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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1] Associate Editor(s)-in-Chief: Sara Zand, M.D.[2] Edzel Lorraine Co, DMD, MD[3] Nehal Eid, M.D.[4]


Overview

There are several other diagnostic tests being done for sudden cardiac death. These include the signal-averaged electrocardiogram (SaECG), exercise testing, provocative diagnostic tests such as the sodium channel blocker testing, adenosine test, and epinephrine test, electrophysiology study, and genetic testing.

Other Diagnostic Studies

There are several other diagnostic tests being done for sudden cardiac death. These include the signal-averaged electrocardiogram (SaECG), exercise testing, provocative diagnostic tests such as the sodium channel blocker testing, adenosine test, and epinephrine test, electrophysiology study, and genetic testing [1] [2] [3] [4] [5] [6] [7] [8] [9] [10] [11] [12] [13] [14] [6] [15] [16] [17].

Signal-averaged Electrocardiogram

Exercise Testing

Provocative Diagnostic Tests

Electrophysiology Study

  • This study includes measurement of programmed electrical stimulation (PES), baseline intervals (His-ventricuar interval and atrial-His interval) and electroanatomical mapping for diagnosis and therapy [9] [10] [11] [12] [13] [14].
  • In case of normally structured heart and ECG inconclusive of arrythmic syndrome, it is required to further evaluate the condition with electrophysiological study (EPS),sodium channel blocker challenge, or stress ECG testing may be performed. Because delta waves in Wolff-Parkinson-White syndrome and Brugada pattern may not be apparent initially on ECGs after resuscitation, an EPS can identify and treat accessory path ways responsible for cardiac arrest.[20] A sodium channel blocker challenge during EPS involves administration of drugs such as flecainide, ajmaline, and pilsicainide to unmask a type 1 Brugada ECG pattern.[18]

Genetic testing

Postmortem Genetic Investigation:
  • Its use increased recently for research purposes and to inform family members about potentially inherited disease. It investigates the association between genotypes and etiology by autopsy.
  • Genetic studies of sudden deaths in young adults demonstrate that the genetic yield for pathogenic or likely pathogenic variants in autopsy-confirmed sudden cardiac deaths ranged from 13% to 34%.[21],[22],[23],[24]-,[25]. These yields are obtained after careful etiologic assessment by comprehensive postmortem investigation (including toxicology) for accurate genotype-phenotype correlation.
  • Sudden arrhythmic death without an apparent cause identified by autopsy is often attributed to arrhythmia syndromes. Of 490 prospectively ascertained sudden cardiac deaths by autopsy in persons aged 1 to 35 years in Australia,[21] 113 were adjudicated as sudden arrhythmic death syndrome (ie,normal structural heart) and underwent genetic testing. Clinically relevant pathogenic or likely pathogenic variants in cardiac genes were found in 27%; major associated disorders included LQTS, Brugada syndrome, arrhythmogenic right ventricular cardiomyopathy, and CPVT.
  • Another study, 103 sudden cardiac deaths defined by autopsy in persons aged 1 to 44years without known CVD referred from 24 US medical examiners’ offices identified pathogenic or likely pathogenic variants associated with dilated cardiomyopathy, hypertrophic cardiomyopathy, LQTS, and arrhythmogenic right ventricular cardiomyopathy in13%.[25]
  • However, the total number of eligible sudden deaths was not reported, so it is unclear how this applies to all young adults with sudden cardiac death. A single center prospective study in the UK revealed that among 303 referred family members of individuals who had sudden arrhythmic death syndrome, 128 (42%) were diagnosed with inherited cardiac diseases including Brugada syn drome,LQTS,and dilated cardiomyopathy.[26]
Genetic Testing of Cardiac Arrest Survivors:

Genetic testing of sudden cardiac arrest survivors and additional cardiac screening of family members may detect previously unknown cardiomyopathy, such as dilated cardiomyopathy, hypertrophic cardiomyopathy, or primary arrhythmia syndrome.[27],[23],[25] Genetic testing of survivors is recommended if the results are likely to aid diagnosis,management, or family screening (classI,level B).[28] However, the yield of genetic testing from studies of survivors with clinically unexplained VT/VF targeting arrhythmia and cardiomyopathy genes ranged from 2% to 22%, which is lower than the percentage of pathogenic or likely pathogenic variants in cardiac genes among those who had sudden cardiac death (ie, nonsurvivors).[29][30][31][32]


