Cases Of Sudden Cardiac Death Research Articles

Retrospective analysis of 769 cases of sudden cardiac death from 2006 to 2015: a forensic experience in China.

Sudden cardiac death (SCD) is a major health challenge. The records of 769 autopsy cases of SCD examined at Tongji Medicolegal Expertise Center from January 2006 to December 2015 were retrospectively reviewed. The mean age of the cases was 46years, excluding 27 victims in whom the exact age could not be confirmed. The highest incidence of SCD occurred among the 40- to 60-year-old group (45.0%). Male preponderance was observed in SCD cases (male: female ratio: 5.0:1), and this preponderance was even higher (8.0:1) in the 10- to 20-year-old and 60- to 70-year-old groups. Death predominantly occurred in hospitals (37.4%) and outdoors (32.5%). The incidence of SCD did not differ significantly between the seasons. Coronary atherosclerotic disease (CAD) was the main cause of SCD (67.9%), followed by unexplained SCD (6.1%), myocarditis (5.7%), cardiomyopathy (4.7%), rupture of aortic dissection (3.9%), and cardiac conduction system disease (3.9%). In terms of the CAD cases, the mean age was 52.0years and coronary artery stenosis exceeding 75% accounted for 73.6% of cases. The left anterior descending branch was involved with atherosclerosis in 92.0% of cases. In conclusion, detailed autopsy and forensic pathology examination is key to diagnosing SCD. Making an early diagnosis and performing early intervention of CAD may reduce the mortality of SCD. Additionally, the use of molecular genetic tests plus forensic pathology diagnosis will help further determine the underlying cause of death in individuals with SCD.

Prevention of Sudden Cardiac Death in Adults With Congenital Heart Disease: Do the Guidelines Fall Short?

Sudden cardiac death (SCD) is a major cause of mortality in adult congenital heart disease (ACHD) patients. SCD may be prevented by implantable cardioverter-defibrillator (ICD) implantation, but patient stratification remains troublesome. The 2014 Consensus Statement on Arrhythmias in ACHD patients and the 2015 European Society of Cardiology Guidelines specified recommendations for ICD implantation in ACHD patients for the first time. We assess the discriminative ability of these ICD recommendations for SCD in ACHD patients. Of 25 790 ACHD patients in an international multicenter registry, we identified all SCD cases, matched to living controls by age, sex, congenital defect, and surgical repair. We assessed all primary prevention ICD recommendations listed in both documents. We used conditional logistic regression models to calculate odds ratios and receiver operating characteristic curves with area under the curve. Consensus Statement: One hundred twenty-four cases (median age at death, 33 years [26-44]; 67% men) and 230 controls were studied. In total, 41% of SCD cases and 17% of controls had an ICD recommendation (odds ratio, 5.9; P<0.001). European Society of Cardiology Guidelines: Of one hundred fifty-seven cases (median age at death, 33 years [26-48]; 64% men) and 292 controls, 35% and 14% had an ICD recommendation, respectively (odds ratio, 4.8; P<0.001). A minority of SCD cases had an ICD recommendation according to these guidelines, whereas the majority of SCD victims remained unrecognized. With an area under the curve of 0.6 to 0.7, the discriminative ability of both guidelines was mediocre. Critical clinical reasoning when deciding on ICD implantation in ACHD patients, therefore, remains vital.

Association between mitochondrial DNA copy number and sudden cardiac death: findings from the Atherosclerosis Risk in Communities study (ARIC).

