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At least 19 recordsLinked to original sources
PubMed1996

[Cardiological fitness examination of the athlete and prevention of sudden death].

Sudden death happening to an athlete is a frightening tragedy. Epidemiological data are quite controversial but sudden death occurring during sporting activity is probably not a rare occurrence. Beside drug abuse and accidental causes, cardiovascular abnormalities represent the principal origin of sudden death. Cardiomyopathy in young athletes and coronary artery disease in older athletes are the underlying pathologic substrates for most incidences. A certain proportion of sudden death in apparently healthy athletes was preceded by symptoms of exercise intolerance; pre participation evaluation directed to detect the cardiovascular abnormalities is probably of more value to reduce sudden cardiac death in athletes than detailed and routine sophisticated investigations.

Adolescent↗
PubMed1998

[Nocturnal sudden death].

Sudden death is natural death which is rapid and unexpected. Various epidemiological surveys indicate that the incidence of sudden death in Japan is about 100,000 annually, of which 60-70% are due to cardiovascular causes. One third of the victims die while sleeping in the night. Several disorders which may cause nocturnal sudden death, including "Pokkuri disease", are reviewed.

Adult↗
PubMed1975

Time, place, event of sudden death.

Sudden death, known since antiquity, is almost always due to cardiovascular disorder, but not exclusively to coronary artery disease. It is postulated that two processes, action of pre-existing risk factors (enlarged heart, abnormal conduction, extra systoles, ischemia) and new, untoward events (acute infarction or ischemia) culminate in the catastrophic event. Sudden death is apparently most likely during waking hours; sleep is a lesser risk. Which subjects are at greatest risk and which circumstances are most dangerous remain unknown and are important topics for further investigation.

Adolescent↗
PubMed1992

Sudden death.

Sudden death in athletes is a tragic, but fortunately infrequent, event. In young athletes (30 years old and younger) structural cardiovascular disease, often congenital, is usually responsible. Athletes over 30 years old who die suddenly are most frequently found to have severe atherosclerotic coronary artery disease. This article discusses the type of cardiovascular diseases underlying sudden death in athletes and approaches to preventing these tragedies.

Adult↗
PubMed1987

Exercise and sudden death.

Sudden death during exercise is rare, but limited data suggest that vigorous physical activity is associated with an increased risk for this event, particularly in individuals with overt cardiac disease or a high coronary risk profile. The mechanism of exercise-associated sudden death is usually a lethal arrhythmia; however, this may vary depending on the underlying cardiovascular disease. In the great majority of cases, cardiovascular disease is present in persons who die during exercise. In young individuals (less than 35 years old) hypertrophic cardiomyopathy and congenital coronary anomalies are the most common conditions, whereas older victims usually have coronary artery disease. Cardiac disease is typically unrecognized prior to death in young persons; in the older population, most have overt coronary disease or recognizable coronary risk factors. Screening asymptomatic individuals to identify increased risk of a cardiac event during exercise presents major problems in terms of logistics, expense, and accuracy, but careful evaluation, including exercise testing, is mandatory before a program of increased activity in patients with overt cardiac disease. In other cases, the extent of any evaluation must be determined on an individual basis.

Adult↗
PubMed1996

[Sudden death].

Sudden death accounts for about 7000 deaths per year in Belgium. Everyone could be concerned, from the newborn to the octogenarian. Due to the scientifical and technical progresses of our rescue teams, our hospitals are more often confronted with resuscitated patients. This syndrome must be considered as a whole clinical entity. Its causes, its physiopathological concepts, its diagnostic and prophylactic tools and its treatment should be fully integrated. The actual conceptions are modifying. Those different aspects are reviewed, in the light of the recent literature.

Adult↗
PubMed1996

The role of catecholamines in cocaine toxicity: a model for cocaine "sudden death".

Sudden death associated with cocaine abuse is preceded by a state of agitated delirium. We postulated that release of catecholamines associated with this stress enhanced toxicity from cocaine. Thus we investigated the effect of catecholamine infusion [(epinephrine (7.25 ugml-1), norepinephrine (4.4 ugml-1) and dopamine (8.0 ugml-1), infused at 6 ml h-1] on the toxicity from concomitant infusion of cocaine (1 mg-kg-1 min-1). Two groups of rats were studied in order to isolate distinct toxicity endpoints: convulsions and respiratory arrest in conscious, and, circulatory arrest in anesthetized and ventilated rats. Catecholamines were administered at either full or 1/2 strength to establish a dose response effect on cocaine toxicity. Catecholamine infusion in a dose dependent fashion provoked earlier convulsions and respiratory arrest in conscious rats and circulatory arrest in anesthetized and ventilated rats. Despite lower cocaine cumulative dose administration, rats receiving catecholamines had similar plasma cocaine concentrations at the onset of convulsions and respiratory arrest compared to those with cocaine infusion alone. The data suggest that catecholamines enhance the convulsive, respiratory and circulatory toxicity of cocaine by a pharmacokinetic interaction.

