 115. Affects the pharmacokinetics of digoxin , warfarin , verapamil — reduced dose</li></li></ul><li>WPW SYNDROME<br /><ul><li>Use of AV nodal blocking agents is dangerous.
  116. 116. Allows the fibrillatory waves to pass freely through the bypass tract--- VF
  117. 117. Type Ia agents which increase refractory period of bypass tract –procainamide
  118. 118. Inhibit both AV node and bypass tract– type Ic and type III ibutilide or amiodarone IV to control ventricular rate.
  119. 119. Or else use EC</li></li></ul><li>Non pharmacologcial control of VR in AF<br /><ul><li>In case of tachycardia induced cardiomyopathy</li></ul>AV nodal ablation : if the VR in AF cannot be controlled by AV Nodal blocking agents AV nodal ablation with permanent ventricular pacemaker is an option<br /><ul><li>Agents should be tried</li></ul>Pulmonary vein isolation:<br /><ul><li>Surgically or RFA</li></li></ul><li>
  120. 120. What is effective rate control?<br /><ul><li>At rest HR , 80 /MIN
  121. 121. HOLTER MONITROING rest --- < 80/min
  122. 122. no hour averaging ----- 90 / min
  123. 123. Moderate exercise 90 – 115 /min
  124. 124. Peak exercise 120 /min
  125. 125. 20- 30 % REDUCTION of age predicted HR
  126. 126. RATE CONTROLLING DRUGS</li></li></ul><li>Rhythm control<br /><ul><li>Not necessary in all patients
  127. 127. In AFFIRM trial (Atrial Fibrillation Follow up Investigation of Rhythm Management)
  128. 128. RACE Rate control vs Electrical Cardioversion for Persistent Atrial Fibrillation
  129. 129. No change in mortality or incidence of stroke in both groups.
  130. 130. Symptomatic and LVFpatients</li></li></ul><li>Methods<br />Electrical cardioversion<br />Pharmacological cardioversion<br /><ul><li>Risk of thromboembolisation
  131. 131. Increased if > 48 hrs.
  132. 132. Spontaneous conversion – many patients of AF
  133. 133. Mostly during the first 24-48 hrs.
  134. 134. Less as duration prolongs
  135. 135. Very less > 7 days
  136. 136. Efficacy of drugs also decrease.</li></li></ul><li>Cardioversion<br /><ul><li>Electrical or pharmacological
  137. 137. When?
  138. 138. Which is better?
  139. 139. In whom?
  140. 140. When --- symptomatic AF,newlyAF,post op AF
  141. 141. Which -------- electrical > pharmacological
  142. 142. Whom? ------- persistent,paroxysmal</li></li></ul><li>Do all need ?<br /><ul><li>Severely symptomatic ,less severe symptomatic acute AF --- to be cardioverted…..
  143. 143. “restoration of SR is a reasonable goal in patients who have a first time diagnosis of AF regardless of symptoms unless some indications shows that AF has been prsent for many years before identification…….” CARDIOLOGY CLINICS
  144. 144. In asymptomatic to slow progression of AF </li></li></ul><li><ul><li>Duration of paroxysmal event  progression of AF
  145. 145. Effective in short duration AF
  146. 146. Not useful in old , asymptomatic
  147. 147. Therapeutic anticoagulation in all..
  148. 148. Biphasic > monophasic
  149. 149. Even in presence of structural heart disease.</li></li></ul><li>Electrical cardioversion<br /><ul><li>Success – adequate current flow
  150. 150. Biphasic > monophasic
  151. 151. Deep sedation required.
  152. 152. No effect of pad size or paddle positioning.
  153. 153. Shock delivery not during vulnerable phase---VF
  154. 154. In synchronized mode— R wave sensing.
  155. 155. In defibrillation mode --- in an asynchronous fashion.
  156. 156. 200/360 J
  157. 157. In emphysema,obesity,asthma---expiratory phase </li></li></ul><li><ul><li>Implanted devices --- AP postioning
  158. 158. Why?--- no effect on device.
  159. 159. Device commanded cardioversion.
  160. 160. In AFL –antitachycardio pacing is required,no sedation.
  161. 161. Internal cardioversion --- by catheters—rtatrium,LCS,LPA. </li></li></ul><li>Aftercardioversion<br /><ul><li>Persistent restoration of AF
  162. 162. IRAF
  163. 163. Failed cardioversion
  164. 164. IRAF---immediate recurrence of AF
  165. 165. 5%-25%
  166. 166. Triggered by APCs
  167. 167. Pretreatment with fleicainide useful.
  168. 168. Failed cardioversion – 10 %
  169. 169. Amiodarone,ibutilide useful.</li></li></ul><li>Positoning of paddles <br />
  170. 170. RHYTHM CONTROL DRUGS<br /><ul><li>Theoretically useful
  171. 171. Less symptoms
  172. 172. Good effort tolerance
  173. 173. Less hospitalisations
  174. 174. But more compications by drug itself</li></li></ul><li>
  175. 175.