Sudden cardiac death (SCD) is a major public health burden. Mitochondrial dysfunction has been implicated in a wide range of cardiovascular diseases including cardiomyopathy, heart failure, and arrhythmias, but it is unknown if it also contributes to SCD risk. We sought to examine the prospective association between mtDNA copy number (mtDNA-CN), a surrogate marker of mitochondrial function, and SCD risk. We measured baseline mtDNA-CN in 11 093 participants from the Atherosclerosis Risk in Communities (ARIC) study. mtDNA copy number was calculated from probe intensities of mitochondrial single nucleotide polymorphisms (SNP) on the Affymetrix Genome-Wide Human SNP Array 6.0. Sudden cardiac death was defined as a sudden pulseless condition presumed due to a ventricular tachyarrhythmia in a previously stable individual without evidence of a non-cardiac cause of cardiac arrest. Sudden cardiac death cases were reviewed and adjudicated by an expert committee. During a median follow-up of 20.4 years, we observed 361 SCD cases. After adjusting for age, race, sex, and centre, the hazard ratio for SCD comparing the 1st to the 5th quintiles of mtDNA-CN was 2.24 (95% confidence interval 1.58-3.19; P-trend <0.001). When further adjusting for traditional cardiovascular disease risk factors, prevalent coronary heart disease, heart rate, QT interval, and QRS duration, the association remained statistically significant. Spline regression models showed that the association was approximately linear over the range of mtDNA-CN values. No apparent interaction by race or by sex was detected. In this community-based prospective study, mtDNA-CN in peripheral blood was inversely associated with the risk of SCD.

Electrical risk score beyond the left ventricular ejection fraction: prediction of sudden cardiac death in the Oregon Sudden Unexpected Death Study and the Atherosclerosis Risk in Communities Study.

There is an urgent need to extend sudden cardiac death (SCD) risk stratification beyond the left ventricular ejection fraction (LVEF). We evaluated whether a cumulative electrocardiogram (ECG) risk score would improve identification of individuals at high risk of SCD. In the community-based Oregon Sudden Unexpected Death Study (catchment population ∼1 million), 522 SCD cases with archived 12-lead ECG available (65.3 ± 14.5 years, 66% male) were compared with 736 geographical controls to assess the incremental value of multiple ECG parameters in SCD prediction. Heart rate, LV hypertrophy, QRS transition zone, QRS-T angle, QTc, and Tpeak-to-Tend interval remained significant in the final model, which was externally validated in the Atherosclerosis Risk in Communities (ARIC) Study. Sixteen percent of cases and 3% of controls had ≥4 abnormal ECG markers. After adjusting for clinical factors and LVEF, increasing ECG risk score was associated with progressively greater odds of SCD. Overall, subjects with ≥4 ECG abnormalities had an odds ratio (OR) of 21.2 for SCD [95% confidence interval (CI) 9.4-47.7; P < 0.001]. In the LVEF >35% subgroup, the OR was 26.1 (95% CI 9.9-68.5; P < 0.001). The ECG risk score increased the C-statistic from 0.625 to 0.753 (P < 0.001), with net reclassification improvement of 0.319 (P < 0.001). In the ARIC cohort validation, risk of SCD associated with ≥4 ECG abnormalities remained significant after multivariable adjustment (hazard ratio 4.84; 95% CI 2.34-9.99; P < 0.001; C-statistic improvement 0.759-0.774; P = 0.019). This novel cumulative ECG risk score was independently associated with SCD and was particularly effective for LVEF >35% where risk stratification is currently unavailable. These findings warrant further evaluation in prospective clinical investigations.

Long-term Non-Invasive ECG-based Risk Stratification of Sudden Cardiac Death: Extended 5-year Results

