Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “DEATH, SUDDEN”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 19 recordsLinked to original sources
PubMed1999

[Sudden death (IV). Sudden death in the athlete. The minimal requirements before performing a competitive sport].

In our society, athletes project the ultimate image of well being in the health status spectrum. Though very uncommon, the sudden death of a young athlete has always great impact on the community and the athlete's surroundings (physicians, athletes, coaches, etc.). Due both to this and to the growing number of physical exercise practitioners, there is an increasing demand for more and precise information on the recommendations of participation in certain sports with the minimum possible risk. Together with the most recent and detailed statistics concerning the cardiovascular causes of sudden death in athletes, the objective of the present article is to review the present controversy regarding the preparticipation medical examination as a useful method to identify those athletes with greater potential risk, as well as to propose a few and simple recommendations concerning the tests that should be performed in each case.

Adolescent↗
PubMedDate not supplied

Risk stratification and primary prevention of sudden cardiac death: sudden death prevention.

The initial challenge in primary prevention of sudden cardiac death (SCD) lies in identifying those at greatest risk, before the index event. Ventricular fibrillation is the leading cause of SCD; however, many clinical conditions predispose fatal ventricular dysrhythmias. In patients with structural heart disease, left ventricular dysfunction is the strongest predictor of SCD. Noninvasive markers such as nonsustained ventricular tachycardia, delayed potentials, decreased heart rate variability and baroreflex sensitivity, and repolarization alternans are further observed to assess risk in ischemic cardiomyopathy; however, most of these markers have poor positive predictive value and lack specificity. The electrophysiologic study has strong positive predictive value, but remains a costly and invasive method for risk stratification. In patients with normal hearts, genetic predisposition may identify patients at risk but clinical markers are not readily recognized. The implantable loop recorder is a useful tool in detecting dysrhythmic causes of syncope and identifying patients at risk for SCD.

Adult↗
PubMedDate not supplied

[Current concepts on sudden death].

Sudden death is defined as the death occurring less than one hour before the onset of the patient's symptoms. It is a severe condition considered a public health issue in several countries and in ours, it accounts for 33 000 to 53 000 annual deaths mainly related to ischemic heart disease. The main cause of sudden death are severe ventricular arrhythmias, but determining what patients are at risk for such an episode is complex, that is why risk stratification is usually a low cost-effective intervention. In the present study, we describe different sudden death risk-stratification strategies. Different sudden death treatment strategies regarding general population have different success rates in different countries, nevertheless, among select high risk populations; the best therapy currently available is the automatic implantable cardioverter-defibrillator. We also discuss other treatment options. In Mexico it is deemed necessary to do an important effort for the early detection, prevention and treatment of sudden death in order to limit the consequences of this problem.

Clinical Trials as Topic↗
PubMed2006

[Psychotropic drugs and sudden death].

Sudden death associated with psychotropic drugs is an issue in clinical practice which is currently debated worldwide in the literature. The objective of this work is to review recent literature on the issue (up to the end of 2004). The literature focuses mainly on the association between unexplained sudden death and antipsychotics and, to a lesser degree, tricyclic antidepressants; there are few references to other classes of psychotropic drugs. Over the last few decades various causal mechanisms have been proposed. However, recent literature refers mostly to sudden cardiac death induced by arrhythmias, and discusses, as a possible mechanism, the prolongation of the QTc interval due to the inhibition of potassium channels, leading to the risk of developing torsade de pointes which can result in sudden death. Although these cases of sudden death are rare, associated risk factors are also discussed because it is believed that a combination of several of these factors may increase the risk. We go on to consider recommendations to diminish the risk of sudden death. Finally, we review sudden death cases that have occurred in the last 5 years in the Acute Psychiatric Ward of S. Francisco Xavier Hospital (January 1999 to December 2004).

Antidepressive Agents, Tricyclic↗
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↗
PubMed2000

The insula and cerebrogenic sudden death.