2022 ESC Guidelines for the management of patients with ventricular arrythymias and the prevention of sudden cardiac death [33]

Recommendations for genetic testing
Class I (Level of Evidence: B)
Class I (Level of Evidence: C)
  • When a putative causative variant is first identified evaluation for pathogenicity is recommended using an internationally accepted framework.
Class I (Level of Evidence: C)
Class I (Level of Evidence: C)
Class I (Level of Evidence: C)
  • It is recommended that class III (variants of uncertain significance) and Class IV variants should be evaluated for segregation in families where possible, and the variant re-evaluated periodically.
Class III (Level of Evidence: C)
Recommendations for public basic life support and access to automated external defibrillators
Class I (Level of Evidence: B)
Class I (Level of Evidence: B)
  • Prompt CPR by bystanders is recommended at out-of-hospital cardiac arrest.
Class I (Level of Evidence: B)
Class IIa (Level of Evidence: B)
  • Mobile phone-based alerting of basic life support-trained bystander volunteers to assist nearby out-of-hospital cardiac arrest victims should be considered.
Recommendations for diagnostic evaluation and general recommendations for ventricular arrhythmia in dilated cardiomyopathy/ hypo kinetic non-dilated cardiomyopathy
Class I (Level of Evidence: B)
Class IIa (Level of Evidence: C)
Class III (Level of Evidence: C)
Recommendations for diagnosis of ventricular arrhythmias in arrhythmogenic right ventricular cardiomyopathy
Class I (Level of Evidence: B)
Class I (Level of Evidence: B)
Class IIb (Level of Evidence: C)
Recommendations for diagnosis of ventricular arrhythmias in hypertrophic cardiomyopathy
Class I (Level of Evidence: B)
Class IIb (Level of Evidence: C)

2017AHA/ACC/HRS Guideline for management of sudden cardiac arrest and ventricular arrhythmia

[34]

Class I, Level of evidence: B
In patients who recovered from SCA due to ventricular arrhythmia suspected ischemic heart disease, coronary angiography and probabley revascularization is recommmended
Class I, Level of evidence:C
In patients with anomalous origin of a coronary artery leading ventricular arrhythmia or SCA, repair or revascularization is recommended
Class IIa, Level of evidence: B
In patients with ischemic or nonischemic cardiomyopathy or congenital heart disease presented with syncope arrhythmia and do not meet criteria for primary prevention ICD, an electrophysiological study is recommended for assessing the risk of sustained VT
Class III, Level of evidence: B
In patients who meet criteria for ICD implantation, an electrophysiological study is not recommended for only inducing ventricular arrhythmia
Class III, Level of evidence: B
An electrophysiological study is not recommended for risk stratification for ventricular arrhythmia in patients with Long QT syndrome, short QT syndrome, cathecolaminergic polymorphic ventricular arrhythmia




Class I (Level of Evidence: C)
  • In patients with SCA or SCD in their family member, genetic tests and genetic counselling is recommended

