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At least 199 records · Page 11Linked to original sources
PubMed2003

Risk factors for unexplained antepartum fetal death in Norway 1967-1998.

OBJECTIVE: To relate unexplained antepartum fetal death with maternal and fetal characteristics in order to identify risk factors. DESIGN: Population-based study based on records of 1,676,160 singleton births with gestational age > or =28 weeks. Unexplained antepartum fetal death was defined as fetal death before labour without known fetal, placental, or maternal pathology. RESULTS: Although unexplained fetal mortality in general declined from 2.4 per 1000 births in 1967-1976 to 1.6 in 1977-1998, the proportion among all fetal deaths increased from 30% to 43% during the same period of observation. Unexplained fetal death occurred later in gestation than explained. From 39 weeks of gestation, the risk increased progressively to 50/10,000 in women aged > or =35 years and <10/10,000 in women <25 years. In birth order > or =5, the risk was particularly high after 39 weeks of gestation. For birth weight percentile 2.5-9.9 and > or =97.5, unexplained fetal death was four and three times more likely to occur, respectively. We found an additive effect of maternal age and birth weight percentile 2.5-9.9. Women with less than 10 years education had higher risk than women with 13 years or more (OR=1.6). Weaker associations were observed with female gender, unmarried mothers, and winter season. CONCLUSIONS: Unexplained antepartum fetal death occurred later in gestation than explained and was associated with high maternal age, multiparity, low education, and moderately low and high birth weight percentile. The increased risk in post-term pregnancies and the additive effect of maternal age and birth weight percentile 2.5-9.9 suggests that older women would benefit from monitoring of fetal growth.

Birth Weight↗
PubMed2001

Validation of death certificate diagnosis for coronary heart disease: the Atherosclerosis Risk in Communities (ARIC) Study.

The validity of the death certificate in identifying coronary heart disease deaths was evaluated using data from the community surveillance component of the Atherosclerosis Risk in Communities Study (ARIC). Deaths in the four ARIC communities of Forsyth Co., NC; Jackson, MS; Minneapolis, MN; and Washington Co., MD were selected based on underlying cause of death codes as determined by the rules of the ninth revision of the International Classification of Diseases (ICD-9). Information about the deaths was gathered through informant interviews, physician or coroner questionnaires, and medical record abstraction, and was used to validate the cause of death. Sensitivity, specificity, and positive predictive value of the death certificate classification of CHD death (ICD-9 codes 410-414 and 429.2) were estimated by comparison with the validated cause of death based on physician review of all available information. Results from 9 years of surveillance included a positive predictive value 0.67 (95% CI 0.66-0.68), sensitivity of 0.81 (95% CI 0.79-0.83), and a false-positive rate (1-specificity) of 0.28 (95% CI 0.26-0.30). Comparing CHD deaths as defined by the death certificate with validated CHD deaths indicated that the death certificate overestimated CHD mortality by approximately 20% in the ARIC communities. Within subgroups, death certificate overestimation was reduced with advancing age (up to age 74), was consistent over time, was not dependent on gender, and exhibited considerable variation among communities.

Abstracting and Indexing↗
PubMed2002

Aneurysm-related death: primary endpoint analysis for comparison of open and endovascular repair.