&lt;p&gt;Objectives: To evaluate predictive value of heart rate turbulence (HRT), deceleration capacity (DC) and microvolt T-wave alternans (mTWA) for risk stratification for sudden cardiac death (SCD) in patients after myocardial infarction (MI) during 60 months of follow-up.&lt;/p&gt;&lt;p&gt;Methods: We studied 111 patients after MI occurred &amp;gt; 60 days (27 [9; 84] months) before enrollment (84 men; mean age 64.1±10.5 years). All subjects had 24-hour ambulatory ECG monitoring with HRT, DC and mTWA evaluation. Follow-up period was 60 months; primary endpoint was SCD, secondary endpoint included all non-sudden cardiovascular deaths.&lt;/p&gt;&lt;p&gt;Results: During follow-up, we registered 19 cases of SCD and 11 cases of non-sudden cardiovascular deaths (including 7 fatal MI and 3 fatal strokes). DC had high negative predictive value (97.4% for all-cause mortality and 93.7% for SCD). DC values below 4.15 for all-cause mortality and 2.0 for SCD significantly increased risk of all-cause mortality (OR 8.5, 95% CI 2.9 to 24.6, р&amp;lt;0.001) и SCD (OR 9.6, 95% CI 3.2 to 28.5, р&amp;lt;0.001). Combined risk assessment at 12 months revealed that the most significant combination was HRT2 and mTWA100 &amp;gt; 53 mcV, which increased risk both of all-cause mortality (30.7-fold) and SCD (63.3-fold); however, at 60 months this predictive value for SCD decreased (OR = 20.8 (95% CI 2.8 to 114.0), p &amp;lt;0.001).&lt;/p&gt;Conclusion: Evaluation of HRT, DC and mTWA during 24-hour ECG monitoring may define the high risk of cardiovascular mortality and SCD in post-MI patients especially during the first 12 months after the baseline examination.

Clinical and Genetic Diagnosis of Nonischemic Sudden Cardiac Death

Introduction and objectivesNonischemic sudden cardiac death (SCD) is predominantly caused by cardiomyopathies and channelopathies. There are many diagnostic tests, including some complex techniques. Our aim was to analyze the diagnostic yield of a systematic diagnostic protocol in a specialized unit. MethodsThe study included 56 families with at least 1 index case of SCD (resuscitated or not). Survivors were studied with electrocardiogram, advanced cardiac imaging, exercise testing, familial study, genetic testing and, in some cases, pharmacological testing. Families with deceased probands were studied using the postmortem findings, familial evaluation, and molecular autopsy with next-generation sequencing (NGS). ResultsA positive diagnosis was obtained in 80.4% of the cases, with no differences between survivors and nonsurvivors (P=.53). Cardiac channelopathies were more prevalent among survivors than nonsurvivors (66.6% vs 40%, P=.03). Among the 30 deceased probands, the definitive diagnosis was given by autopsy in 7. A diagnosis of cardiomyopathy tended to be associated with a higher event rate in the family. Genetic testing with NGS was performed in 42 index cases, with a positive result in 28 (66.6%), with no differences between survivors and nonsurvivors (P=.21). ConclusionsThere is a strong likelihood of reaching a diagnosis in SCD after a rigorous protocol, with a more prevalent diagnosis of channelopathy among survivors and a worse familial prognosis in cardiomyopathies. Genetic testing with NGS is useful and its value is increasing with respect to the Sanger method.

Early markers of myocardial ischemia: from the experimental model to forensic pathology cases of sudden cardiac death.

The goal of this study was to assess whether early markers of myocardial ischemia, identified in a previous experimental work, can be applied in forensic pathology cases of sudden, ischemic cardiac death. These markers include desphosphorylated connexin 43 (Cx43), JunB, TUNEL assay, myoglobin, and troponin T. Fourteen cases of sudden cardiac death with gross and/or histological signs of myocardial infarction and 14 cases of sudden cardiac death with signs of early ischemia at histology and positive immunoreactions for fibronectin and C5b-9 were investigated. The control group was represented by 15 hanging (global hypoxia) cases. Immunohistochemical reactions were classified into four degrees and compared among groups. Cx43 and JunB were significantly more expressed in hanging than in ischemia/infarction, but they showed a different distribution in the tissue (sub-endocardial in ischemia/infarction, diffuse in hanging) and a different intensity of the signal. TUNEL assay was significantly more expressed in the group of early ischemia than in myocardial infarction. Myoglobin and troponin T did not show any significantly different expression among the three groups. Depletion markers have a limited application in forensic cases, and this is mostly because positive (depleted) areas are difficult to distinguish from artifactually paler areas. Nuclear markers (JunB and TUNEL), on the other hand, require a well-trained eye and a high magnification in order to be distinguished. Cx43, JunB, and TUNEL assays were confirmed to be early, sensitive markers for myocardial ischemia. Nonetheless, they are not specific, as they are expressed in global hypoxia as well, but with a different tissular distribution.