  176. 176. Pharmacolocigalcardioversion<br /><ul><li>No IV sedation
  177. 177. < 7 days of onset
  178. 178. Less effective than electric
  179. 179. Toxic effects of drugs
  180. 180. Type Ia agents – procainamide,quinidine,disopyramide
  181. 181. Type Ic agents – propafenone , fleicainide
  182. 182. Type IIIagents -- ibutilide, dofetilideamiodarone
  183. 183. Hospitalised
  184. 184. Exception is amiodarone</li></li></ul><li>Type Ia and Ic convert AF –AFL<br />BB or CCBs to be given half n hour before them.<br />Agents <br /><ul><li>AF< 7 days :
  185. 185. Class I recommendation
  186. 186. Class Icfleicainide or propafenone
  187. 187. Class IIa Class III dofetilide or ibutilide
  188. 188. Class IIb – amiodarone
  189. 189. class III --- sotalol,digoxin</li></li></ul><li>Preserved systolic function<br />Flecainide:<br /><ul><li>Class I recommendation
  190. 190. Orally or IV
  191. 191. 200-300 mg given once
  192. 192. Only after effective response in hospitalisation –pill in pocket approach to be used.
  193. 193. IV Dose is 1.5 -3.0 mg/kg given over 10-20 min </li></ul>Propafenone:<br /><ul><li>Class I recommendation
  194. 194. Oral –600mg given once
  195. 195. IV dose 1.5-2.0 mg /kg over 10-20 min
  196. 196. 56-83%</li></li></ul><li>Ibutilide:<br /><ul><li>IV only
  197. 197. 1 mg over 10 min
  198. 198. Dose repeated</li></ul>Dofetilide:<br /><ul><li>c/I in renal dysfunction
  199. 199. 500 mcg bid
  200. 200. 500-100 mcg daily
  201. 201. QT interval to be monitored</li></li></ul><li>Amiodarone:<br /><ul><li>5-7 mg/ kg IV over 30- 60 min
  202. 202. 1.2 -1.8 g/day of infusion—10 gms
  203. 203. 200-400mg/day is maintenance</li></ul>Quinidine:<br /><ul><li>0.75-1.5 gm in divided doses
  204. 204. Digitalis toxicity </li></li></ul><li>In LVD<br /><ul><li>Only amiodarone and dofetilide
  205. 205. 100-400 mg daily
  206. 206. >7 days:
  207. 207. Class III agents are effective</li></li></ul><li>Choice of anti arrhythmic drugs in the treatment of AF with assosciated co morbidities <br />
  208. 208. In brief<br /><ul><li>Short duration AF --- highly symptomatic , no structural heart disease.
  209. 209. Adjunctive therapy
  210. 210. For short duration –class Ic drugs
  211. 211. Pill in pocket approach only after intial hospital response --- based on symptoms prsent outside,
  212. 212. >70 kg--- flecainide 300mg, propafenone 600mg
  213. 213. <70 kg --- flecainide 200 mg , propafenone 450 mg
  214. 214. Long duration 20-30 % cases</li></li></ul><li>Surgical ablation:<br /><ul><li>Maze procedures –atrial incisions
  215. 215. In conjunction with other surgical operations
  216. 216. Replacemnt of mirtal valve
  217. 217. CABG </li></li></ul><li>Pacemakers<br />RV placed pacemaker..<br />Prevents AV asynchrony<br />Prevents reentry<br />Prevents bradycardia induced dispersion of atrialdepolarisation.<br />
  218. 218. Other drugs<br />Beneficial role<br /><ul><li>ACEI
  219. 219. ARBS</li></ul>Prevents structural remodelling.<br />Blocks RAAS<br /><ul><li>STATINS
  220. 220. OMEGA 3 FATTY ACIDS
  221. 221. VITAMIN C
  222. 222. STEROIDS
  223. 223. RANOLAZINE-RANEXA
  224. 224. --- MERLIN AF TRIAL Na channel blocking drug.. </li></li></ul><li>New drugs<br /><ul><li>DRONEDARONE( multaq):sanofiaventis
  225. 225. Amiodarone like compound
  226. 226. Lacks iodine moiety
  227. 227. Spans all classes
  228. 228. K currents,INa,Ikr,Ikach,L type ca ,βblocking,prolongs AP,
  229. 229. T ½ --24 hrs
  230. 230. Dronedarone AF study after EC—prevention of AF 800mg optimal dose.
  231. 231. ANDROMEDA study– tolerability in CHF
  232. 232. DANE trial
  233. 233. ADONIS,EURIDIS
  234. 234. 400mg bid</li></li></ul><li><ul><li>CELIVARONE: SSR 149744C
  235. 235. Benzofuran derivative
  236. 236. Structurally related to amiodarone
  237. 237. Inhibits k currents
  238. 238. 300mg or 600 mg.