PURPOSE: The purpose of this study was to utilize an objective endpoint analysis of aneurysm treatment, which is based on the primary objective of aneurysm repair, and to apply it to a consecutive series of patients undergoing open and endovascular repair. METHOD: Aneurysm-related death was defined as any death that occurred within 30 days of primary aneurysm treatment (open or endovascular), within 30 days of a secondary aneurysm or graft-related treatment, or any death related to the aneurysm or graft at any time following treatment. We reviewed 417 consecutive patients undergoing elective infrarenal aortic aneurysm repair: 243 patients with open repair and 174 patients with endovascular repair. RESULTS: There was no difference between the groups (open vs endovascular) with regard to mean age +/- standard deviation (73 +/- 8 years vs 74 +/- 8 years) or aneurysm size (64 +/- 2 mm vs 58 +/- 10 mm) (P = not significant [NS]). The 30-day mortality for the primary procedure after open repair was 3.7% (9/243) and after endovascular repair was 0.6% (1/174, P <.05). The 30-day mortality for secondary procedures after open repair was 14% (6/41) compared to 0% after endovascular repair (P <.05). The aneurysm-related death rate was 4.1% (10/243) after open surgery and 0.6% (1/174) after endovascular repair (P <.05). Mean follow-up was 5 months longer following open repair (P <.05). Secondary procedures were performed in 41 patients following open surgery and 27 patients following endovascular repair (P = NS). Secondary procedures following open repair were performed for anastomotic aneurysms (n = 18), graft infection (n = 6), aortoenteric fistula (n = 5), anastomotic hemorrhage (n = 4), lower extremity amputation (n = 4), graft thrombosis (n = 3), and distal revascularization (n = 1). Secondary procedures following endovascular repair consisted of proximal extender cuffs (n = 11), distal extender cuffs (n = 11), limb thrombosis (n = 3), and surgical conversion (n = 2). The magnitude of secondary procedures following open repair was greater with longer operative time 292 +/- 89 minutes vs 129 +/- 33 minutes (P <.0001), longer length of stay 13 +/- 10 days vs 2 +/- 2 days (P <.0001) and greater blood loss 3382 +/- 4278 mL vs 851 +/- 114 mL (P <.0001). CONCLUSIONS: The aneurysm-related death rate combines early and late deaths and should be used as the primary outcome measure to objectively compare the results of open and endovascular repair in the treatment of infrarenal abdominal aortic aneurysms. In our experience, endovascular aneurysm repair reduced the overall aneurysm-related death rate when compared to open repair. Secondary procedures are required after both open and endovascular repair. However, the magnitude, morbidity, and mortality of secondary procedures are reduced significantly with endovascular repair.

Aged↗
PubMed2003

Defining senescence and death.

This article evaluates features of leaf and flower senescence that are shared with, or are different from, those of other terminal events in plant development. Alterations of plastid structure and function in senescence are often reversible and it is argued that such changes represent a process of transdifferentiation or metaplasia rather than deterioration. It may be that the irreversible senescence of many flowers and some leaves represents the loss of ancestral plasticity during evolution. Reversibility serves to distinguish senescence fundamentally from programmed cell death (PCD), as does the fact that viability is essential for the initiation and progress of cell senescence. Senescence (particularly its timing and location) requires new gene transcription, but the syndrome is also subject to significant post- transcriptional and post-translational regulation. The reversibility of senescence must relate to the plastic, facultative nature of underlying molecular controls. Senescence appears to be cell-autonomous, though definitive evidence is required to substantiate this. The vacuole plays at least three key roles in the development of senescing cells: it defends the cell against biotic and abiotic damage, thus preserving viability, it accumulates metabolites with other functions, such as animal attractants, and it terminates senescence by becoming autolytic and facilitating true cell death. The mechanisms of PCD in plants bear a certain relation to those of apoptosis, and some processes, such as nucleic acid degradation, are superficially similar to aspects of the senescence syndrome. It is concluded that, in terms of physiological components and their controls, senescence and PCD are at best only distantly related.

Apoptosis↗
PubMed2004

Use of the newborn screening card to define cause of death in a 12-year-old diagnosed with epilepsy.

Post-mortem investigation of sudden death in young people frequently reveals no overt cause for the death. Full investigation is hampered if tissue or blood is not retained for DNA analysis. We report a post mortem molecular diagnosis of long QT syndrome in a 12-year-old boy diagnosed with epilepsy who died suddenly playing sport. The DNA was extracted from an archived blood spot on his newborn screening ('Guthrie') card, which had been taken from him at 6 days of age. A missense mutation was detected in exon 5 of the KCNQ1 gene; R243C (835C > T), associated with long QT type 1. The same mutation was found in the mother (who now takes effective preventative therapy), but not in the sib who has now been reassured that she is not at risk of sudden death.

Arginine↗
PubMedDate not supplied

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↗
PubMed2002

Long-term efficacy of empirical chronic amiodarone therapy in patients with sustained ventricular tachyarrhythmia and structural heart disease.

