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Definition af VT 2

Inddeling af VT (1). Monomorf regelmssigt ensartet elektrokardiografisk prgPolymorf med vekslende elektrokardiografisk mnster. Inddeling af VT (2). Ventrikelflagren hvis QRS-komplekser og T-segmenter ikke kan skelnesVentrikelflimren ved uregelmssig vekslende amplitude og frekvens

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Definition af VT 2

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    2. Definition af VT (2) For praktiske formål bør enhver takykardi med breddeøget QRS-mønster opfattes som ventrikulær takykardi indtil anden mekanisme er sandsynliggjort

    3. Inddeling af VT (1) Monomorf – regelmæssigt ensartet elektrokardiografisk præg Polymorf – med vekslende elektrokardiografisk mønster

    4. Inddeling af VT (2) Ventrikelflagren – hvis QRS-komplekser og T-segmenter ikke kan skelnes Ventrikelflimren – ved uregelmæssig vekslende amplitude og frekvens Torsades des pointes – ved en vis regelmæssighed i amplitudeskift

    5. Inddeling af VT (3) Sustained VT > 30 sekunders varighed Selvlimiterende non-sustained VT < 30 sekunders varighed

    6. Ventrikulær takykardi

    7. Polymorf VT af typen - torsades des pointes

    8. Tre klinisk betydende arytmimekanismer Re-entry - over 95 % af arytmier - post MI-VT, idiopatisk venstre VT Efterdepolarisering (“eftersvingninger”) - RVOT VE/VT Øget automaticitet - RVOT VE/VT

    9. Ætiologi og forekomst Som ledsagefænomen til en række strukturelle hjertesygdomme Ved sygdomme med strukturelt normalt hjerte som selvstænding arytmimanifestation Som proarytmi udløst af antiarytmisk behandling

    10. VT og morfologi ved strukturel hjertesygdom

    11. VT og morfologi ved strukturelt normalt hjerte

    12. Klassisk inddeling af antiarytmika (Vaughan Williams) Ia: Na-blokker + let K-blokade (kinidin) Ib: Na-blokker (lidokain) Ic: Na blokker (flecainid, propafenon) II: Beta-blokkere III: K-blokkere: (sotalol, amiodaron) IV: Ca-antagonister (verapamil, diltiazem)

    13. Symptomer og kliniske fund Non-sustained VT asymptomatisk til kortvarig takykardi-fornemmelse, palpitationer, varmefornemmelse, svimmelhed eller regulær synkope Sustained VT ofte almen svækkelse men lige fra træthed, svedudbrud, svimmelhed, dyspnø, oppression, shock, hjertestop

    14. Behandling af VT (1) DC konvertering (200-360 J) ved kliniske tegn på shock, lungestase eller ved angina pectoris Anfaldsbrydende medicinsk behandling hvis patienten er upåvirket med BT over 100 mmHg systolisk (Amiodaron 150 + 150 mg iv) – NB Fare for kredsløbskollaps!

    15. Ventrikulære ekstrasystoler i bigemini fra RVOT

    16. Benign repetitiv monomorf VT fra RVOT (Gallavardin)

    17. Ventrikulær takykardi ved ARVD

    18. Hvad er det ?

    20. Kort-lang-kort

    21. Lang QT-syndrom - gener

    22. Start på torsades des pointes hos sotalolbehandlet patient

    24. Behandling af torsades des pointes VT Lang QT-associeret - bradykardi-afhængig. Behandling: Ved congenit form: betablokker, pace Drug induceret: isoprenalin, pace, Mg Ses også ved normal QT og iskæmi-hjerteinsufficiens: kort-lang-udløst og behandles med revaskularisering, NTG, amiodarone, betablokker, pace.

    26. Behandling af VT (2) Medicinsk behandling af VT er ofte ineffektiv. ICD behandling kan terminere VT episoder, men forebygger dem ikke. Dog livsforlængende. RFA har potentialet til at ”fjerne” VT substratet, men procedurerne er ofte ”udfordrende” og langt mindre effektive end for RFA af SVT.  Effektiviteten og sikkerhed af RFA af VT er dog meget afhængig af VT typen

    27. ICD - Implanterbar cardioverter og defibrillator Automatisk detektion og behandling af ventrikulære takyarytmier (”farlig hjerteflimmer/hjertestop)” 1980 Baltimore USA 1989 Danmark Implantation af 300/år i Danmark