  239. 239. ATI 2001
  240. 240. Synthetic analogue of amiodarone
  241. 241. More potent than amiodarone in atrial properties
  242. 242. T1/2 –12min </li></li></ul><li>Class III drugs<br />AZEMILIDE:<br /><ul><li>125 mg daily
  243. 243. Neutropenia,torsades de pointes</li></ul>TEDISAMIL:<br /><ul><li>Multiple k channels
  244. 244. Decreases rate
  245. 245. Increases AP in atria
  246. 246. Antianginal drug</li></ul>BERTOSAMIL on clinical trials<br />
  247. 247. Atrial depolarization delaying agents<br /><ul><li>VERNAKALANT
  248. 248. Na ,k blockers
  249. 249. Atrial selectivity
  250. 250. 61 % conversion
  251. 251. 3mg/kg over 10 min --- 2 mg /kg
  252. 252. Dysguesia,nausea,vomting
  253. 253. AVE 0118
  254. 254. Ikur,ito,ikach
  255. 255. No QT prolongation
  256. 256. AZ7009
  257. 257. SEROTONIN type 4 antagonists
  258. 258. RS 100302 </li></li></ul><li>New drugs<br /><ul><li>Adenosine agonists CVT –510 :
  259. 259. Slowed av conduction
  260. 260. No negative inotropic ,vasodialtion,hypotension effects.
  261. 261. Ambasilide
  262. 262. Almokalant
  263. 263. Sematilide
  264. 264. Tedisamil
  265. 265. Ximelgatran –SPORT IF trial
  266. 266. Rotigaptide---gap junction modulator</li></li></ul><li>
  267. 267.
  268. 268. WHAT DOES TRIALS SAY?<br />AFFIRM trial :<br />RACE trial :<br />AF –CHF trial<br />ALL reveal no change in mortality in both groups.<br />Treatment is individuialised<br />
  269. 269. AFFIRM trial : management of AF with the rhythm control strategy offers no survival advantage over the rate control strategy.anticoagualtion to be continued in this group of high risk patients .<br />ATHENA trial :a trial with dronaderone to prevent hospitalisation or death in AF<br />400mg bid dose<br />ANDROMEDA –european trial of dronedarone in moderate to severe CHF---400 mg bid<br />CAFÉ trial : canadian AF evaluation study.<br />SAFIRE –D study –doefetilide use in AF 500ug dose.<br />CRAFT <br />REL-Y TRIAL 110mg -150 mg of dabigatran.<br />RECOVER –in dvt<br />ROCKET AF –rivaroxaban<br />EINSTEIN ---vte<br />ATLAS ACS –in ACS <br />
  270. 270.
  271. 271. Ongoing trials/new trials<br /><ul><li>625 trials so far
  272. 272. 1.Apixaban– novel factor X a inhibitor
  273. 273. 5mg bid
  274. 274. AVERROES study –phase III
  275. 275. Compared with aspirin
  276. 276. Double blinded RCT
  277. 277. 2.efficacy of olmesartan in paroxysmal AF
  278. 278. ANTI PAF trial –40 mg OD
  279. 279. 3.EPLERAF study ---eplerenone in the prevention of AF recurrence after cardioversion
  280. 280. 4.vernakalant hcl efficacy in AF
  281. 281. 5.WISDOM trial –withdrawal or continuation of amiodarone in successfully treated patients with persistent AF
  282. 282. 6.w 3 fatty acids for prevention of post OP AF--- OPERA</li></li></ul><li>Recent advances<br />ACC/AHA 2010 guidelines<br />How to handle rate control therapy<br />Recently introduced antiarryhtmic drugs<br />Catheter based treatment<br />Antithrombotic therapy<br /><ul><li>No benefit of achieving strict heart rate control <80 bpm at rest <110 bpm on exercise ---class IIIevidence b
  283. 283. Dronedarone not to be used in LVD
  284. 284. Catheter ablation –class Ia –A evidence in paroxysmal Afnormalatria,class II b --- paroxysmal with LVD,Iia –persistent
  285. 285. Dabigatran –seminal event in AF management</li></li></ul><li>Take home message<br /><ul><li>Most common sustained cardiac arrhythmia
  286. 286. All three properties of arryhtmia play a role.
  287. 287. Foci of intiation diagnosed.
  288. 288. Treatment depends upon duration.
  289. 289. Treatment changes on age,presence of LVD
  290. 290. Anticoagualtion or antithrombotic based on assessment of risk factors..
  291. 291. Rate control = rhytm control on long term
  292. 292. theoretically rhythm control is better.
  293. 293. Not useful in permanent AF.
  294. 294. Catheter ablation is becoming the major option in treatment.
  295. 295. Effects of antiarryhthmic drugs are overcome by new drugs.
  296. 296. INR need not be monitored witndagibatran</li></li></ul><li>
  297. 297. Ganong<br />Samson and wright physiology<br />Guyton<br />www.emedicine.com<br />www.aha.org<br />www.atrialfibrillation.com<br />And finally I landed up in AF ---DOCTORS SYMDROME….THANK YOU for your attention<br />
  298. 298. Professor: define seminar<br />Student :seminar is defined as process in which one spoils his sleep for one night in an effort to make others sleep.<br />
  299. 299. Thank you<br />Dr.P.L.JOHN ISRAEL<br />H.O.D OF GENERAL MEDICINE<br />
  300. 300. Thank you<br />

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