China
Africa
Explore chapters and articles related to this topic
Investigation of Sudden Cardiac Death
Published in Mary N. Sheppard, Practical Cardiovascular Pathology, 2022
Sudden arrhythmic death syndrome (SADS) refers to a subset of SCD, where, despite thorough and expert post-mortem histological and toxicological examinations, a cause of death cannot be identified. There is no disease of any other organ and toxicology is negative.7 In such cases, the medical history should be reviewed. There are some conditions such as epilepsy, psychiatric disorders, and alcoholic liver disease in which there appears to be an excess of sudden deaths. A prior history of syncopal attacks or fainting episodes may point to a cardiac arrhythmia as the cause. It is considered that there are up to 600 cases per year in the UK.7,8 The concept of the morphologically normal heart in sudden death is of major importance with the emergence of the molecular channelopathies giving rise to lethal cardiac arrhythmias. Once the pathologist establishes these facts about a case, it is important to tell the coroner/medical examiner and the family that primary electrical abnormalities have to be considered.
Prescribing for minor illness
Published in Gina Johnson, Ian Hill-Smith, Chirag Bakhai, The Minor Illness Manual, 2018
Gina Johnson, Ian Hill-Smith, Chirag Bakhai
Full information on which drugs prolong the QT interval can be found at the Sudden Arrhythmic Death Syndrome (SADS) website (www.sads.org.uk) or the American site CredibleMeds (www.crediblemeds.org). Below is a list of medications commonly prescribed in primary care or available over the counter (OTC) in the United Kingdom that are known to affect the QT interval. Not all carry the same risk. The drugs in bold type are associated with higher risk (Table 14.2).
Arrhythmias
Published in Clive Handler, Gerry Coghlan, Nick Brown, Management of Cardiac Problems in Primary Care, 2018
Clive Handler, Gerry Coghlan, Nick Brown
all close blood relatives of a person who has died of sudden arrhythmic death syndrome should be referred to a specialist centre for investigation. Only 50% of relatives show evidence of a genetic problem, because the victim may have had a mutation or the family members may be carriers but have no signs of disease.
Brugada syndrome and the story of Dave
Published in Neuropsychological Rehabilitation, 2018
Samira Kashinath Dhamapurkar, Barbara A Wilson, Anita Rose, Gerhard Florschutz
There are several abnormal ECG patterns that identify BrS including a heart block affecting the right ventricle so that it is not directly activated by impulses travelling through the right bundle branch (known as the right bundle branch block). ST-segment elevations noted in leads v1–v3, prolonged PR and negative T wave may also indicate BrS (Brugada, 2016). This segment is part of the ECG. An ST segment elevation myocardial infarction (STEMI) is the name for one type of heart attack that arises from an acute interruption of blood supply to a part of the heart. Initially, it was believed that people with BrS had a structurally normal heart but this has been challenged (Frustaci et al., 2005) and the syndrome can also occur as a consequence of subtle structural changes in the right ventricular outflow tract (Antzelevitch, Brugada, Brugada, & Brugada, 2005; Nademanee et al., 2011). Other terms for this syndrome include sudden unexplained death syndrome; sudden unexplained nocturnal death syndrome and sudden arrhythmic death syndrome (Nademanee et al., 1997; Vatta et al., 2002). Symptoms vary from palpitations and giddiness to recurrent fainting, nocturnal agonal respiration (breathing with short, sporadic gasps) and sudden cardiac death (Antzelevitch & Patocskai, 2016; Wilde et al., 2002). The condition is accountable for 4% of all sudden deaths and 20% of sudden deaths reported to be in those without structural heart disease (Vohra & Rajagopalan, 2015). A family history is present in about 20 to 30% of patients.
Sudden unexplained cardiac deaths in young adults: a call for multidisciplinary approach
Published in Acta Cardiologica, 2018
Bartosz Hudzik, Michal Hudzik, Andrzej Lekston, Mariusz Gasior
The investigation of death in young (usually under 35 years of age), previously healthy persons calls for an in-depth autopsy with considerable attention drawn to the examination of the heart. Oftentimes, post-mortem examination can detect cardiovascular abnormalities responsible for sudden cardiac death (SCD) (Table 1). The relative predominance of ARVC over HCM in the European (namely Italian) SCD registries may arise from different genetic predisposition or be associated with a substantial reduction in HCM-associated SCD due to pre-participation screening programmes [1,2]. However, a substantial portion of SCDs remains unexplained even after comprehensive medicolegal investigation and such SCDs are labelled as autopsy-negative sudden unexplained deaths (SUDs) [3]. Data show a high prevalence of SUD in young adults, young athletes in particular, with a morphologically normal heart. Although American and European data somewhat differ, most deaths occur due to some form of cardiomyopathy, arrhythmia, or coronary artery disease (Table 2, Figure 1) [2,4,5]. It is estimated that as many as 30% of deaths of children, adolescents, and young adults have no identifiable structural abnormality found at autopsy [6]. Most SUDs are reported to occur during or directly after exertion or exercise. Therefore, the issue is of paramount importance among athletes. Although likely underestimated, the incidence of SUD among endurance athletes ranges between 1 per 50,000 and 1 per 300,000. Annually, great number of sudden deaths involving young individuals remains unexplained even following a thorough medicolegal investigation including an autopsy. In fact, several epidemiologic studies have estimated that the prevalence of no morphologic abnormalities identifiable at autopsy varies widely and can be as high as 53% of sudden deaths among previously healthy children and young adults [6]. Margey et al. have reported that sudden arrhythmic death syndrome (SADS) was the commonest cause of SCD in the young (14- to 35-year olds). They have demonstrated the incidence of SADS to be more than five times that in official reports of the Irish Central Statistics Office [5]. In a recent study, Ullal et al. have reported that hypertrophic cardiomyopathy is not a more common finding at death than structurally normal hearts in young subjects with SCD. The authors emphasise that increased attention should be directed toward identifying causes of death associated with a structurally normal heart in subjects with SCD [7].