Refining the World Health Organization Definition: Predicting Autopsy-Defined Sudden Arrhythmic Deaths Among Presumed Sudden Cardiac Deaths in the POST SCD Study.
Adolescent
Adult
Aged
Aged, 80 and over
Autopsy
Cause of Death
Death, Sudden, Cardiac
/ epidemiology
Echocardiography
Electrocardiography
Female
Humans
Incidence
Male
Middle Aged
Predictive Value of Tests
Reproducibility of Results
Risk Assessment
Risk Factors
San Francisco
/ epidemiology
Tachycardia, Ventricular
/ classification
Terminology as Topic
Ventricular Fibrillation
/ classification
Young Adult
arrhythmias
autopsy
sudden cardiac death
ventricular fibrillation
Journal
Circulation. Arrhythmia and electrophysiology
ISSN: 1941-3084
Titre abrégé: Circ Arrhythm Electrophysiol
Pays: United States
ID NLM: 101474365
Informations de publication
Date de publication:
07 2019
07 2019
Historique:
entrez:
29
6
2019
pubmed:
30
6
2019
medline:
17
3
2020
Statut:
ppublish
Résumé
Conventional definitions of sudden cardiac death (SCD) presume cardiac cause. We studied the World Health Organization-defined SCDs autopsied in the POST SCD study (Postmortem Systematic Investigation of SCD) to determine whether premortem characteristics could identify autopsy-defined sudden arrhythmic death (SAD) among presumed SCDs. Between January 2, 2011, and January 4, 2016, we prospectively identified all 615 World Health Organization-defined SCDs (144 witnessed) 18 to 90 years in San Francisco County for medical record review and autopsy via medical examiner surveillance. Autopsy-defined SADs had no extracardiac or acute heart failure cause of death. We used 2 nested sets of premortem predictors-an emergency medical system set and a comprehensive set adding medical record data-to develop Least Absolute Selection and Shrinkage Operator models of SAD among witnessed and unwitnessed cohorts. Of 615 presumed SCDs, 348 (57%) were autopsy-defined SAD. For witnessed cases, the emergency medical system model (area under the receiver operator curve 0.75 [0.67-0.82]) included presenting rhythm of ventricular tachycardia/fibrillation and pulseless electrical activity, while the comprehensive (area under the receiver operator curve 0.78 [0.70-0.84]) added depression. If only ventricular tachycardia/fibrillation witnessed cases (n=48) were classified as SAD, sensitivity was 0.46 (0.36-0.57), and specificity was 0.90 (0.79-0.97). For unwitnessed cases, the emergency medical system model (area under the receiver operator curve 0.68 [0.64-0.73]) included black race, male sex, age, and time since last seen normal, while the comprehensive (area under the receiver operator curve 0.75 [0.71-0.79]) added use of β-blockers, antidepressants, QT-prolonging drugs, opiates, illicit drugs, and dyslipidemia. If only unwitnessed cases <1 hour (n=59) were classified as SAD, sensitivity was 0.18 (0.13-0.22) and specificity was 0.95 (0.90-0.97). Our models identify premortem characteristics that can better specify autopsy-defined SAD among presumed SCDs and suggest the World Health Organization definition can be improved by restricting witnessed SCDs to ventricular tachycardia/fibrillation or nonpulseless electrical activity rhythms and unwitnessed cases to <1 hour since last normal, at the cost of sensitivity.
Sections du résumé
BACKGROUND
Conventional definitions of sudden cardiac death (SCD) presume cardiac cause. We studied the World Health Organization-defined SCDs autopsied in the POST SCD study (Postmortem Systematic Investigation of SCD) to determine whether premortem characteristics could identify autopsy-defined sudden arrhythmic death (SAD) among presumed SCDs.
METHODS
Between January 2, 2011, and January 4, 2016, we prospectively identified all 615 World Health Organization-defined SCDs (144 witnessed) 18 to 90 years in San Francisco County for medical record review and autopsy via medical examiner surveillance. Autopsy-defined SADs had no extracardiac or acute heart failure cause of death. We used 2 nested sets of premortem predictors-an emergency medical system set and a comprehensive set adding medical record data-to develop Least Absolute Selection and Shrinkage Operator models of SAD among witnessed and unwitnessed cohorts.