References

  1. ↑ Goldberger JJ, Cain ME, Hohnloser SH, Kadish AH, Knight BP, Lauer MS; et al. (2008). "American Heart Association/American College of Cardiology Foundation/Heart Rhythm Society scientific statement on noninvasive risk stratification techniques for identifying patients at risk for sudden cardiac death: a scientific statement from the American Heart Association Council on Clinical Cardiology Committee on Electrocardiography and Arrhythmias and Council on Epidemiology and Prevention". Circulation. 118 (14): 1497–1518. PMID 18833586.
  2. ↑ 2.0 2.1 Gatzoulis KA, Arsenos P, Trachanas K, Dilaveris P, Antoniou C, Tsiachris D; et al. (2018). "Signal-averaged electrocardiography: Past, present, and future". J Arrhythm. 34 (3): 222–229. doi:10.1002/joa3.12062. PMC 6010001. PMID 29951136.
  3. ↑ 3.0 3.1 Marcus FI, McKenna WJ, Sherrill D, Basso C, Bauce B, Bluemke DA; et al. (2010). "Diagnosis of arrhythmogenic right ventricular cardiomyopathy/dysplasia: proposed modification of the Task Force Criteria". Eur Heart J. 31 (7): 806–14. doi:10.1093/eurheartj/ehq025. PMC 2848326. PMID 20172912.
  4. ↑ 4.0 4.1 Giudicessi JR, Ackerman MJ (2019). "Exercise testing oversights underlie missed and delayed diagnosis of catecholaminergic polymorphic ventricular tachycardia in young sudden cardiac arrest survivors". Heart Rhythm. 16 (8): 1232–1239. doi:10.1016/j.hrthm.2019.02.012. PMID 30763784.
  5. ↑ 5.0 5.1 Roston TM, Kallas D, Davies B, Franciosi S, De Souza AM, Laksman ZW; et al. (2021). "Burst Exercise Testing Can Unmask Arrhythmias in Patients With Incompletely Penetrant Catecholaminergic Polymorphic Ventricular Tachycardia". JACC Clin Electrophysiol. 7 (4): 437–441. doi:10.1016/j.jacep.2021.02.013. PMID 33888264 Check |pmid= value (help).
  6. ↑ 6.0 6.1 6.2 Priori SG, Wilde AA, Horie M, Cho Y, Behr ER, Berul C; et al. (2013). "Executive summary: HRS/EHRA/APHRS expert consensus statement on the diagnosis and management of patients with inherited primary arrhythmia syndromes". Europace. 15 (10): 1389–406. doi:10.1093/europace/eut272. PMID 23994779.
  7. ↑ 7.0 7.1 Govindan M, Batchvarov VN, Raju H, Shanmugam N, Bizrah M, Bastiaenen R; et al. (2010). "Utility of high and standard right precordial leads during ajmaline testing for the diagnosis of Brugada syndrome". Heart. 96 (23): 1904–8. doi:10.1136/hrt.2010.201244. PMID 20962343.
  8. ↑ Churet M, Luttoo K, Hocini M, Haïssaguerre M, Sacher F, Duchateau J (2019). "Diagnostic reproducibility of epinephrine drug challenge interpretation in suspected long QT syndrome". J Cardiovasc Electrophysiol. 30 (6): 896–901. doi:10.1111/jce.13926. PMID 30907461.
  9. ↑ 9.0 9.1 Bourke JP, Richards DA, Ross DL, Wallace EM, McGuire MA, Uther JB (1991). "Routine programmed electrical stimulation in survivors of acute myocardial infarction for prediction of spontaneous ventricular tachyarrhythmias during follow-up: results, optimal stimulation protocol and cost-effective screening". J Am Coll Cardiol. 18 (3): 780–8. doi:10.1016/0735-1097(91)90802-g. PMID 1907984.
  10. ↑ 10.0 10.1 Gatzoulis KA, Tsiachris D, Arsenos P, Archontakis S, Dilaveris P, Vouliotis A; et al. (2014). "Prognostic value of programmed ventricular stimulation for sudden death in selected high risk patients with structural heart disease and preserved systolic function". Int J Cardiol. 176 (3): 1449–51. doi:10.1016/j.ijcard.2014.08.068. PMID 25150471.