    28. ICD patienten Typisk 60 år (17–79 år) ”Blodprop”/”åreforkalkning” i hjertet Hjertestop eller farlig hurtig hjerteflimren Forebyggelse af pludselig død efter blodprop i hjertet hos patienter i høj risiko Forebyggelse af pludselig død ved særlige former for ”arvelige” hjertesygdomme

    29. ICD terapi

    31. The Survival Trial for Amiodarone Therapy in Congestive Heart Failure (STAT-CHF) randomized 674 patients to placeob or amiodarone. Patients were NYHA class II or III with a mean LVEF of 0.25 and all had NSVT on Holter. The Kaplan-Meier curves showed no benefit for amiodarone compared to placebo, neither for arrhythmic, nor for all-cause mortality.The Survival Trial for Amiodarone Therapy in Congestive Heart Failure (STAT-CHF) randomized 674 patients to placeob or amiodarone. Patients were NYHA class II or III with a mean LVEF of 0.25 and all had NSVT on Holter. The Kaplan-Meier curves showed no benefit for amiodarone compared to placebo, neither for arrhythmic, nor for all-cause mortality.

    32. Antiarrhythmics Vs Implantable Defibrillator (AVID) AVID concluded with 1016 patients enrolled, and showed an overall hazard ratio of 0.62 (p < 0.02) in favor of ICD therapy. The mortality reductions were 39%, 27% and 31% in the first, second and third years, respectively. Additionally, investigators concluded that the ICD should be offered as first-line therapy to such patients. (D. Zipes et al. NEJM 1997). A similar study, the Canadian Implantable Defibrillator Study (CIDS), compared ICDs to only amiodarone. Upon its conclusion, with 659 patients enrolled, the ICD superiority was 20%, but the sample size was insufficient to show statistical significance (S. Connoly; Circulation 2000). Also, the CIDS outcome was weakened by a 20% crossover rate ( patients assigned to amiodarone who were switched to ICDs within 2 years - usually following VT/VF episodes), but continued on intention-to-treat analysis to be considered withing the amiodarone group. AVID concluded with 1016 patients enrolled, and showed an overall hazard ratio of 0.62 (p < 0.02) in favor of ICD therapy. The mortality reductions were 39%, 27% and 31% in the first, second and third years, respectively. Additionally, investigators concluded that the ICD should be offered as first-line therapy to such patients. (D. Zipes et al. NEJM 1997). A similar study, the Canadian Implantable Defibrillator Study (CIDS), compared ICDs to only amiodarone. Upon its conclusion, with 659 patients enrolled, the ICD superiority was 20%, but the sample size was insufficient to show statistical significance (S. Connoly; Circulation 2000). Also, the CIDS outcome was weakened by a 20% crossover rate ( patients assigned to amiodarone who were switched to ICDs within 2 years - usually following VT/VF episodes), but continued on intention-to-treat analysis to be considered withing the amiodarone group.

    33. Cardiac Arrest Study Hamburg (CASH) At two years of follow-up, patients randomized to ICDs had a 38% lower mortality compared to patients on amiodarone or metoprolol, with a one-sided p-value of 0.047 (K Kuck, R. Cappato, ACC 1998 [press release]) . Sub-group analysis indicated that the ICD superiority was even stronger in the second half of the study, where only non-thoracotomy ICDs were implanted. Another very small European study was the Netherlands Cost-Effectiveness Study (R. Hauer, E. Wever; Circulation 1995), which compared ICD as initial therapy versus electrophysiologyically -guided therapy. This study enrolled only 60 patients and proved the hypothesis of ICD cost-effenctiveness. But it also demonstrated a 73% signicantly higher mortality rate (p = .02) for patients randomized to the contol limb versus those who received ICD as first line therapy. At two years of follow-up, patients randomized to ICDs had a 38% lower mortality compared to patients on amiodarone or metoprolol, with a one-sided p-value of 0.047 (K Kuck, R. Cappato, ACC 1998 [press release]) . Sub-group analysis indicated that the ICD superiority was even stronger in the second half of the study, where only non-thoracotomy ICDs were implanted. Another very small European study was the Netherlands Cost-Effectiveness Study (R. Hauer, E. Wever; Circulation 1995), which compared ICD as initial therapy versus electrophysiologyically -guided therapy. This study enrolled only 60 patients and proved the hypothesis of ICD cost-effenctiveness. But it also demonstrated a 73% signicantly higher mortality rate (p = .02) for patients randomized to the contol limb versus those who received ICD as first line therapy.