Sudden death is an "electrical accident" caused by fatal cardiac arrhythmias. While brain-heart control has physiological advantages, cerebrogenic sudden death and nonfatal cardiovascular disturbances can complicate stroke of all types, seizures and epilepsy, head injury, other neurological conditions, neurosurgical procedures, and intense emotional states. Cerebrogenic cardiovascular and autonomic disturbances include electrocardiographic changes, elevation of cardiac enzymes, cardiac arrhythmias, disturbances of blood pressure regulation, and cerebrogenic pulmonary edema. Evidence from experimental studies and clinical observations indicates a crucial role of the insula in cerebrogenic cardiovascular disturbances and sudden death. Future studies should focus on identification of at-risk patients, confirmation of a vulnerable period of cerebrogenic sudden death in those with different neurological conditions and intense emotional states, and clarification of the neurochemical mediators.

Animals↗
PubMed2002

Cocaine-induced channelopathies: emerging evidence on the multiple mechanisms of sudden death.

Sudden death due to cocaine in the absence of myocardial infarction has been attributed to the precipitation of life-threatening arrhythmias not unlike that due to antiarrhythmic drugs. Cocaine is a slow on-off sodium blocker and a fast on-off potassium blocker. Effects on repolarization are biphasic: At low concentrations, cocaine delays ventricular recovery, whereas at higher levels, cocaine hastens it. Two distinct clinical profiles emerge from case reports of electrocardiographically documented life-threatening arrhythmias attributed to cocaine. The first is monomorphic slow ventricular tachycardia or idioventricular rhythm that occurs in overdose situations and appears to reflect excessive sodium channel block; it may respond to sodium bicarbonate. The second is torsade de pointes that occurs in recreational users who have underlying risks for this tachycardia (such as fully or partially expressed congenital long QT syndrome) and reflects potassium channel blockade. These clinical observations can be explained by recent findings regarding the electrophysiologic effects of cocaine. Other patterns of severe arrhythmias due to cocaine may yet emerge.

Adult↗
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↗
PubMed2000

Debate: Do all patients with heart failure require implantable defibrillators to prevent sudden death?

Sudden death is a major cause of mortality in patients with ventricular dysfunction. The highest risk occurs among patients with less severe functional impairment. Current methods of risk stratification are inadequate, and a rational therapy for prevention of sudden death is not available. The implantable cardioverter-defibrillator (ICD) has proven to be more effective than drugs in reducing sudden-death risk in some subsets of patients. Empiric ICD therapy, targeting the general population with mild to moderate heart failure, will maximize the impact of such a strategy to prevent sudden death and improve long-term survival.

Journal Article↗
PubMed1993

Helping survivors cope with sudden death.

Sudden death is extremely traumatic for survivors. Sudden death allows no preparation or special moments of farewell and thus leaves survivors with feelings of guilt as well as grief. Caring for survivors presents a challenge to the nurse and an opportunity to utilize strategies around a crisis intervention model that can assist survivors in coping. Helping survivors can be crucial in encouraging those who remain to experience successful bereavement and to cope with the loss.

Adaptation, Psychological↗
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↗
PubMed2005

[Heart failure and sudden death].

Sudden death in patients with heart failure (HF) is a topic of great complexity. Neurohumoral activation including adrenergic and renin-angiotensin-aldosterone system has been a suspected trigger for lethal ventricular arrhythmias and sudden deaths. Randomized clinical trials have demonstrated that angiotensin converting enzyme inhibitors, angiotensin II receptor antagonists and beta-adrenergic blockers improve survivals in patients with HF. Although prophylactic implantable cardioverter defibrillator (ICD) therapy is effective reducing mortality in patients with left ventricular (LV) systolic dysfunction, the ICD is unlikely to be appropriate for all patients with LV systolic dysfunction. In addition, the effect of routine prophylactic use of ICDs on health care costs must be carefully considered. The care of patients with LV systolic dysfunction should be individualized for each patient.