  11. ↑ 11.0 11.1 Gatzoulis KA, Vouliotis AI, Tsiachris D, Salourou M, Archontakis S, Dilaveris P; et al. (2013). "Primary prevention of sudden cardiac death in a nonischemic dilated cardiomyopathy population: reappraisal of the role of programmed ventricular stimulation". Circ Arrhythm Electrophysiol. 6 (3): 504–12. doi:10.1161/CIRCEP.113.000216. PMID 23588627.
  12. ↑ 12.0 12.1 Brilakis ES, Shen WK, Hammill SC, Hodge DO, Rea RF, Lexvold NY; et al. (2001). "Role of programmed ventricular stimulation and implantable cardioverter defibrillators in patients with idiopathic dilated cardiomyopathy and syncope". Pacing Clin Electrophysiol. 24 (11): 1623–30. doi:10.1046/j.1460-9592.2001.01623.x. PMID 11816631.
  13. ↑ 13.0 13.1 Brembilla-Perrot B, Suty-Selton C, Beurrier D, Houriez P, Nippert M, de la Chaise AT; et al. (2004). "Differences in mechanisms and outcomes of syncope in patients with coronary disease or idiopathic left ventricular dysfunction as assessed by electrophysiologic testing". J Am Coll Cardiol. 44 (3): 594–601. doi:10.1016/j.jacc.2004.03.075. PMID 15358027.
  14. ↑ 14.0 14.1 Schmitt C, Barthel P, Ndrepepa G, Schreieck J, Plewan A, Schömig A; et al. (2001). "Value of programmed ventricular stimulation for prophylactic internal cardioverter-defibrillator implantation in postinfarction patients preselected by noninvasive risk stratifiers". J Am Coll Cardiol. 37 (7): 1901–7. doi:10.1016/s0735-1097(01)01246-3. PMID 11401129.
  15. ↑ Ingles J, Lind JM, Phongsavan P, Semsarian C (2008). "Psychosocial impact of specialized cardiac genetic clinics for hypertrophic cardiomyopathy". Genet Med. 10 (2): 117–20. doi:10.1097/GIM.0b013e3181612cc7. PMID 18281919.
  16. ↑ Ackerman MJ, Priori SG, Willems S, Berul C, Brugada R, Calkins H; et al. (2011). "HRS/EHRA expert consensus statement on the state of genetic testing for the channelopathies and cardiomyopathies this document was developed as a partnership between the Heart Rhythm Society (HRS) and the European Heart Rhythm Association (EHRA)". Heart Rhythm. 8 (8): 1308–39. doi:10.1016/j.hrthm.2011.05.020. PMID 21787999.
  17. ↑ Conte G, Wilde A, Behr ER, Scherr D, Lenarczyk R, Gandjbachkh E; et al. (2021). "Importance of Dedicated Units for the Management of Patients With Inherited Arrhythmia Syndromes". Circ Genom Precis Med. 14 (2): e003313. doi:10.1161/CIRCGEN.120.003313. PMC 8284353 Check |pmc= value (help). PMID 33797288 Check |pmid= value (help).
  18. ↑ 18.0 18.1 Zeppenfeld K,Tfelt-Hansen J, de Riva M, et al; ESC Scientific Document Group.2022 ESC guidelines for the management of patients with ventricular arrhythmias and the prevention of sudden cardiac death. EurHeartJ. 2022;43(40): 3997-4126. doi:10.1093/eurheartj/ehac262
  19. ↑ Sy RW, van der Werf C, Chattha IS, et al. Derivation and validation of a simple exercise-based algorithm for prediction of genetic testing in relatives of LQTS probands. Circulation. 2011;124 (20):2187-2194. doi:10.1161/CIRCULATIONAHA.111. 028258
  20. ↑ Al-Khatib SM, Stevenson WG, Ackerman MJ, et al. 2017 AHA/ACC/HRS guideline for management of patients with ventricular arrhythmias and the prevention of sudden cardiac death: executive summary: a Report of the American College of Cardiology/American Heart Association Task Force on Clinical Practice Guidelines and the Heart Rhythm Society.Heart Rhythm.2018;15(10):e190-e252. doi:10.1016/j.hrthm. 2017.10.035
  21. ↑ 21.0 21.1 Bagnall RD, Weintraub RG, Ingles J, et al. A prospective study of sudden cardiac death among children and young adults. NEnglJMed.2016;374 (25):2441-2452. doi:10.1056/NEJMoa1510687