RESULTS
Of 615 presumed SCDs, 348 (57%) were autopsy-defined SAD. For witnessed cases, the emergency medical system model (area under the receiver operator curve 0.75 [0.67-0.82]) included presenting rhythm of ventricular tachycardia/fibrillation and pulseless electrical activity, while the comprehensive (area under the receiver operator curve 0.78 [0.70-0.84]) added depression. If only ventricular tachycardia/fibrillation witnessed cases (n=48) were classified as SAD, sensitivity was 0.46 (0.36-0.57), and specificity was 0.90 (0.79-0.97). For unwitnessed cases, the emergency medical system model (area under the receiver operator curve 0.68 [0.64-0.73]) included black race, male sex, age, and time since last seen normal, while the comprehensive (area under the receiver operator curve 0.75 [0.71-0.79]) added use of β-blockers, antidepressants, QT-prolonging drugs, opiates, illicit drugs, and dyslipidemia. If only unwitnessed cases <1 hour (n=59) were classified as SAD, sensitivity was 0.18 (0.13-0.22) and specificity was 0.95 (0.90-0.97).
CONCLUSIONS
Our models identify premortem characteristics that can better specify autopsy-defined SAD among presumed SCDs and suggest the World Health Organization definition can be improved by restricting witnessed SCDs to ventricular tachycardia/fibrillation or nonpulseless electrical activity rhythms and unwitnessed cases to <1 hour since last normal, at the cost of sensitivity.
Identifiants
pubmed: 31248279
doi: 10.1161/CIRCEP.119.007171
pmc: PMC6738572
mid: NIHMS1527956
doi:
Types de publication
Journal Article
Research Support, N.I.H., Extramural
Validation Study
Langues
eng
Sous-ensembles de citation
IM
Pagination
e007171Subventions
Organisme : NHLBI NIH HHS
ID : R01 HL102090
Pays : United States
Commentaires et corrections
Type : CommentIn
Références
J Gen Intern Med. 1993 Apr;8(4):179-84
pubmed: 8515327
N Engl J Med. 2018 Sep 27;379(13):1205-1215
pubmed: 30280654
Circulation. 2018 Jun 19;137(25):2689-2700
pubmed: 29915095
Ann Emerg Med. 2009 Nov;54(5):674-683.e2
pubmed: 19394110
J Am Coll Cardiol. 2018 Jun 26;71(25):2957-2969
pubmed: 29753563
World Health Organ Tech Rep Ser. 1985;726:5-25
pubmed: 3936284
Europace. 2018 Apr 1;20(4):614-621
pubmed: 28339816
Circulation. 2016 Sep 13;134(11):806-16
pubmed: 27542394
Eur Heart J. 2018 Nov 21;39(44):3961-3969
pubmed: 30169657
Mayo Clin Proc. 2016 Oct 8;:
pubmed: 27810088
JAMA Cardiol. 2018 Jul 1;3(7):591-600
pubmed: 29801082
Circ Cardiovasc Qual Outcomes. 2017 Jan;10(1):e000022
pubmed: 27993943
Epidemiology. 2010 Jan;21(1):128-38
pubmed: 20010215
Circulation. 1982 Mar;65(3):457-64
pubmed: 7055867
J Am Coll Cardiol. 2004 Sep 15;44(6):1268-75
pubmed: 15364331
Environ Health Perspect. 2016 Jan;124(1):120-5
pubmed: 26090776
N Engl J Med. 2008 Feb 28;358(9):873-5
pubmed: 18305264
JAMA Cardiol. 2018 Jul 1;3(7):556-558
pubmed: 29800957
Circulation. 2006 Dec 5;114(23):2534-70
pubmed: 17130345
Sci Rep. 2017 Oct 24;7(1):13889
pubmed: 29066841
Eur Heart J. 2017 Dec 7;38(46):3443-3448
pubmed: 29020391
MMWR Morb Mortal Wkly Rep. 2009 Oct 30;58(42):1171-5
pubmed: 19875978