    34. Canadian Implantable Defibrillator Study (CIDS)

    38. MADIT I - Probability of Survival The Kaplan-Meier curves showing probability of survival from all-cause mortality showed a 0.46 hazard ratio (54% lower risk of death) in favor of ICD therapy, with a p-value of 0.0085. The curves separate very early but continue to diverge out through 4 years follow-up. The Kaplan-Meier curves showing probability of survival from all-cause mortality showed a 0.46 hazard ratio (54% lower risk of death) in favor of ICD therapy, with a p-value of 0.0085. The curves separate very early but continue to diverge out through 4 years follow-up.

    40. MUSTT - Total Mortality Figure 4. Kaplan–Meier Estimates of the Rates of Overall Mortality According to Whether the Patients Received Treatment with a Defibrillator. The P value refers to two comparisons: between the patients in the group assigned to electrophysiologically guided (EPG) therapy who received treatment with a defibrillator and those who did not receive such treatment, and between the patients assigned to electrophysiologically guided therapy who received treatment with a defibrillator and those assigned to no antiarrhythmic therapy. Figure 4. Kaplan–Meier Estimates of the Rates of Overall Mortality According to Whether the Patients Received Treatment with a Defibrillator. The P value refers to two comparisons: between the patients in the group assigned to electrophysiologically guided (EPG) therapy who received treatment with a defibrillator and those who did not receive such treatment, and between the patients assigned to electrophysiologically guided therapy who received treatment with a defibrillator and those assigned to no antiarrhythmic therapy.

    41. MADIT II - Total Mortality Figure 2. Kaplan–Meier Estimates of the Probability of Survival in the Group Assigned to Receive an Implantable Defibrillator and the Group Assigned to Receive Conventional Medical Therapy. The difference in survival between the two groups was significant (nominal P=0.007, by the log-rank test). Figure 3. Hazard Ratios and 95 Percent Confidence Intervals for Death from Any Cause in the Defibrillator Group as Compared with the Group Assigned to Receive Conventional Medical Therapy, According to Selected Clinical Characteristics. The hazard ratios in the various subgroups were similar, with no statistically significant interactions. The dotted vertical line represents the results for the entire study (nominal hazard ratio, 0.66, without adjustment for the stopping rule). The horizontal lines indicate nominal 95 percent confidence intervals. LVEF denotes left ventricular ejection fraction, and NYHA New York Heart Association. Figure 2. Kaplan–Meier Estimates of the Probability of Survival in the Group Assigned to Receive an Implantable Defibrillator and the Group Assigned to Receive Conventional Medical Therapy. The difference in survival between the two groups was significant (nominal P=0.007, by the log-rank test). Figure 3. Hazard Ratios and 95 Percent Confidence Intervals for Death from Any Cause in the Defibrillator Group as Compared with the Group Assigned to Receive Conventional Medical Therapy, According to Selected Clinical Characteristics. The hazard ratios in the various subgroups were similar, with no statistically significant interactions. The dotted vertical line represents the results for the entire study (nominal hazard ratio, 0.66, without adjustment for the stopping rule). The horizontal lines indicate nominal 95 percent confidence intervals. LVEF denotes left ventricular ejection fraction, and NYHA New York Heart Association.

    43. Videre perspektiver De ”smalle” MADIT 1-kriterier afløses sandsynligvis af simple MADIT-2 kriterier: EF < 30 % Dette sker formentlig samtidig med behandling af baggrundsbefolkningen Skønsmæssigt vil virkningen af MADIT-2 være en permanent fordobling af implantationsraten sammenlignet med i dag

    46. Virkning af kateterbaseret radiofrekvensstrømablation Arytmi Varig kurativ effekt Supraventrikulær WPW-takykardi >95% AV-nodal takykardi >95% Atrial takykardi >80% Atrieflagren >90% Atrieflimren >70% Ventrikulær Højre udløbsdelstakykardi >90% Venstre fascikeltakykardi >90% Grenbundts takykardi >90% Postiskæmisk takykardi >50% Takykardi ved kardiomyopati uegnet Torsades des pointes uegnet Ventrikelflimren uegnet

    47. RVOT VE/non-sust VT 52 år gammel kvinde Palpitationer gennem 5 år TTE normal Aldrig sustained VT Negativ familieanamnese Beta-blokkere og Ca-antagonister uden effekt Holter: bigemini og masser af løb

    48. Ventrikulær ekstrasystoli

    49. Idiopatisk VT fra RVOT

    50. RVOT VE: Sinus Map

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