Hjärtarytmier- sjukdomshistoria och behandling Nils Edvardsson

1. Hjärtarytmier- sjukdomshistoria och behandling Nils Edvardsson

2. Normal sinusknutefunktion • * intrinsic rate • ** 90-120 slag/min (ex. denervering vid • hjärttransplantation • ** sjunker med åldern • ** kronotropi – frekvensökning • * autonom styrning • ** vagus dominerar (avtar med åldern) • *** vid max atropin HR 110-120 • ** sympaticus • *** vid max arbete HR 220 - åldern

3. Sjuk sinusknuta – diagnostik • * Förmaksbradyarytmi (paroxysmal eller generell) • ** sinusbradycardi (<40 slag/min) • ** sinus arrest (> 3 s) • ** sino-atrialt block • ** kronotrop insufficiens • * Paroxysmalatachyarytmier • ** oftast förmaksflimmer

4. Sjuk sinusknuta – incidens, prevalens • * svårbestämd - unga friska kan ha bradycardier, • idrottsmän har ofta HR<40. • * incidens ca 0.2% • * ökar med åldern • Symptom • * specifika - syncope, yrsel, hjärtsvikt • * ospecifika - trötthet, orkselöshet, apati, depression • * hjärtklappning • ** paroxysmala FF, FFl, andra tachycardier • ** inappropriate sinus nodetachycardia, IST • ** trombembolism!

5. ”Sinus noderemodelling” * En inaktiv sinusknuta ”somnar in” ** fungerar inte normalt efter en tid ** kan ses övergående efter elkonvertering (riskperiod för proarytmi) ** avtagande sinusfrekvens - nodalrytm * Kronotrop insufficiens ** välbekant men ej lättdefinierat begrepp ** ”otillräcklig frekvensvariation i samband med fysisk ansträngning”

6. AV-block * AV-block I (PR>0.22 s) * AV-block II:I (Wenchebach) ** oftast beläget I AV-noden (intra-nodalt) * AV-block II:II ** oftast beläget nedanför AV-noden (infra- nodalt) ** pacemakerindikation * AV-block III (oberoende förmaks- och kammarrytm)

7. Vänstergrenblock - LBBB * alltid ett observandum - markör! * någon gång rest efter myokardit – i princip ofarligt om myokardiet friskt * vanligt vid allvarliga tillstånd som klaffel (aortastenos), VK-kardiomyopati, kranskärlssjukdom, VK-svikt, etc.

8. V1 LBBB V6

9. V1 V2 V3 V4 V5 V6 LBBB – normal electrical axis

10. LAH-block = extremt vänsterställd el-axel • * QRS-komplexet ofta <120 ms • * Vanligt hos äldre, avspeglar (lindrig) hjärtsjukdom • hos ca 50% • Enkel diagnostik: • ** om R/S-kvoten är 0 eller negativ i II • ** och mer negativ i III • ** föreligger extremt vänsterställd el-axel (minst -30º)

11. RBBB

12. Högergrenblock - RBBB * vanligt med partiella RBBB, anomali, ”högersidigt intraventrikulärt ledningshinder” * hos yngre - tänk på ASD * hos äldre vanligare - ingen ökad risk Ovanligt men viktigt: högerkammarsjukdom, t.ex. ARVD (arytmogenhögerkammardysplasi)

13. Uttalat vänstersidigt intraventrikulärt ledningshinder • * QRS >120 ms, oftast betydligt mer • * uppfyller inte strikta kriterier för LBBB • * betyder att konduktionen är drabbad mer • perifert på grund av utbredd myokardskada

14. Bifascikulärt block – BBBB • * oftast RBBB+LAH, mycket sällan RBBB+LPH: • * BBBB utan symptom: expektans • * BBBB med yrsel/syncope: risk för AV- • block III cirka 6% per år • * BBBB+AV-block I: risk för AV-block III • cirka 30% per år – pacemaker!

15. Primary VF

16. Monomorphic VT

17. Moe Mirowski

18. Appropriate shocks

20. Behandling av VT/VF • * Farmakologisk behandling kan vara riskabel, • risk för proarytmi • * Implanterbar defibrillator • ** overdrive pacing vid VT • ** shock vid snabb VT och VF • * Shockreduktion (betablockad, amiodarone, • sotalol)

21. V1 V2 V3 V4 V5 V6

23. 921003 22 y, professional ice-hockey goalkeeper WPW-syndrome In total 5 procedures at three centres in the US before cured 921006

24. ♂ 19 y, soccer goalkeeper Palpitations during match, cured by RF ablation

25. WPW syndrome Preexcitation in 0.1-0.3 ‰ in general population Tachyarrhythmias in abouthalf of them High risk patients rare - multiple pathways - antidromictachycardia - preexcited AF Sudden cardiac death very rare RF ablation is an effectivecure

26. WPW syndrome Left lateral pathway – RF ablation

27. AVNRT ♂23y, professional tennis player. Paroxysmal tachycardias, before, but not enough to motivate treatment Had to give up an important match in 5th set when in winning position. Tachycardia started during game and stopped only after end of ”injury time” Cured by RF ablation