The efficacy of empirical chronic oral amiodarone therapy in 129 patients with sustained ventricular tachyarrhythmia (VTNVF) and structural heart disease is evaluated. Twenty-nine patients were treated with class I drugs and monitored by electrophysiological study (EPS) and Holter electrocardiogram (ECG) (class I). The remaining 100 non-responders to the class I drugs were treated with oral amiodarone, of whom 70 were tolerant (AMD+) and 30 were intolerant (AMD-). Patients were followed up to 36 months. The primary and secondary end-points were recurrence of VT/VF and hypothetical death, respectively; whereby, hypothetical death was defined as actual death and the event of rapid VT.VF (heart rate >240beats/min) in patients with an implantable cardioverter defibrillator. Class I and AMD+ patients showed a better prognosis than AMD- patients. The VT/VF event free at 36 months in class I (64.8%) and AMD+ (56.1%) patients were significantly higher than that in AMD- (27.2%) (p<0.01) patients. Hypothetical survival rates in class I (92.0%) and AMD+ (83.6%) patients were significantly higher than that in AMD- (57.0%) (p<0.001) patients, but there were no significant differences in the actual survival rate among the 3 patient groups. The independent clinical factors suppressing the recurrence of VT/VF (Cox hazard) were treatment with amiodarone (p=0.02, 95% confidence interval (CI) =0.19-0.86) and EPS/Holter ECG-guided Class I drugs (p=0.04, 95% CI=0.14-0.94). The results demonstrate that empirical amiodarone has a substantial long-term benefit that is comparable to EPS/Holter ECG-guided class I drugs in the treatment of high-risk patients with VT/VF and structural heart disease.

Amiodarone↗
PubMed1994

[A case-control study on the risk factors of sudden death. An analysis of 44 cases in a company by health care records].

A case-control study was conducted on sudden deaths in a company having about 40,000 workers to determine the risk factors of sudden death. Sudden death was defined as internal death within 24 hours from the onset of the event. Two controls whose sex and age were matched with a case were selected from the employees of the company. The risk factors studied were age, sex, obesity, blood pressure, serum glucose, total cholesterol, triglyceride, uric acid, urinary, protein, urinary sugar, electrocardiographic (ECG) findings, diabetes mellitus, smoking history and drinking history. These data were collected from the latest health care record including health examinations performed annually in the company. t test, U test and Fisher's test were applied to each of the variables. Multiple logistic regression analysis and canonical discriminant analysis were applied, using mean systolic blood pressure for 5 years, body mass index (BMI), abnormal Q wave on ECG, and serum glucose as explanatory variables. From 1984 to 1990 44 sudden death cases composed of 42 males and two females were identified. The age-specific mortality rate increased exponentially with age with a peak at the sixth decade. The most frequent cause of sudden death was heart disease (77%) followed by cerebrovascular disease (18%). Statistical analysis showed that significant risk factors were high blood pressure, low BMI, diabetes mellitus, and ST-T change on ECG.

Adult↗
PubMed1995

[A clinical and pathological study of 46 cases of sudden and unexpected death].

A series of 46 autopsied adult cases of sudden and unexpected natural death were investigated. In this study, sudden and unexpected death was defined as any death occurring with 24 hours of onset of symptoms in a person with or without probable cause of death suggested by medical history. The cases included 31 males and 15 females aged 26 to 85 years (mean 66.6 years). Age distribution peaked in seventies. The lesions causing sudden and unexpected death according to the most frequent organ systems were, diseases of the heart (acute myocardial infarction with or without old infarct, 20; old myocardial infarction without acute infarction, 2; dilated cardiomyopathy, 2; sarcoidosis, 1; amyloidosis, 2; and valvular disease, 2), the aorta (ruptured aneurysm, 6; dissecting aneurysm, 2), the respiratory tract (pulmonary embolism, 7; pulmonary hypertension, 1), the alimentary tract (intestinal obstruction, 1), and other diseases (cause unknown, 1). The cardiovascular lesions were found in 78.2% of cases autopsied. The sudden and unexpected death caused by acute myocardial infarction was found in 47.8%, and acute myocardial infarction seemed to play a major role in cardiac sudden death in these series. The respiratory lesions were found in 17.4%. Four of seven cases with pulmonary embolism died in two weeks after surgical operation. The most common underlying disease was post-operative condition.