Animals↗
PubMed1995

Cardiac sarcoidosis: an unforeseen cause of sudden death.

Sudden death occurring in a male with established coronary artery disease is inevitably assumed to result from the atherosclerotic process, and an autopsy is rarely requested to confirm the cause. On occasions, however, an autopsy reveals the unexpected, such as cardiac sarcoidosis.

Autopsy↗
PubMed1998

Circumstances of death in sudden death in epilepsy: interviews of bereaved relatives.

OBJECTIVES: To study the circumstances of death in sudden death in epilepsy. METHODS: Self referred bereaved relatives of patients with epilepsy who had died suddenly were interviewed with information obtained substantiated through other sources-namely, coroners' officers' reports, postmortem reports, previous medical records, and EEG reports. RESULTS: Of 34 cases, 26 were classified as sudden unexpected deaths in epilepsy (SUDEP). Twenty four of 26 cases of SUDEP were unwitnessed. Evidence indicative or suggestive of a seizure was found in most. In 11 of 26 the position of the head was such that breathing could have been compromised. Cases included both localisation related and idiopathic primary generalised epilepsy. Only three were in remission at the time of death. Most relatives expressed the view that they would have preferred to have known that epilepsy could be fatal. CONCLUSIONS: Although the deaths in question were largely unwitnessed, the available evidence suggested that most cases of SUDEP represented ictal or postictal seizure deaths, occurring in people with a history of generalised tonic clonic seizures, and in both primary generalised and localisation related epilepsy. These interviews highlight the needs of bereaved relatives and their sense of isolation in the face of an entirely unexpected and apparently unexplained loss.

Adolescent↗
PubMed1998

Comparison of anti-epileptic drug levels in different cases of sudden death.

Sudden unexplained death syndrome (SUDS) in epilepsy is identified as death in an epileptic individual with no anatomic cause found at autopsy. SUDS appears to be associated with subtherapeutic levels of anticonvulsants. Sudden death with no demonstrable cause at autopsy accounts for 5% to 30% of deaths in epileptic individuals. In the majority of cases, however, the cause of death in epileptic individuals can be demonstrated at autopsy. We examined the anti-epileptic drug concentrations in decedents who died as a direct result of epilepsy and compared these findings with those from a control population of epileptic patients who died suddenly due to some unrelated cause. This retrospective study was conducted on all deaths involving patients with epilepsy examined at the Jefferson County Coroner/Medical Examiner office from 1986-95. Out of 115 total cases the underlying cause of death was epilepsy in 60 cases--52 cases of SUDS and 8 deaths caused by an accident precipitated by a seizure. In 44 cases death was unrelated to the decedent's epilepsy. In 11 cases the contribution of epilepsy to death could not be determined. Published articles on SUDS report subtherapeutic anti-epileptic medication levels in 63% to 94% of cases. We found subtherapeutic drug levels in 69% of the 52 cases of SUDS, in 75% of the 8 cases where a seizure precipitated an accident causing death, and in 34% of the control population. The incidence of subtherapeutic anticonvulsants is significantly greater in patients dying as a direct result of their epilepsy than in those dying of an unrelated cause.

Adolescent↗
PubMed1995

[The current status of the prevention and treatment of sudden death].

Sudden cardiac death is a major medical problem. The techniques to identify high risk patients have a limited value. Only betablockers, and perhaps amiodarone, are useful for primary prevention of sudden cardiac death. Prospective studies being carried out today with implantable cardioverter-defibrillator, will show us if these are the best way of treatment (secondary prevention) of sudden cardiac death.

Cardiovascular Agents↗
PubMed1985

Post-mortem examination of the heart in cases of sudden death.

Sudden unexpected death is an important topic of forensic medicine. Several papers have been published on the morphological changes of the coronary arteries and the myocardium in sudden cardiac death. Forensic pathology demands more and more accurate methods of postmortem diagnosis of early ischaemic lesions of the heart muscle that occur shortly before death and which, in the absence of other explanations, may presumably be related to the cause of death. The cause of death is often evident from post-mortem findings, still in a number of cases the diagnosis may be doubtful. The application of electron microscopy has increased rapidly over recent years and the electron microscopic investigation of post-mortem biopsy material may be useful in narrowing down the cause of death. This report presents the results of electron microscopic and cytochemical studies of the myocardium in cases when death had occurred at a precisely recorded time.

Calcium↗
PubMed1984

The electrophysiologic features of sudden death.

Sudden or instantaneous death is nearly always of cardiac origin. The most common mechanism is a severe electrical dysfunction, which is apparent on Holter monitoring tapes. Identifying patients at risk of sudden cardiac death is difficult, and Holter monitoring has proved to be limited in its diagnostic usefulness. However, in patients who have experienced cardiac arrest Holter monitoring has shown that the electrical abnormalities leading to death vary. These abnormalities usually take time to develop, and during this time the cerebral circulation is partially maintained. In this brief period, lasting less than 2 minutes, the individual may become aware that something is wrong and have time to react.

