Refining the World Health Organization Definition: Predicting Autopsy-Defined Sudden Arrhythmic Deaths Among Presumed Sudden Cardiac Deaths in the POST SCD Study.

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 ß-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.

Prospective Countywide Surveillance and Autopsy Characterization of Sudden Cardiac Death: POST SCD Study.

BACKGROUND: Studies of out-of-hospital cardiac arrest and sudden cardiac death (SCD) use emergency medical services records, death certificates, or definitions that infer cause of death; thus, the true incidence of SCD is unknown. Over 90% of SCDs occur out-of-hospital; nonforensic autopsies are rarely performed, and therefore causes of death are presumed. We conducted a medical examiner-based investigation to determine the precise incidence and autopsy-defined causes of all SCDs in an entire metropolitan area. We hypothesized that postmortem investigation would identify actual sudden arrhythmic deaths among presumed SCDs. METHODS: Between February 1, 2011, and March 1, 2014, we prospectively identified all incident deaths attributed to out-of-hospital cardiac arrest (emergency medical services primary impression, cardiac arrest) between 18 to 90 years of age in San Francisco County for autopsy, toxicology, and histology via medical examiner surveillance of consecutive out-of-hospital deaths, all reported by law. We obtained comprehensive records to determine whether out-of-hospital cardiac arrest deaths met World Health Organization (WHO) criteria for SCD. We reviewed death certificates filed quarterly for missed SCDs. Autopsy-defined sudden arrhythmic deaths had no extracardiac cause of death or acute heart failure. A multidisciplinary committee adjudicated final cause. RESULTS: All 20 440 deaths were reviewed; 12 671 were unattended and reported to the medical examiner. From these, we identified 912 out-of-hospital cardiac arrest deaths; 541 (59%) met WHO SCD criteria (mean 62.8 years, 69% male) and 525 (97%) were autopsied. Eighty-nine additional WHO-defined SCDs occurred within 3 weeks of active medical care with the death certificate signed by the attending physician, ineligible for autopsy but included in the countywide WHO-defined SCD incidence of 29.6/100 000 person-years, highest in black men (P<0.0001). Of 525 WHO-defined SCDs, 301 (57%) had no cardiac history. Leading causes of death were coronary disease (32%), occult overdose (13.5%), cardiomyopathy (10%), cardiac hypertrophy (8%), and neurological (5.5%). Autopsy-defined sudden arrhythmic deaths were 55.8% (293/525) of overall, 65% (78/120) of witnessed, and 53% (215/405) of unwitnessed WHO-defined SCDs (P=0.024); 286 of 293 (98%) had structural cardiac disease. CONCLUSIONS: Forty percent of deaths attributed to stated cardiac arrest were not sudden or unexpected, and nearly half of presumed SCDs were not arrhythmic. These findings have implications for the accuracy of SCDs as defined by WHO criteria or emergency medical services records in aggregate mortality data, clinical trials, and cohort studies.

Sudden Death in Patients With Cardiac Implantable Electronic Devices.

IMPORTANCE: Interrogations and autopsies of sudden deaths with cardiac implantable electronic devices (CIEDs) are rarely performed. Therefore, causes of sudden deaths with these devices and the incidence of device failure are unknown. OBJECTIVE: To determine causes of death in individuals with CIEDs in a prospective autopsy study of all sudden deaths over 35 months as part of the San Francisco, California, Postmortem Systematic Investigation of Sudden Cardiac Death (POST SCD) study. DESIGN, SETTING, AND PARTICIPANTS: Full autopsy, toxicology, histology, and device interrogation were performed on incident sudden cardiac deaths with pacemakers or implantable cardioverter defibrillators (ICDs). The setting was the Office of the Chief Medical Examiner, City and County of San Francisco. Participants included all sudden deaths captured through active surveillance of all deaths reported to the medical examiner and San Francisco residents with an ICD (January 1, 2011, to November 30, 2013). MAIN OUTCOMES AND MEASURES: Identification of a device concern in sudden deaths with CIEDs, including hardware failures, device algorithm issues, device programming issues, and improper device selection. For the ICD population, outcomes were the cumulative incidence of death and sudden cardiac death and the proportion of deaths with an ICD concern. RESULTS: Twenty-two of 517 sudden deaths (4.3%) had CIEDs, and autopsy revealed a noncardiac cause of death in 6. Six of 14 pacemaker sudden deaths and 7 of 8 ICD sudden deaths died of ventricular tachycardia or ventricular fibrillation. Device concerns were identified in half (4 pacemakers and 7 ICDs), including 3 hardware failures contributing directly to death (1 rapid battery depletion with a sudden drop in pacing output and 2 lead fractures), 5 ICDs with ventricular fibrillation undersensing, 1 ICD with ventricular tachycardia missed due to programming, 1 improper device selection, and a pacemaker-dependent patient with pneumonia and concern about lead fracture. Of 712 San Francisco residents with an ICD during the study period, 109 died (15.3% cumulative 35-month incidence of death), and the 7 ICD concerns represent 6.4% of all ICD deaths. CONCLUSIONS AND RELEVANCE: Systematic interrogation and autopsy of sudden deaths in one city identified concerns about CIED function that might otherwise not have been observed. Current passive surveillance efforts may underestimate device malfunction. These methods can provide unbiased data regarding causes of sudden death in individuals with CIEDs and improve surveillance for CIED problems.