Adult↗
PubMed2001

Balance between autocrine interleukin-1beta and caspases defines life versus death of polymorphonuclear cells.

The role of endogenous IL-1beta in regulating spontaneous and Fas-triggered apoptosis of human PMN has been studied in relation to the activity of the IL-1beta-generating enzyme ICE (caspase-1), an enzyme also involved in the mechanism of cell death. Upon in vitro culture, PMN undergo spontaneous apoptosis and express increasing levels of IL-1beta, caspase-1- and caspase-3-like enzymes. Endogenous IL-1beta protects PMN from apoptosis, since inhibition of either IL-1beta or caspase-1 activity can accelerate PMN apoptotic death. Thus, in spontaneous PMN apoptosis caspase-1 essentially plays an anti-apoptotic role by inducing maturation of protective IL-1beta, whereas other molecules are responsible of driving apoptosis. Upon Fas triggering, PMN apoptosis is greatly accelerated, in correlation with increased caspase activity, whereas IL-1beta production is not augmented. Inhibition of IL-1beta activity can increase Fas-induced apoptosis, whereas caspase-1 inhibitors are without significant effect. It is hypothesized that in Fas-induced PMN apoptosis caspase-1 has a double role: it can protect from apoptosis through generation of protective IL-1beta, as in spontaneous apoptosis, and it can also exert pro-apoptotic activity which counterbalances the protective effect and allows accelerated apoptosis.

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↗
PubMed1990

[Sudden deaths among male employees: a six-year epidemiological survey].

To elucidate the circumstances involving sudden death, deaths among 20,685 male employees of "K" company during a six-year period from April 1981 to March 1987 were reviewed. The subject age ranged from 19 through 59 years, and averaged 38.6 years. Information concerning each death was obtained from the death reports prepared by officials of the Safety and Health Division of the Labor Affairs Department of this company, based on the death certificate and interviews with questionnaires to the deceased's family, colleagues, and attending physicians. In this study, "sudden death" was defined as the death of a full-time employee who had been capable of performing ordinary work and who died within 24 hours after the onset of a sudden disease. When the cause of death could not be determined, the cause was categorized as unknown. A total of 233 employees died during the six-year period. The causes were malignant tumors in 107 (45.9%), heart diseases (including all of the sudden deaths from "unknown cause") in 41 (17.6%), cerebral vascular accidents in 20 (8.6%) and other causes in 64. "Sudden death" occurred in 39 employees. This accounted for 12 to 33% (17% average) of the total deaths. The mortality of sudden death by age group (adjusted to the annual deaths per 100,000 persons) was six in the age of 30-34 years, 20 for 35-39 years, 22 for 40-44 years, 54 for 45-49 years, 51 for 50-54 years and 107 for 55-59 years, an average of 33. In seven sudden death cases, the last medical examinations before death indicated "no abnormalities".(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1988

[The host-defense index predicting the risk of operative mortality in esophageal cancer patients].

A "host defense index" (HDI) has been developed that predicts the risk of operative mortality based on the impairment of host defense in patients with esophageal cancer. The function of host defense was assessed on admission in 32 patients. Assessment included 21 parameters of nutritional status, cellular immunity, humoral immunity, neutrophil levels, complement levels and serum factors. Operative deaths, which were defined as deaths due to operative complications occurring within 120 days after esophagectomy or by-pass operation, were in 10 out of 32 patients. A discriminant analysis was then performed using 21 parameters in 32 patients, and an equation to calculate HDI was generated. The equation consisted of 10 parameters. The values of HDI more than -0.90 predicted no operative deaths while those less than -0.90 did predict operative deaths. The percentage of patients correctly classified was 87.5%. For clinical application, the predictive risk of operative mortality based on HDI was classified as high (HDI less than or equal to -1.80), intermediate (-1.80 less than HDI less than 0) or low (HDI greater than or equal to 0). The values of HDI in 32 patients were compared with those of the prognostic nutritional index or nutritional assessment index but no significant correlation between HDI and those indices was recognized.

Antibody Formation↗