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PubMed2002

Sudden death in patients with right isomerism (asplenism) after palliation.

OBJECTIVE: To define the risk of sudden death in patients with right isomerism (asplenia) after palliation. STUDY DESIGN: A total of 154 patients with right isomerism was identified from 1980 to 1999. Sudden death was defined as acute cardiovascular collapse from which death occurred within 24 hours. RESULTS: A total of 620 patient-years were evaluated. The 1-year and 5-year survival was 72% and 50%, respectively. There were 22 sudden unexpected deaths (14%, 35 events/1000 patient-years). Sudden death tended to occur in infancy or early childhood (12 +/- 9 months; median, 9 months). The mechanisms were classified as sudden tachyarrhythmic in 2 (9%), sudden cardiac but nontachyarrrhythmic (sudden onset severe cyanosis) in 15 (68%), and sudden noncardiac in 5 (23%)(fulminant sepsis with positive blood culture: streptococcus pneumonia (3), Escherichia coli (1), and yeast-like organism (1)). The incidence of sudden death steadily decreased with age until the age of 3 years. CONCLUSION: The incidence of sudden death in patients with right isomerism after initial palliation remained high. Sudden death was related to complex cardiac anomalies, a susceptibility to fulminant infection, and arrhythmia.

Adolescent↗
PubMed2006

Management of unsuccessful thrombolysis in acute massive pulmonary embolism.

BACKGROUND: The management of patients with acute massive pulmonary embolism (PE) who do not respond to fibrinolytic therapy remains unclear. We aimed to compare rescue surgical embolectomy and repeat thrombolysis in patients who did not respond to thrombolysis. METHODS: We conducted a prospective single-center registry of PE patients who underwent thrombolytic therapy. Lack of response to thrombolysis within the first 36 h was prospectively defined as both persistent clinical instability and residual echocardiographic right ventricular dysfunction. Patients underwent surgical embolectomy or repeat thrombolysis, at the discretion of the attending physician. The clinical end point was a combined end point including recurrent PE, bleeding complications, or PE-related death, which was defined as death from recurrent PE or cardiogenic shock. Long-term adverse outcomes included death, recurrent thromboembolic events, and congestive heart failure. RESULTS: From January 1995 to January 2005, 488 PE patients underwent thrombolysis, of whom 40 (8.2%) did not respond to thrombolysis. Fourteen patients were treated by rescue surgical embolectomy, and 26 were treated by repeat thrombolysis. There was no significant difference in baseline characteristics between the two groups. The in-hospital course was uneventful in 11 of the surgically treated patients (79%) and in 8 patients (31%) treated by repeat thrombolysis (p = 0.004). There was a trend for higher mortality in the medical group than in the surgical group (10 vs 1 deaths, respectively; p = 0.07). There were significantly more recurrent PEs (fatal and nonfatal) in the repeat-thrombolysis group (35% vs 0%, respectively; p = 0.015). While no significant difference was observed in number of major bleeding events, all bleeding events in the repeat-thrombolysis group were fatal. The rate of uneventful long-term evolution was the same in the two groups. CONCLUSION: Rescue surgical embolectomy led to a better in-hospital course when compared with repeat thrombolysis in patients with massive PE who have not responded to thrombolysis. The transfer of patients who have not responded to thrombolysis to tertiary cardiac surgery centers could be considered as an alternative option.

Acute Disease↗
PubMed2003

Autonomic responses to sighs in healthy infants and in victims of sudden infant death.

OBJECTIVE: Sigh, defined as an isolated breath with an increased tidal volume, can be associated with abrupt changes in heart rate (HR) or blood oxygenation. Sigh may be followed by a central apnea. As impairment of autonomic control was postulated in future SIDS victims, we hypothesized that their autonomic responses to sighs were different from those of healthy control infants. METHODS: Sighs followed by central apnea were studied in the sleep recordings of 18 infants who eventually died of SIDS and of 18 control infants. The infants of the two groups were matched for sex, gestational age, postnatal age, weight at birth and sleep position during sleep recording. HR autoregressive power spectral analysis was performed on RR intervals preceding and following sighs. RESULTS: In all infants, most sighs followed by an apnea were found in NREM sleep. Compared to the control infants, the future SIDS victims were characterized by a greater sympathovagal balance and a lower parasympathetic tonus before the sighs. Following the sighs, no more differences were found in NREM sleep. CONCLUSION: Based on the present findings, it can be postulated that sighs contribute to reset autonomic tonus during NREM sleep.