Usefulness and limitation of postmortem computed tomography in bath-related death: Four case reports

Abstract Bath-related death occurs relatively frequently in Japan; however, there is room for improvement in the investigation of such deaths. Here, we describe four autopsy cases of bath-related death (one case of drowning; one of drowning under the influence of drinking; and two cases of sudden cardiac death without drowning) in which postmortem computed tomography (PMCT) was performed before autopsy. Based on analysis of autopsy and PMCT findings of these cases, we further discuss the utility and limitation of PMCT when applied to bath-related death. Comparison of the autopsy findings and PMCT findings between the cases suggests that combinations of several PMCT findings in bath-related death cases (e.g., signs suggestive of overinflated lungs, hemodilution, and excessive water intake in the gastrointestinal tract) can serve to distinguish drowning cases from non-drowning cases. Many bath-related deaths have been reported to have drowning signs at autopsy, although elderly victims with cardiovascular diseases tend to be diagnosed as death due to disease without employing PMCT or autopsy. Therefore, this case series suggests that implementation of PMCT in bath-related death might prevent underestimation of drowning as a cause of death. Although PMCT alone has several limitations, such as inability to evaluate toxicology or heart pathology, implementation of PMCT may trigger a more detailed investigation of the background regarding bath-related death, especially in drowning cases. Based on this case report, we emphasize that PMCT should be performed routinely in bath-related death for compilation of accurate mortality statistics of bath-related death for developing future prevention strategies.

Early repolarization is associated with a significantly increased risk of ventricular arrhythmias and sudden cardiac death in patients with structural heart diseases

Early repolarization pattern (ERP) has been proved to increase risk of arrhythmia death in the general population, but its prognostic significance in patients with structural heart disease (SHD) is controversial. The purpose of this study was to conduct a meta-analysis of studies assessing the association between ERP and risk of ventricular arrhythmias (VTAs) and sudden cardiac death (SCD) in patients with SHD. We performed a literature search using MEDLINE (January 1, 1966, to September 25, 2016) and EMBASE (January 1, 1980, to September 25, 2016) with no restrictions. Studies that reported odds ratio (OR) estimates with 95% confidence intervals (CIs) for the associations of interest were included. The search yielded 19 observational studies, involving 7268 patients that reported 1127 cases of VTAs or SCD. In the selected studies, the point estimates of the ORs were consistently greater than 1. Compared with those without ERP, patients with ERP experienced a significantly increased risk of developing VTAs or SCD (OR 4.76; 95% CI 3.62-6.26), ventricular fibrillation (OR7.14; 95% CI 4.31-11.82), and SCD (OR 4.07; 95% CI 1.58-10.51). The results were consistent and statistically significant in all subgroups. ERP with J-point elevation in inferior leads, notching configuration, and horizontal or descending ST segment connote higher risk. ERP is associated with a significant increased risk of VTAs or SCD in patients with SHD. Future research should attempt to understand the exact mechanisms for the arrhythmia risk and to introduce ERP in the risk stratification in this patient group.

Sudden cardiac death in adults with congenital heart disease: does QRS-complex fragmentation discriminate in structurally abnormal hearts?

Sudden cardiac death (SCD) causes a large portion of all mortality in adult congenital heart disease (ACHD) patients. However, identification of high-risk patients remains challenging. Fragmented QRS-complexes (fQRS) are a marker for SCD in patients with acquired heart disease but data in ACHD patients are lacking. We therefore aim to evaluate the prognostic value of fQRS for SCD in ACHD patients. From a multicentre cohort of 25790 ACHD patients, we included tachyarrhythmic SCD cases (n = 147), and controls (n = 266) matched by age, gender, congenital defect and (surgical) intervention. fQRS was defined as ≥1 discontinuous deflection in narrow QRS-complexes, and ≥2 in wide QRS-complexes (>120 ms), in two contiguous ECG leads. We calculated odds ratios (OR) using univariable and multivariable conditional logistic regression models correcting for impaired systemic ventricular function, heart failure and QRS duration >120 ms. ECGs of 147 SCD cases (65% male, median age of death 34 years) and of 266 controls were assessed. fQRS was present in 51% of cases and 34% of controls (OR 2.0, P = 0.003). In multivariable analysis, fQRS was independently associated with SCD (OR 1.9, P = 0.01). The most common diagnose of SCD cases was tetralogy of Fallot (ToF, 34 cases). In ToF, fQRS was present in 71% of cases vs. 43% of controls (OR for SCD 2.8, P = 0.03). fQRS was independently associated with SCD in ACHD patients in a cohort of SCD patients and matched controls. fQRS may therefore contribute to the decision when evaluating ACHD patients for primary prevention of SCD.

