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Life Threatening EKG's in the Office

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Life Threatening EKG's in the Office Life Threatening EKG’s In The Office Joseph A Manfredi, MD, FACC, FHRS GHS Cardiovascular Symposium January 24th, 2015 Disclosures Speaker Honorariums: STJM, Boston Scientific Advisory role: Medtronic Stock: Boston Scientific Willem Einthoven 1903 Willem Einthoven’s Nobel Prize Lecture December 11, 1925 PERICARDITIS Wolff-Parkinson-White Syndrome 45 year old woman Presented with syncope No prior cardiac history Recently started on Azithromycin Prior history of a “seizure disorder” LONG QT SYNDROME What is a prolonged QTc ? >0.44 s M vs. >0.46s F Symptoms Range from SCD to syncope or near syncope Patients who have suffered a SCA have a ominous prognosis with a 12.9 RR of experiencing another event. Reference: 1. Moss AJ, Zareba W, Hall WJ, et al. Effectiveness and limitations of beta-blocker therapy in congenital long-QT syndrome. Circulation. 2000;101:616-623. Beta-blocker Therapy for LQTS 17 Reference: 1. Moss AJ, Zareba W, Hall WJ, et al. Effectiveness and limitations of beta-blocker therapy in congenital long-QT syndrome. Circulation. 2000;101:616-623. Management Beta-Blockers (Less helpful in LQT3) Exercise restriction Pace or Isoproterenol Avoid QT prolonging drugs www.qtdrugs.org Ischemia/electrolytes AICD Cervico-sympathectomy Beta-Blockers immediate post-partum Probability of Any Cardiac Event Sauer, A. J. et al. J Am Coll Cardiol 2007;49:329-337 Copyright ©2007 American College of Cardiology Foundation. Restrictions may apply. Suggested Risk-Stratification Scheme for ACA or SCD in LQTS Patients Goldenberg, I. et al. J Am Coll Cardiol 2008;51:2291-2300 Copyright ©2008 American College of Cardiology Foundation. Restrictions may apply. Medications to Avoid Cardiac: Sotalol, Amiodarone, Quinidine, Dofetilide, and Procainamide Psychiatric: Haldol, Fluoxetine, Sertraline Antibiotics: Flouroquinolones, Mycins Narcotics: Methadone Torsades de Pointes SHORT QT SYNDROME Background No evidence on whether specific triggers precipitate events Mutations in at least 3 genes have been identified……. KCNQ1 (Iks), KCNH2 (Ikr), nd KCNJ2 (Ikl) These are similar to LQTS but with gain of function as opposed to loss of function Autosomal Dominant Inheritence EPS ? (usually shows easily inducible ventricular Arrhythmias but it is not known if this is predictive of adverse outcomes) When to Suspect SQT Atrial fibrillation at a very young age Family member with short QT Family member with SCD EKG with tall/peaked T waves QT interval of < 350 ms at 60 BPM 15 year old presents to the ER with atypical chest pain Brugada Syndrome Brugada Syndrome Risk Stratification Original Brugada description Circ 1998;97;457-460. 63 patients 30% risk of cardiac arrest at 3 years EPS is predictive of high risk 60 –90 % inducible ICD usually advised Brugada Syndrome ST elevation V1 and V2, RBBB ECG changes are variable and dynamic (can be provoked by sodium channel blocking agents – ajmaline, procainamide) M > F 3rd and 4th decades Worldwide, but common in SE Asia Brugada Syndrome Genetics 30% with mutations in SCN5A Autosomal Dominant Usually a loss of function mutation (this gene is also implicated in LQTS3) At least 28 different mutations identified Clinical Presentation Syncope SCA Usually in males in the 3rd to 4th decade of life (Reported cases of SCA in Neonates) Fever is a predisposing factor for SCA Patients with Syncope and a spontaneous Type I ECG have a 6 fold higher risk of SCA than those without syncope and Type I ECG BRUGADA EKG ECGs from a 35-year-old male who has been successfully resuscitated 1 5 Wilde, A. A.M. et al. Circulation 2002;106:2514-2519 Brugada Syndrome Risk Stratification High risk pts: baseline ST elevation and syncope – 44% had cardiac arrest; therefore ICD Intermediate risk patients: spontaneous ST elevation > 2mm without syncope –14% had cardiac arrest; treatment undefined (? ICD) Low risk patient: diagnostic ECG only after provocation – 5% had cardiac arrest over 4 decades of follow up – reassurance – no ICD –avoid Na channel blockers and TCA’s Presymptomatic screening of family members without resting ECG abnormalities is not useful Sudden Cardiac Death Rapid VF or PMVT frequently occurring at rest or during sleep Holter monitoring does not usually show frequent PVC’s or NSVT Bidirectional VT Catecholaminergic Polymorphic Ventricular Tachycardia (CPMVT) CPMVT Background Is one of the most lethal channelopathies if not recognized and treated. Characterized by ventricular arrhythmias induced by emotional stress or exercise (present with syncope during exercise, similar to Long QT but with a normal EKG) Onset usually in childhood and adolescence Caused by mutations in the cardiac ryanodine receptor (RyR2) in the Autosomal Dominant form Resting EKG is usually normal Challenges in Diagnosing CPMVT Exercise stress testing is an important part of a CPVT workup. - However, in as many as 20% of CPVT patients, formal exercise stress testing will not produce ventricular ectopy. During exercise stress testing, bidirectional VT with a beat-to-beat 180 degree rotation of the QRS complex is often observed.1 References: 1. Mohamed U, Napolitano C, Priori SG. Molecular and electrophysiological bases of catecholaminergic polymorphic ventricular tachycardia. J Cardiovasc Electrophysiol. 2007;18(7):791-797. 2. Kontula K, Laitinen PJ, Lehtonen A, Toivonen L, Viitasalo M, Swan H. Catecholaminergic polymorphic ventricular tachycardia: recent mechanistic insights. Cardiovasc Res. 2005;67:379-387. 16 year old boy Cardiac arrest while playing high school basketball Successfully resuscitated No prior history of cardiac disease Hypertrophic Cardiomyopathy Sudden Death in Young Athletes NEJM 2003;349:1064 Hypertrophic Cardiomyopathy Apical Variant Hypertrophic Cardiomyopathy Hypertrophic Cardiomyopathy Risk Stratification Clinical: syncope, FH of SCD, younger age Testing: VT-NS, Exercise decrease in BP. LVH (septum > 30 mm), LVOT gradient > 30 mm Hg (NEJM 2003;348:295.) 3 Risk Factors 6%/yr SCD risk Hypertrophic Cardiomyopathy NEJM 2003;349:1064 14 year old boy Passed out while swimming competitively Required CPR but no defibrillation No prior history of cardiac disease No family history of SCD ARVD-Epsilon wave ARVD - MRI ARVD Treatment Minimal data Ablation – multiple foci and high rate of recurrence Antiarrhythmic drugs - ? Sotalol ICD Avoid competitive athletics Thank you .
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