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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

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

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

[Sudden, unexplained infant death--sudden infant death syndrome. Forensic pathological aspects].

Delimitation of the sudden unexplained infant death syndrome (SIDS) is difficult as the diagnosis is made by exclusion. The difficulties in the differential diagnosis are concentrated on interpretation of the significance of positive viral and bacterial findings, inflammatory changes in the respiratory organs, heart and central nervous system together with malformations. Classification of SIDS appears, therefore, to vary according to time and place. New techniques, e.g. DNA analysis, have explained the etiology in a few per cent of the cases but have not yet solved the riddle of SIDS. The article reviews hypotheses about apnoea, arrhythmia, overheating and inefficient surveillance of the infant. It is emphasized that assessment of risk factors for SIDS requires valid epidemiological investigations where the basis for the diagnosis is a uniform classification of SIDS infants as compared with other groups of sudden death in infancy. An investigation of this nature has been initiated in the Nordic countries. It is important to examine and treat infants with abnormal sleep apnoea but generalized employment of monitoring has not reduced the number of unexplained infantile deaths.

Autopsy

A prospective study of sudden death in "high-risk" bundle-branch block.

We prospectively followed 257 patients with bifascicular and trifascicular conduction-system disease and intact atrioventricular conduction who had undergone His-bundle studies. Forty-seven per cent had associated coronary-artery disease, and 23 per cent primary conduction-system disease. His-ventricular interval was moderately prolonged in 43 per cent and markedly prolonged in 12 per cent. During an average follow-up period of 25 months 50 patients died. However, death was sudden in only 27, and 17 of the sudden deaths were not due to bradyarrhythias. Actuarial analysis showed an overall mortality rate (mean +/- S.E.) of 19 +/- 2.6 per cent at two years, mortality from sudden death being 10 +/- 2.6 per cent. Permanent heart block occurred in 12. No clinical symptoms (including syncope), electrocardiographic findings, electrophysiologic data or their combination identified patients at high risk of sudden death. Sudden death due to bradyarrhythmia is uncommon in patients with bundle-branch block and intact atrioventricular conduction. Therefore, routine prophylactic use of permanent pacemakers in all such patients is inappropriate. Pacemaker implantation should be reserved for those with documented symptomatic bradyarrhythmias.

Adult

Sudden death from stroke.

Sudden death is defined as any death that occurs less than 24 hours after the onset of first symptoms. Strokes account for 10 to 20% of all sudden deaths. The records of all residents of Rochester, Minn., who had their first stroke during the period 1955 through 1969 were analyzed. Among 255 deaths caused by the first stroke, 52 were sudden. Twenty-six of the deaths were due to primary intracerebral hemorrhage, and 20 to primary subarachnoid hemorrhage. Only two of the sudden deaths were caused by infarction: one by pontine and cerebellar infarct and the second by a cortical infarct, which resulted in death from status epilepticus. Among the nine patients who died within 2 hours of the onset of symptoms, six had primary subarachnoid hemorrhage. Hypertension was noted in 23 of the 26 patients (88%) who died of primary intracerebral hemorrhage; 8 patients with primary intracerebral hemorrhage were on long-term oral anticoagulant therapy, and all 8 were hypertensive.

Adult

Sudden death in severe aortic stenosis following cardiac catheterization.

Five patients with critical aortic stenosis (aortic valve area 0.6 cm2 or less) died 2 days to 21 days following cardiac catheterization performed in anticipation of cardiac surgery. A sixth patient was successfully resuscitated for spontaneous ventricular fibrillation, and successful aortic valve replacement was accomplished. Two patients had prior history of syncope; one patient, of ventricular tachycardia; three patients, of pulmonary edema; and three patients, of crescendo angina. One patient had severe hypotension during maintenance hemodialysis for chronic renal failure. The mode of death was sudden but not witnessed in two patients. The terminal cardiac rhythms were slow junctional in one patient, idioventricular in one, ventricular tachycardia in one, and ventricular fibrillation in the fourth patient. We conclude that symptomatic patients with critical aortic stenosis should be monitored after cardiac catheterization, and surgery should be performed as soon as possible since sudden death is not unusual.

Aged

Pulmonary hypertension and sudden death in aortic stenosis.

Sudden death is now an infrequent occurrence in severe aortic stenosis. However, an impressive increase in pulmonary arteriolar resistance has been found in some patients with end-stage aortic stenosis dying suddenly or deteriorating suddenly after catheterisation. Pulmonary hypertension does not seem to cause sudden death, but, in conjunction with decreased cardiac output, a critical reduction in aortic orifice area, and left ventricular failure, pulmonary hypertension identifies a population at significant risk. The rare finding of severe pulmonary hypertension in aortic stenosis should be considered an important marker for sudden death and in association with left ventricular failure may indicate an urgent need for valve replacement, regardless of the apparent clinical condition of the patient. In a small number of subjects catheterised postoperatively, increased pulmonary arteriolar resistance lessened rapidly.