Postmortem genetic testing should be recommended in sudden cardiac death cases due to thoracic aortic dissection.

Acute thoracic aortic dissections and ruptures, the main life-threatening complications of the corresponding aneurysms, are an important cause of sudden cardiac death. Despite the usefulness of the molecular diagnosis of these conditions in the clinical setting, the corresponding forensic field remains largely unexplored. The main goal of this study was to explore and validate a new massive parallel sequencing candidate gene​assay as a diagnostic tool for acute thoracic aortic dissection autopsy cases. Massive parallel sequencing of 22 thoracic aortic disease candidate genes performed in 17 cases of thoracic aortic dissection using AmpliSeq and Ion Proton technologies. Genetic variants were filtered by location, type, and frequency at the Exome Aggregation Consortium and an internal database and further classified based on the American College of Medical Genetics and Genomics (ACMG) recommendations published in 2015. All prioritized results were confirmed by traditional sequencing. From the total of 10 potentially pathogenic genetic variants identified in 7 out of the 17 initial samples, 2 of them were further classified as pathogenic, 2 as likely pathogenic, 1 as possibly benign, and the remaining 5 as variants of uncertain significance, reaching a molecular autopsy yield of 23%, approximately. This massive parallel sequencing candidate gene approach proved useful for the molecular autopsy of aortic dissection sudden cardiac death cases and should therefore be progressively incorporated into the forensic field, being especially beneficial for the anticipated diagnosis and risk stratification of any other family member at risk of developing the same condition.

Sudden Cardiac Death: Pharmacotherapy and Proarrhythmic Drugs: A Nationwide Cohort Study in Denmark.

This study sought to describe the use of pharmacotherapy in a nationwide cohort of young patients withsudden cardiac death (SCD). Several drugs have been associated with an increased risk of SCD and sudden arrhythmic death syndrome (SADS). It remains unclear how pharmacotherapy may contribute to the overall burden of SCD in the generalpopulation. This was a nationwide study that included all deaths that occurred between 2000 and 2009 and between 2007 and 2009 in people age 1 to 35 years and 36 to 49 years, respectively. Two physicians identified all SCDs throughreview of death certificates. Autopsy reports were collected. Pharmacotherapy prescribed within 90 days before SCD was identified in the Danish Registry of Medicinal Product Statistics. We identified 1,363 SCDs; median age was 38 years (interquartile range: 29 to 45 years), and 72% (n= 975) were men. Autopsy was performed in 55%. Overall, 58% of SCD cases (n= 786) received at least 1 drug within 90 days before death. The most common drugs were analgesic drugs (n= 239; 18%), antihypertensive drugs (n= 234; 17%), andantibiotic drugs (n= 218; 16%). After multivariable adjustment, prescription of "brugadogenic" drugs or >1 QT-prolonging drug was associated with an increased risk of SADS compared with explained SCD (odds ratio: 2.16 [95%confidence interval: 1.12 to 4.17] and 2.91 [95% confidence interval: 1.46 to 5.81], respectively). Pharmacotherapy was identified in 58% of the SCD cases. After multivariable adjustment, there wasa2- and 3-fold increased risk of SADS compared with explained SCD in patients receiving brugadogenic drugs or>1QT-prolonging drug, respectively. Identification of high-risk patients is warranted to lower the burden of SCD.