Death, Sudden↗
PubMed1983

[Epidemiology of sudden infant death (sudden infant death syndrome, SIDS) in the Lübeck area. Catamnestic studies of 155 observed cases from 1971 to 1981].

The 155 cases of SIDS investigated at the Institut für Rechtsmedizin of the Medizinische Hochschule in Lübeck (northern part of the Federal Republic of Germany) between 1971 and 1981 have been analysed retrospectively under epidemiological aspects. The incidence was 2.17 cases of SIDS/1,000 live-born babies, 63.9% were male, 79.3% of the infants died during the first 6 months of life with a clear peak in the 2nd month. There was no seasonal accumulation; 68.4% of the infants died between 8.00 p.m. and 8.00 a.m., in 75% the socio-economic factors were inconspicuous, but we observed a significantly higher incidence of infants from mothers younger than 25 years. In 58% of our cases no signs of illness or changed behaviour had been observed during the 48 h before death. The results of our study are compared with the literature and discussed with special regard to a possible prevention.

Age Factors↗
PubMed1987

Behavior of chickens prior to death from sudden death syndrome.

A study was made to determine if chickens dying from sudden death syndrome (SDS) showed any unusual behavioral characteristics during the final 12 h preceding death. Continuous video recordings were made of floor pens of 50 to 120 individually marked male broiler chickens between 3 and 10 wk of age. Behavioral data were obtained from video tapes played back following death of chickens from SDS. Analysis of the video tapes revealed no significant differences between 10 SDS chickens and their matched controls in the frequencies or proportions of time spent in each of 19 different behavioral activities. All SDS chickens exhibited a sudden attack prior to death lasting an average of 53 s and characterized by loss of balance, violent flapping, and strong muscular contractions. There was no evidence that death was preceded by a particular environmental or behavioral event. It was concluded that there were no consistent behavioral symptoms which could be used to identify SDS chickens prior to death.

Animals↗
PubMed1987

[Bronchial hyperreactivity in asthma at high risk of sudden death].

Sudden severe life threatening attack (SSA) may occasionally develop in some patients who have had until that event a mild asthma without detectable baseline airway obstruction. Airway responsiveness (AR) measurement could be a useful mean to characterize or identify them. No data exist regarding the baseline non specific AR of such patients. We studied 5 patients having had a SSA during their past few weeks. Methacholine (MCH) challenges were performed only when standard pulmonary function tests were close to normal (FEV1 greater than or equal to 80% pred.); the patients were off medication at the time of MCH challenges. 3 to 8 evaluations were performed over a time span of 4 to 24 months. The level of AR ranged from moderately increased (PC20 = 24 mg/ml). Mean PC20 was 7,8 mg/ml. This level of AR did not differ significantly from that found in a population of 67 mild asthmatics who also were evaluated in the absence of baseline bronchial obstruction and were off medication (PC20 = 5,5mg/ml). In any individual asthmatic having sustained SSA, AR was strikingly stable. However in two patients we detected a marked decrease in PC20 which was followed within 2 weeks by a SSA. We conclude that: 1. Asthmatics who have had SSA do not demonstrate particularly AR, which is not related to the severity of their asthma. 2. Baseline AR is usually stable. 3. The measurement of AR in these patients is not very useful, specially for substantiating medication needs. 4. A marked increase in AR can be observed before SSA.

Adult↗
PubMed1977

Effect of aortocoronary saphenous vein bypass grafting on death and sudden death. Comparison of nonrandomized medically and surgically treated cohorts with comparable coronary disease and left ventricular function.

The effect of saphenous vein bypass grafting on the incidence of sudden cardiac death and total cardiovascular death was studied by comparing the survival of subsets of surgically and medically treated patients with coronary disease who were similar in two major prognostic variables: extent of coronary disease and ejection fraction. Significant differences in some baseline variables existed between medical and surgical subgroups with similar ejection fraction and extent of coronary disease. Medically treated patients tended to be in a lower functional class, to have more extensive ventricular contraction abnormalities, to have a larger end-diastolic volume, and to have fewer distal vessels feasible for grafting. Surgically treated patients with two vessel disease and normal or moderately reduced election fraction had improved survival when compared with medically treated patients with two vessel disease and similar ejection fraction. Improved survival of borderline statistical significance was also seen in surgically treated patients with three vessel disease and moderately reduced ejection fraction. When categorized according to end-diastolic volume, surgically treated patients with two vessel disease and normal or moderately increased end-diastolic volume also had improved survival over similarly defined medically treated patients. The sudden death rates for subgroups of mecically treated patients were 1.8 to 10.9 times higher than the rates in subgroups of surgically treated patients with a comparable extent of coronary disease and ejection fraction.

Adult↗