Electroencephalography↗
PubMed2006

Condensin I recruitment and uneven chromatin condensation precede mitotic cell death in response to DNA damage.

Mitotic cell death (MCD) is a prominent but poorly defined form of death that stems from aberrant mitosis. One of the early steps in MCD is premature mitosis and uneven chromatin condensation (UCC). The mechanism underlying this phenomenon is currently unknown. In this study, we show that DNA damage in cells with a compromised p53-mediated G2/M checkpoint triggers the unscheduled activation of cyclin-dependent kinase 1 (Cdk1), activation and chromatin loading of the condensin I complex, and UCC followed by the appearance of multimicronucleated cells, which is evidence of MCD. We demonstrate that these processes engage some of the players of normal mitotic chromatin packaging but not those that drive the apoptotic chromatin condensation. Our findings establish a link between the induction of DNA damage and mitotic abnormalities (UCC) through the unscheduled activation of Cdk1 and recruitment of condensin I. These results demonstrate a clear distinction between the mechanisms that drive MCD-associated and apoptosis-related chromatin condensation and provide mechanistic insights and new readouts for a major cell death process in treated tumors.

Adenosine Triphosphatases↗
PubMed1996

Infant mortality rate inequalities in the Western Cape Province of South Africa.

BACKGROUND: Cape Town is undergoing rapid urbanization. South African vital statistics have routinely been stratified by racial categories but intra-urban and peri-urban geographical variations have been neglected. METHODS: To examine variations in infant mortality rates (IMR) and proportional infant mortality between urban, rural and informally settled areas, stratified by racial category, birth notifications and infant death certifications recorded by a large health authority were analysed. RESULTS: The IMR per 1000 livebirths was as high for coloureds on rural farms (34, 95% confidence interval 29-40) as for blacks in informal settlements (35, 95% CI: 32-37) and an exceptionally high IMR (60, 95% CI: 43-82) was found for coloureds in informal settlements. Inequalities between racial categories (11 (95% CI: 9-14) for whites, 19 (95% CI: 18-21) for coloureds and 33 (95% CI: 31-35) for blacks) were as expected from other South African studies. Of rural farm deaths, 22% were ascribed to ill-defined causes. Low birthweight was the most common defined cause of death in all areas except rural farm areas (14% ascribed to pneumonia), and gastro-enteritis was important in informally settled areas (18%). CONCLUSIONS: Routine mortality data are more informative if stratified by robust and readily available indicators of socio-economic status such as residential area and racial category. Place of residence may distinguish risk strata as well as racial category, but the latter is helpful within socioeconomically heterogeneous residential areas.

Black or African American↗
PubMed2001

Fetal death. A 10-year retrospective study.

Fetal death has been defined by the World Health Organization as death before complete expulsion or extraction from its mother of a product of conception, irrespective of the duration of pregnancy. Certain causes of fetal death, including syphilis, Rh isoimmunization, toxemia, and diabetes, have shown significant declines over the past several decades. However, many fetal losses continue to occur from intrauterine infections, lethal malformations, fetal growth retardation, and abruptio placentae. Fetal death with no identifiable specific cause is another consideration when dealing with these cases. Other risk factors can include maternal, sociodemographic, and medical care factors. The authors reviewed all forensic cases referred for autopsy to the Forensic Section of the Medical University of South Carolina, Medical Examiners' Office over the 10-year period 1990-1999. All cases listed as fetal death or stillbirth were included. The 42 cases were analyzed as to fetus' gestational age, sex, race, weight, location of delivery, history of prenatal care, maternal drug use, chromosomal abnormalities, cause and manner of death, and autopsy findings. The black:white ratio was approximately 2:1, and the male:female ratio was virtually 1:1. Most fetuses were older than 20 weeks' gestational age, with one third between 20 and 29 weeks. The majority were externally normal aside from maceration. Only 7.5% had congenital anomalies. Twenty-one of 38 placentas were grossly and microscopically normal. Of cases with toxicologic analysis, 21% were positive for drugs, and 17% were positive for cocaine/benzoylecgonine. The manner of death was classified as natural (28), accident (2), and undetermined (12). Few studies have reported the specific causes of fetal death, and the lack of uniformity in data collection and classification of causes of fetal death has made comparisons difficult. The authors present this retrospective study to better determine the factors leading to fetal demise in the hope of assisting death investigators in this challenging arena.