Ten-year outcomes of monomorphic ventricular tachycardia catheter ablation in repaired tetralogy of Fallot

Monomorphic ventricular tachycardia (MVT) is common in adults with repaired tetralogy of Fallot (TOF), and is associated with sudden cardiac death. Management of MVT is not defined, and results of catheter ablation (CA) are limited. To evaluate long-term outcomes of MVT CA in repaired TOF. Thirty-four patients (mean age 32±10.3 years; 59% male) with repaired TOF underwent CA for symptomatic MVT between 1990 and 2012 in our centre; direct-current ablation (DCA) was used in 6%, radiofrequency followed by DCA in 29% and radiofrequency alone in 65%. Right ventricular (RV) dysfunction was present in 35% and left ventricular (LV) dysfunction in 21%. Mean numbers of clinical and induced MVTs were 1 and 2, respectively. Mean VT rate was 225±95bpm. Ablation targeted a single site (range 1-2), which was RV outflow tract in 85%. Primary success, defined as ventricular tachycardia (VT) termination during CA and final non-inducibility, was obtained in 82%. Seven patients (21%) required redo ablation in the first 3 months (before 2004; DCA). No death related to CA occurred. Mean follow-up time was 9.5±5.2 years. Antiarrhythmic therapy was discontinued in 71%. There were two cases of sudden cardiac death and four VT recurrences. Freedom from death and arrhythmia recurrence was 94% at 5 years, 81% at 10 years and 70% at 20 years. Global survival was 91% at 20 years. Baseline LV ejection fraction<60% was significantly associated with ventricular arrhythmia recurrence (hazard ratio 16.4, 95% confidence interval 1.8-147; P=0.01). CA can safely address macroreentrant MVT in repaired TOF patients with an acceptable long-term rate of recurrence in this high-risk population. Anatomical classification of isthmuses with electroanatomical mapping provides reproducible endpoints for CA. Attention should be given to LV systolic function in risk assessment and selection of candidates for implantable cardioverter-defibrillator.

Technical note: EnVision™ FLEX improves the detectability of depletions of myoglobin and troponin T in forensic cases of myocardial ischemia/infarction.

Immunohistochemistry is a well-established technique used in many research laboratories as well as in clinical diagnostics. The method allows to visualize the expression of proteins in biological tissues, as well as to evaluate this expression semi-quantitatively. For diagnosis, an optimal staining, based on a straightforward protocol, is crucial. In many sudden cardiac death cases, immunohistochemistry is the only tool enabling the diagnosis of myocardial ischemia/infarction, thus the diagnosis of the cause of death. Improvements in immunoreactions are actually possible thanks to optimized detection systems. The recently introduced detection system EnVision Flex™ by Dako allows to dramatically improve (in terms of intensity of the signal and practically absence of background) the visualization of antigens in formalin-fixed paraffin-embedded (FFPE) tissue sections. We tested this method for the detection of myoglobin and troponin T in human postmortem cases of myocardial infarction, as the results obtained by using the « classical » ABC (avidin-biotin complex) method have proven to be sub-optimal, thus rendering any interpretation very difficult, if not impossible.

Diagnóstico clínico y genético de la muerte súbita cardiaca de origen no isquémico

Introduction and objectivesNonischemic sudden cardiac death (SCD) is predominantly caused by cardiomyopathies and channelopathies. There are many diagnostic tests, including some complex techniques. Our aim was to analyze the diagnostic yield of a systematic diagnostic protocol in a specialized unit. MethodsThe study included 56 families with at least 1 index case of SCD (resuscitated or not). Survivors were studied with electrocardiogram, advanced cardiac imaging, exercise testing, familial study, genetic testing and, in some cases, pharmacological testing. Families with deceased probands were studied using the postmortem findings, familial evaluation, and molecular autopsy with next-generation sequencing (NGS). ResultsA positive diagnosis was obtained in 80.4% of the cases, with no differences between survivors and nonsurvivors (P=.53). Cardiac channelopathies were more prevalent among survivors than nonsurvivors (66.6% vs 40%, P=.03). Among the 30 deceased probands, the definitive diagnosis was given by autopsy in 7. A diagnosis of cardiomyopathy tended to be associated with a higher event rate in the family. Genetic testing with NGS was performed in 42 index cases, with a positive result in 28 (66.6%), with no differences between survivors and nonsurvivors (P=.21). ConclusionsThere is a strong likelihood of reaching a diagnosis in SCD after a rigorous protocol, with a more prevalent diagnosis of channelopathy among survivors and a worse familial prognosis in cardiomyopathies. Genetic testing with NGS is useful and its value is increasing with respect to the Sanger method.Full English text available from:www.revespcardiol.org/en