Aged

[Analysis of 59 cases of non-traumatic sudden death in various neurological diseases].

Sudden death is a common complication of myocardial infarction, necrotic pancreatitis and other diseases. Physicians usually neglect the possibility of neurological disorders. 59 cases of sudden death among 314 autopsied cases with neurological diseases were analyzed. The most frequent cause of neurological sudden death was cerebrovascular disease (CVD). It was present in 53 (89.9%) cases. 48 of them had hemorrhagic CVD. 37 of these 48 cases were due to hypothalamic lesions. In 37 cases general autopsy was performed; pathological abnormalities of heart, lungs, stomach etc, were found in 28 of them. In conclusion, the size and location of the lesion correlated with the prognosis of the disease. Concomitant multiple organ damage may deteriorate the lesion. Awareness of sudden death resulting from CVD may elevate the rate of correct diagnosis.

Cerebral Hemorrhage

Sudden death in adolescence.

The majority of adolescent deaths are sudden and unexpected; of these, the great majority result from violence. These violent deaths largely accounted for the 25% increase in total adolescent mortality during the 1960s. Yet, sudden death in adolescence is not a distinct entity and receives little study from either pediatricians or pathologists. Some cases of sudden death in adolescence are puzzling and difficult to classify. The pathologist must in each case obtain a detailed history, usually perform a complete autopsy, and obtain consultation when necessary. Only then will each case be adequately studied, and related medical questions and other problems be properly resolved.

Accidents, Traffic

Magnesium deficiency and sudden death.

A link between Mg deficiency and sudden death is suggested by a substantial number of studies published over the past three decades. Data come from epidemiologic, autopsy, clinical, and animal studies. They suggest that: (1) Sudden death is common in areas where community water supplies are Mg-deficient. (2) Myocardial Mg content is low in people who die of sudden death. (3) Cardiac arrhythmias and coronary artery vasospasm can be caused by Mg deficiency and (4) Intravenous Mg reduces the risk of arrhythmia and death immediately after acute myocardial infarction. Because of these data, Mg supplementation has been proposed as a possible method of reducing the risk of sudden death. Suggested ways of supplementing Mg include public education to change dietary habits, addition of Mg to community water supplies, fortification of foods, and oral supplementation. Despite the substantial number of studies linking Mg deficiency with sudden death, no prospective studies have yet investigated whether large-scale Mg supplementation is useful for the primary prevention of sudden death.

Animals

Sudden death.

The threat of sudden death due to a myocardial infarct inevitably places a severe strain on the patient, who may realize the severity of his condition, on the family who are justifiably concerned about the life threatening situation the patient is in, and on the coronary care nurse who is involved in his care. Each one reacts to this stress in his own way. If the nurse can begin to understand her own reactions and the reactions of the family and patient, she will be better equipped to help them cope with this crisis situation.

Adaptation, Psychological

Sudden deaths among Finnish conscripts.

The epidemiology of sudden deaths was studied among conscripts in Finland in 1948-72 (660 000 man-years) and among Finnish men aged 15-24 years in 1969-70 (900 000 man-years). The incidence of sudden deaths among the conscripts was 6-8/100 000 man-years. The onset of acute symptoms occurred during strenuous exercise in a third of the conscripts but in only a few of the other young men. Cardiovascular diseases caused two-thirds of the deaths in both groups. Sudden death tended to be more common among conscripts than among other young men during the corresponding period, but overall non-violent deaths were less common among conscripts than among other young men. On the basis of health records an attempt was made to separate the sudden deaths among conscripts from those among the controls by multiple discriminant analysis. For all practical purposes, however, the separation power proved poor.

Adolescent

Sudden death and sport.

Of 21 sudden deaths in sportsmen, 18 were thought to be caused by heart attacks either during or after sport. There was firm evidence of ischaemic heart-disease in 9, strongly suggestive evidence in 7, but in 2 there was only suggestive clinical evidence. As a group, these subjects were characterised by (1) a mean age above thirty (above twenty-five for rugby players); (2) a family history of early heart-attacks; and (3) antecedent symptoms of chest pain or pressure in 9, fatigue or blackout in 4, and minor complaints in 2. Most were known to their medical practitioners. Psychological factors were thought to be important in 8. Doctors, players and referees should be aware that severe sporting exertion as in rugby football involves a risk which for most players is relatively minor, but in the minority predisposed to heart-attacks by family history, smoking, or age (as in referees) the risk is more serious. To reduce hazard of sudden death in exercise, players and referees should be warned against smoking and informed of the serious implications of the development of chest pain, pressure, or undue tiredness before, during, or after sport.

Cholesterol