Arrhythmias, Cardiac↗
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↗
PubMed1999

Sudden death in the general population in Okinawa: incidence and causes of death.

Sudden unexpected death is generally considered to be caused by acute myocardial infarction and/or arrhythmia. To document the incidence and causes of sudden death in Japan, where the incidence of myocardial infarction is low, the present study examined death certificates, hospital records, the forensic medical records, and the police records of residents of the southern part of Okinawa island who died at the age of 20-74 years during a 3-year period from January 1, 1992 to December 31, 1994. Sudden death was defined as death within 24 h from the onset of unexpected symptoms. The study documented 126 (87 men and 39 women) sudden deaths. The crude incidence rate was 0.37/1,000 person per year (0.51 in men and 0.23 in women). According to the death certificates, 78 cases died of heart diseases. However, the cause of death could be determined by examination of all available records in only 64 cases: myocardial infarction in 10, non-ischemic heart diseases in 13, and stroke in 23 cases. Even when the analysis was limited to the cases who died within 1 h from the onset of symptoms, heart disease was the cause of death in only 22% of the cases while the cause of death could not be determined in 53% of the cases. Only 13% of those diagnosed as heart diseases on the death certificate were verified. The agreement rate between the diagnosis reached by the re-evaluation of the records and that on the death certificate was 82% for stroke and 33% for other diseases. In Okinawa, Japan, the frequencies of heart disease and stroke as the cause of sudden death may be similar. Except for stroke, the diagnosis appearing on the death certificate has substantial inaccuracy.

Adult↗
PubMed2002

Antipsychotic-related QTc prolongation, torsade de pointes and sudden death.

Sudden unexpected deaths have been reported with antipsychotic use since the early 1960s. In some cases the antipsychotic may be unrelated to death, but in others it appears to be a causal factor. Antipsychotics can cause sudden death by several mechanisms, but particular interest has centred on torsade de pointes (TdP), a polymorphic ventricular arrhythmia that can progress to ventricular fibrillation and sudden death. The QTc interval is a heart rate-corrected value that represents the time between the onset of electrical depolarisation of the ventricles and the end of repolarisation. Prolongation of the QTc interval is a surrogate marker for the ability of a drug to cause TdP. In individual patients an absolute QTc interval of >500 msec or an increase of 60 msec from baseline is regarded as indicating an increased risk of TdP. However, TdP can occur with lower QTc values or changes. Concern about a relationship between QTc prolongation, TdP and sudden death applies to a wide range of drugs and has led to the withdrawal or restricted labelling of several. Among antipsychotics available in the UK, sertindole was voluntarily suspended, droperidol was withdrawn, and restricted labelling introduced for thioridazine and pimozide. The degree of QTc prolongation is dose dependent and varies between antipsychotics reflecting their different capacity to block cardiac ion channels. Significant prolongation is not a class effect. Among currently available agents, thioridazine and ziprasidone are associated with the greatest QTc prolongation. Virtually all drugs known to cause TdP block the rapidly activating component of the delayed rectifier potassium current (I(kr)). Arrhythmias are more likely to occur if drug-induced QTc prolongation coexists with other risk factors, such as individual susceptibility, presence of congenital long QT syndromes, heart failure, bradycardia, electrolyte imbalance, overdose of a QTc prolonging drug, female sex, restraint, old age, hepatic or renal impairment, and slow metaboliser status. Pharmacodynamic and pharmacokinetic interactions can also increase the risk of arrhythmias. Further research is needed to quantify the risk of sudden death with antipsychotics. The risk should be viewed in the context of the overall risks and benefits of antipsychotic treatment. It seems prudent, where possible, to select antipsychotics that are not associated with marked QTc prolongation. If use of a QTc-prolonging drug is warranted, then measures to reduce the risk should be adopted.

Antipsychotic Agents↗
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↗