Sudden Cardiac Death: Autopsy Findings in 7200 Cases Between 2001 and 2015.

Sudden cardiac death (SCD) is a sudden unexpected event, from a cardiac cause, that occurs in less than 1 hour after the symptom onset in a person without any previous condition that would seem fatal or who was seen without any symptoms 24 hours before being found dead. The aims of the study were to describe the features of SCD in Brasov County, Romania (400,000 inhabitants) according to local forensic department autopsy files. We retrospectively chart reviewed a number of 7200 autopsy reports between 2001 and 2015 to identify cases of SCD. Data included cause of death, demographics, location of the event, prior known illnesses, as well as psychiatric comorbidities. Of 7200 autopsies effectuated during the 15-year period, we excluded 276 cases with incomplete data. The rest of the 6924 cases included 3000 autopsies (43.3%) of individuals with a violent death: accidents, suicides, and homicides. In 3924 cases (56.7%), the death was nonviolent. Of 3924 nonviolent deaths, based on the registry of Forensic department, we identified 1085 cases of SCD (749 males [69%]; mean age, 56 ± 17.4 years). Sudden death with a cardiac etiology remained a major cause of unexpected end of life in the vast majority of cases autopsied during the study period.

Post-mortem toxicology in young sudden cardiac death victims: a nationwide cohort study.

Several drugs increase the risk of ventricular fibrillation and sudden cardiac death (SCD). We aimed to investigate in detail the toxicological findings of all young SCD throughout Denmark. Deaths in persons aged 1-49 years were included over a 10-year period. Death certificates and autopsy reports were retrieved and read to identify cases of sudden death and establish cause of death. All medico-legal autopsied SCD were included and toxicological reports collected. Positive toxicology was defined as the presence of any substance (licit and/or illicit). All toxicological findings had previously been evaluated not to have caused the death (i.e. lethal concentrations were excluded). We identified 620 medico-legal autopsied cases of SCD, of which 77% (n = 477) were toxicologically investigated post-mortem, and 57% (n = 270) had a positive toxicology profile. Sudden cardiac death with positive toxicology had higher rates of sudden arrhythmic death syndrome (SADS), compared with SCD with negative toxicology (56% vs. 42%, P < 0.01). In total, 752 agents were detected, and polypharmacy (defined as the presence of more than one drug) was present in 61% (n = 164), all substances combined. Psychotropic drugs were the most frequent (62%, n = 467), and 82% (n = 385) were in pharmacological or subpharmacological levels. We found that more than half of all toxicologically investigated SCD victims have positive post-mortem toxicological findings, and polypharmacy is displayed in a considerable proportion. SCD with positive toxicology had higher rate of SADS, suggesting that the compounds may play a proarrhythmic role in these cases.

Use of Cardiac Injury Markers in the Postmortem Diagnosis of Sudden Cardiac Death.

In the daily practice of forensic pathology, sudden cardiac death (SCD) is a diagnostic challenge. Our aim was to determine the usefulness of blood biomarkers [creatine kinase CK-MB, myoglobin, troponins I and T (cTn-I and T), and lactate dehydrogenase] measured by immunoassay technique, in the postmortem diagnosis of SCD. Two groups were compared, 20 corpses with SCD and 8 controls. Statistical significance was determined by variance analysis procedures, with a post hoc Tukey multiple range test for comparison of means (p < 0.05). SCD cases showed significantly higher levels (p < 0.05) of cTn-T and cTn-I compared to the control group. Although only cases within the first 8 h of postmortem interval were included, and the control group consisted mainly of violent death cases, our results suggest that blood troponin levels may be useful to support a diagnosis of SCD.