28. AV nodal reentry tachycardia AVNRT 3 %o in general population Women:men 6:1 Palpitations, syncope, urina spastica Sudden onset, sudden offset Heart rate during tachycardia (140) 180-240 bpm Fast pathway Slow pathway Adenosin stops tachycardia by short block in AV node

29. AVNRT - Slow pathway ablation HBE SC Efficacy >95% Patient cured for life RF RV

30. 14 mån efter RF-ablation av AVNRT Startkänslan

32. Maj 2004 AVNRT

33. EAT ♂ 23 y, soccer defender in elite division PP 380 ms

34. Ectopic atrial tachycardia, EAT * focal or reentry * intermittent or persistent * may cause LV dysfunction * can be life-threatening in children and young patients

35. Start of atrial fibrillation P on T PAC PAC – atrial fibrillation

36. Requisits for atrial fibrillation Regulator AV node Autonomic tone Terminator Trigger • Premature atrial beats • Bursts from pulmonary veins • Bradycardia AF Initiator Perpetuator • Large atria • Diseased areas • Anatomical blocks • Short wave length • Short excitable gap • Triggers • Spatial dispersion ofrefractory periods • Short wave length • Functional blocks

37. Autonomic trigger patterns Euro Heart Survey, 1517 pts with paroxysmal AF De Vos et al., Eur Heart J 2008

38. Acute, paroxysmal AFSelf-terminating <7d, mostly <48h Symptoms: palpitations, anxiety, dizziness etc Risk: depending on additional factors Treatment goal: symptom relief, eliminate or reduce attacks, reduce heart rate during attacks Strategy: rhythm control (and rate control), consider anticoagulation

39. Persistent:duration >7d, will not stop spontaneously but can be converted. Long-standing persistent, duration > 1 year May be asymptomatic, little or very symptomatic: at rest?, on exertion? Risk: depending on additional risk factors Treatment goal: relief of symptoms, reduce risk Treatment: rhythm control (+ rate control) + antithrombotic treatment

40. Permanent or ”accepted”: will not stop spontaneously and/or cannot be converted May be asymptomatic, little or very symptomatic: at rest?, on exertion? Risk: depending on comorbidity Treatment goal: relief of symptoms, reduce risk Treatment: rate control + antithrombotic treatment

41. Atrial fibrillation Variable conduction via the AV node to the ventricles II Right atrium Atrial rate 350-500 bpm Left atrium

42. Patient 1 51 years old, male, accountant with own company, two elder brothers with AF, while he himself is sofar healthy. PAF diagnosed one year ago after golf and whisky, propranolol (Inderal). Increasing number of episodes, almost always after tennis, skiing, golf, often starting during the night afterwards. Sotalol (Sotacor), better. Worse again, tested dispopyramide (Dirytmin), verapamil (Isoptin). More frequent episodes, longer duration, more easily starting, need for DC. Amiodarone (Coradrone). AF interfering with work.

43. Patient 1 Finally very limited in his life, can not sport, can not participate in social life, no wine/whisky. Persistent AF alternating with self-terminating episodes. Ready for non-pharmacological treatment. Duration from first attack to heavily symptomatic, therapy resistant AF was 8 years.

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45. Atrial flutter:more organized, one circuit, atrial rate 280 bpm, various degrees of blocked conduction to the ventricles, here 3:1 Occurs as an entity of its own but very often together with atrial fibrillation. Treated mainly in the same way but often difficult to treat pharmacologically. Ablation!

46. ACC/AHA/ESC Guidelines for Management of Atrial Fibrillation Progression of AF Permanent Persistent Paroxysmal Sinus Rhythm DC Atrial Fibrillation

47. AF is associated with increased morbidity and mortality Adjusted relative risk 3.5 Mortality Morbidity 3.0 2.5 2.0 1.5 1.0 0.5 0 Stroke mortality Non-stroke mortality Non-CV mortality CV mortality Totalmortality Stroke MI CHF Manitoba Heart Study; Am J Med 1995

48. <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 AF- a problem growing with age U.S. populationx 1000 Population with AFx 1000 Population withatrial fibrillation 500 30,000 400 20,000 300 U.S. population 200 10,000 100 0 0 Age, yr Adapted from Feinberg WM. Arch Intern Med 1995;155:469-473

49. Atrial fibrillation – the future Adults with atrial fibrillation, in millions 7.0 6.0 5.61 5.42 5.16 5.0 4.78 4.34 4.0 3.80 3.33 3.0 2.94 2.66 2.44 2.26 2.0 2.08 1.0 0 1990 2000 2010 2020 2030 2040 2050 Go et al., JAMA 2001

50. AF limits patients´ lifes “I‘d love to go skiing again. It makes me quite sad” (UK, parox) “Always worried …always scared about tomorrow” (F, parox) “I used to do all the housework but now…I feel unable…to look after my home” (Fr, Parox) “No more sport, nothing…physically diminished. Heavy work, cycling, sport; all out of the question ” (Fr, Parox) “I like going out, going to parties…enjoying life…now I can’t” (Fr, perm) “To cook, to have twelve people for dinner, I can’t do those things” (US, Perm) “When it was bad we couldn’t have sex” (Ge, pers) “In the short-term, I have trouble going up and down the stairs” (US, Parox) “Even just considering walking, it’s noticeable” (Fr, Parox) “Everything is an effort, I have no bounce” (Fr, Parox)