Vertebral artery dissection complicating occipital injection of heparin for treatment of thoracic outlet syndrome.

A 38-year-old woman with a 2-year history of chronic neck pain radiating down her right arm underwent radiological and neurological evaluations, which revealed no anatomical cause for her pain. She sought alternative therapies including intramuscular heparin injections. Following a right occipital injection of heparin, cyanocobalamin, and lidocaine, she had a sudden cardiorespiratory arrest and was successfully resuscitated, but did not regain consciousness.Computed tomography of the head and neck and subsequent autopsy revealed a right vertebral artery dissection, but at autopsy, no significant subarachnoid hemorrhage was noted at the base of the brain. This is the first case report where heparin (a potent anticoagulant) used in an occipital injection was documented to cause a vertebral artery dissection. It is also the first reported case where radiographically and histologically documented vertebral artery dissection did not present with overwhelming subarachnoid hemorrhage at the base of the brain. The subtle gross anatomical findings in this case highlight the importance of evaluating the cervical spinal cord in any case of sudden cardiorespiratory arrest following even apparently minor neck injury.

Characteristics of sudden arrhythmic death in a diverse, urban community.

BACKGROUND: Sudden cardiac death (SCD) remains a major public health problem; however, its true burden remains unknown with widely variable estimates of its incidence. We aimed to examine the contemporary epidemiology and autopsy characteristics of SCD in an ethnically diverse community. METHODS: Three physicians reviewed all deaths of individuals aged ≥20 years reported to the San Francisco medical examiner in 2007 for presentations fitting World Health Organization (WHO) SCD criteria-within 1 hour of symptom onset (witnessed) or within 24 hours of being observed alive and symptom free (unwitnessed). After comprehensive review of medical examiner investigation, WHO SCDs were classified as sudden arrhythmic death (SAD) or nonarrhythmic death. Coronary artery disease (CAD) and cardiac mass were evaluated in all SADs undergoing autopsy and compared with demographically similar accidental trauma control deaths. RESULTS: We identified 252 WHO SCDs; 145 were SADs. Men had a 2.2-fold higher SAD rate (P < .0005). Blacks had a 3.15-fold higher SAD rate compared with whites (P = .003). Significant CAD was present in 38.9% of SADs and associated with higher SAD risk compared with control deaths (OR 2.58, 95% CI 1.12-5.97, P = .026). Mean cardiac mass was linearly associated with risk for SAD in cases without significant CAD (OR 2.06 per 100 g, 95% CI 1.43-2.98, P < .0005). CONCLUSIONS: In a diverse, urban population, SAD incidence varied substantially by gender and race. Significant CAD accounted for far fewer SADs than previous studies but remained associated with a 2.6-fold higher risk as compared with control deaths. These findings may reflect the evolving contemporary epidemiology of SCD.

Childhood status epilepticus and excitotoxic neuronal injury.

This report describes the case of an 11-year-old girl with a prior history of epilepsy and multiple episodes of status epilepticus who presented with generalized convulsive status epilepticus and left hemiclonic seizures. Magnetic resonance imaging, including diffusion-weighted sequences and spectroscopy, and neuropathology at autopsy were consistent with excitotoxic neuronal injury to the hippocampus, cortex, thalamus, mammillary bodies, and cerebellum. Review of the literature revealed 11 similar cases that support the hypothesis of excitotoxic neuronal cell death after status epilepticus.

Autopsy artifact created by the Revivant AutoPulse resuscitation device.

In certain cases, the evaluation and correct identification of resuscitative artifacts is critical to the correct diagnosis and determination of the cause and manner of death. Resuscitative artifacts can resemble homicidal or accidental injury and thus possibly be misinterpreted. Occasionally, new technologies and/or medical procedures will create original and/or distinctive artifacts. In 2003, the San Francisco Fire Department emergency personnel began field-testing the Revivant AutoPulse, an automated chest compression device. This device is currently being used in two other counties in the San Francisco Bay Area as well as regions of Florida, Virginia, and Ohio. We present three cases of resuscitative artifact that could be potentially confused with homicidal or accidental injury. These cases illustrate resuscitative artifacts, specifically lateral chest and horizontally oriented upper abdomen cutaneous abrasions created by this automated chest compression device.