  22. ↑ Christiansen SL, Hertz CL, Ferrero-Miliani L, et al. Genetic investigation of 100 heart genes in sudden unexplained death victims in a forensic setting. Eur J HumGenet.2016;24(12):1797-1802. doi:10.1038/ejhg.2016.118
  23. ↑ 23.0 23.1 Lahrouchi N, Raju H, Lodder EM, et al.Utility of post-mortem genetic testing in cases of sudden arrhythmic death syndrome.JAmCollCardiol. 2017;69(17):2134-2145. doi:10.1016/j.jacc.2017.02. 046
  24. ↑ Hansen BL, Jacobsen EM, Kjerrumgaard A, et al. Diagnostic yield in victims of sudden cardiac death and their relatives. Europace. 2020;22(6): 964-971. doi:10.1093/europace/euaa056
  25. ↑ 25.0 25.1 25.2 Webster G,Puckelwartz MJ,Pesce LL, et al. Genomic autopsy of sudden deaths in young individuals. JAMA Cardiol. 2021;6(11):1247-1256. doi:10.1001/jamacardio.2021.2789
  26. ↑ Papadakis M, Papatheodorou E,Mellor G, et al. The diagnostic yield of Brugada syndrome after sudden death with normal autopsy.JAmColl Cardiol. 2018;71(11):1204-1214. doi:10.1016/j.jacc. 2018.01.031
  27. ↑ Krahn AD, Healey JS, Chauhan V, et al. Systematic assessment of patients with unexplained cardiac arrest: Cardiac Arrest Survivors With Preserved Ejection Fraction Registry (CASPER). Circulation. 2009;120(4):278-285. doi:10.1161/CIRCULATIONAHA.109.853143
  28. ↑ Stiles MK, Wilde AAM, Abrams DJ, et al.2020 APHRS/HRS exper tconsensus statement on the investigation of decedents with sudden unexplained death andpatients with sudden cardiac arrest, and of their families. Heart Rhythm. 2021;18(1):e1-e50. doi:10.1016/j.hrthm.2020.10.010
  29. ↑ Mellor G, Laksman ZWM, Tadros R, et al. Genetic testing in the evaluation of unexplained cardiac arrest: from the CASPER(Cardiac Arrest Survivors With Preserved Ejection Fraction Registry). Circ Cardiovasc Genet. 2017;10(3):e001686. doi:10.1161/CIRCGENETICS.116.001686
  30. ↑ Visser M, Dooijes D, van der Smagt JJ, et al. Next-generation sequencing of a large gene panel in patients initially diagnosed with idiopathic ventricular fibrillation. Heart Rhythm. 2017;14(7): 1035-1040. doi:10.1016/j.hrthm.2017.01.010
  31. ↑ Leinonen JT, Crotti L, Djupsjöbacka A, et al. The genetics underlying idiopathic ventricular fibrillation: a special role for catecholaminergic polymorphic ventricular tachycardia? Int J Cardiol. 2018;250:139-145. doi:10.1016/j.ijcard.2017.10.016
  32. ↑ Asatryan B, Schaller A, Seiler J, et al. Usefulness of genetic testing in sudden cardiac arrest survivors with or without previous clinical evidence of heart disease. AmJCardiol. 2019;123 (12):2031-2038. doi:10.1016/j.amjcard.2019.02.061
  33. ↑ Zeppenfeld K, Tfelt-Hansen J, de Riva M, Winkel BG, Behr ER, Blom NA; et al. (2022). "2022 ESC Guidelines for the management of patients with ventricular arrhythmias and the prevention of sudden cardiac death". Eur Heart J. 43 (40): 3997–4126. doi:10.1093/eurheartj/ehac262. PMID 36017572 Check |pmid= value (help).
  34. ↑ Al-Khatib, Sana M.; Stevenson, William G.; Ackerman, Michael J.; Bryant, William J.; Callans, David J.; Curtis, Anne B.; Deal, Barbara J.; Dickfeld, Timm; Field, Michael E.; Fonarow, Gregg C.; Gillis, Anne M.; Granger, Christopher B.; Hammill, Stephen C.; Hlatky, Mark A.; Joglar, José A.; Kay, G. Neal; Matlock, Daniel D.; Myerburg, Robert J.; Page, Richard L. (2018). "2017 AHA/ACC/HRS Guideline for Management of Patients With Ventricular Arrhythmias and the Prevention of Sudden Cardiac Death". Circulation. 138 (13). doi:10.1161/CIR.0000000000000549. ISSN 0009-7322.

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