Temporal Trends in Sudden Cardiac Death From 1997 to 2010: A Data Linkage Study.

Community-wide trends data for sudden cardiac death (SCD) are scarce, unlike widely reported declines in cardiovascular disease (CVD) mortality. Using administrative data, we aimed to examine population-level trends in SCD, stratified by sex, age and prior CVD hospitalisation. Person-linked mortality and hospital morbidity data were used to identify SCD and determine hospitalisation and comorbidity using a 10-year hospitalisation lookback period. Log-linear Poisson regression was used to calculate annual rate changes and rate ratios. In Western Australia, 7160 SCD cases were identified from 1997 to 2010 with males comprising 69%. Overall age-standardised SCD rates decreased by 17% in men and 31% in women from 1997-2001 to 2007-2010. The annual rate reduction was higher in women than men (-4.0%/year versus -2.3%/year; p=0.0039). Significant reductions were observed for 55-69 year-old and 70-84 year-old men and women but not for the 35-54 year-olds. The overall relative risk comparing men to women increased slightly from 2.4 in 1997 to 3.0 in 2010 (trend p=0.0039) but differed across age groups. The relative risk declined in 35-54 year-olds from 5.1 to 3.2 whereas it increased from 2.9 to 3.9 in 55-69 year-olds and 1.9 to 2.3 in 70-84 year-olds. Declining trends in SCD rates were observed in those with and without prior CVD and were similar to CVD mortality trends (-4.9%/year in men and -5.5%/year in women). Trends in rates of SCD fell in middle to older aged men and women, with and without CVD, and mirrored the fall in fatal CVD. Limited improvement in 35-54 year-olds requires further investigation.

SUDDEN DEATH IN HYPERTROPHIC CARDIOMYOPATHY: SEARCH FOR NEW RISK FACTORS

Regardless the developed algorithms for risk stratification in sudden cardiac death (SCD) among patients with hypertrophy cardiomyopathy (HCM) there are SCD cases with no common risk factors. The issue for prediction of SCD in this pathology does not lose its importance. Aim. To study the risk factors for SCD in HCM patients. Material and methods. During 14 years, 198 HCM patients studied (mean age — 60,0±13,8 y.o., 105 males) with ECG, EchoCG, Holter ECG, veloergometry done. During 14 years, 15 died. There was 7 SCD cases with 2 successful resuscitations. Results. In HCM patients there was relation of SCD with the following clinical and instrumental parameters: age (r=-0,19, p=0,015), syncopes in anamnesis (r=0,17, p=0,03), high flow velocity in outflow tract of the left ventricle (LV) in exertion (Ex) (VmaxLVOT) (r=0,3, p=0,04), low Ex tolerance (r=-0,34, p=0,009), abnormal Ex response of blood pressure (ABPR) (r=0,36, p=0,00001), high minimal heart rate (HR) on Holter ECG (r=0,26, p=0,01). Applying the binary logistic regression with inclusion of the most significant predictors, the model was formulated for SCD prediction in HCM patients: SCD=22,28хABPR-6,9хEx Duration+12,5хVmaxLVOT+0,32хMinHR-0,4478хAge-14,7 If the result of equation more than 0 — the patient has high risk of SCD. In negative — SCD risk is minimal. Value of χ2 for the proposed equation is 19,3 (p=0,002). Conclusion. Regardless the common (age, syncopes, severity of LVOT obstruction, ABPR in Ex) there are additional SCD risk factors in HCM patients: low Ex tolerance and high minimal HR on Holter ECG. the mathematic model proposed, making to, based on the age of patient and presence of ABPR in Ex, Ex tolerance, maximal flow velocity in LVOT in Ex, as minimal HR by Holter ECG, to reveal patients with high risk of SCD.