Adolescent↗
PubMed1996

Apoptosis: molecular regulation of cell death.

The field of apoptosis is unusual in several respects. Firstly, its general importance has been widely recognised only in the past few years and its surprising significance is still being evaluated in a number of areas of biology. Secondly, although apoptosis is now accepted as a critical element in the repertoire of potential cellular responses, the picture of the intra-cellular processes involved is probably still incomplete, not just in its details, but also in the basic outline of the process as a whole. It is therefore a very interesting and active area at present and is likely to progress rapidly in the next two or three years. This review emphasises recent work on the molecular mechanisms of apoptosis and, in particular, on the intracellular interactions which control this process. This latter area is of crucial importance since dysfunction of the normal control machinery is likely to have serious pathological consequences, probably including oncogenesis, autoimmunity and degenerative disease. The genetic analysis of programmed cell death during the development of the nematode Caenorhabditis elegans has proved very useful in identifying important events in the cell death programme. Recently defined genetic connections between C. elegans cell death and mammalian apoptosis have emphasised the value of this system as a model for cell death in mammalian cells, which, inevitably, is more complex. The signals inducing apoptosis are very varied and the same signals can induce differentiation and proliferation in other situations. However, some pathways appear to be of particular significance in the control of cell death; recent analysis of the apoptosis induced through the cell-surface Fas receptor has been especially important for immunology. Two gene families are dealt with in particular detail because of their likely importance in apoptosis control. These are, first, the genes encoding the interleukin-1 beta-converting enzyme family of cysteine proteases and, second, those related to the proto-oncogene bcl-2. Both of these families are homologous to cell death genes in C. elegans. In mammalian cells the number of members of both families which have been identified is growing rapidly and considerable effort is being directed towards establishing the roles played by each member and the ways in which they interact to regulate apoptosis. Other genes with established roles in the regulation of proliferation and differentiation are also important in controlling apoptosis. Several of these are known proto-oncogenes, e.g. c-myc, or tumour suppressors, e.g. p53, an observation which is consistent with the importance of defective apoptosis in the development of cancer. Viral manipulation of the apoptosis of host cells frequently involves interactions with these cellular proteins. Finally, the biochemistry of the closely controlled cellular self-destruction which ensues when the apoptosis programme has been engaged is also very important. The biochemical changes involved in inducing phagocytosis of the apoptotic cell, for example, allow the process to be neatly integrated within the tissues, under physiological conditions. Molecular defects in this area too may have important pathological consequences.

Amino Acid Sequence↗
PubMed2004

Out-of-hospital care of critical drug overdoses involving cardiac arrest.

OBJECTIVES: Death from acute drug poisoning, also termed drug overdose, is a substantial public health problem. Little is known regarding the role of emergency medical services (EMS) in critical drug poisonings. This study investigates the involvement and potential mortality benefit of EMS for critical drug poisonings, characterized by cardiovascular collapse requiring cardiopulmonary resuscitation (CPR). METHODS: The study population was composed of death events caused by acute drug poisoning, defined as poisoning deaths and deaths averted (persons successfully resuscitated from out-of-hospital cardiac arrest by EMS) in King County, Washington, during the year 2000. RESULTS: Eleven persons were successfully resuscitated and 234 persons died from cardiac arrest caused by acute drug poisoning, for a total of 245 cardiac events. The EMS responded to 79.6% (195/245), attempted resuscitation in 34.7% (85/245), and successfully resuscitated 4.5% (11/245) of all events. Among the 85 persons for whom EMS attempted resuscitation, opioids, cocaine, and alcohol were the predominant drugs involved, although over half involved multiple drug classes. Among the 11 persons successfully resuscitated, return of circulation was achieved in six following EMS cardiopulmonary resuscitation alone, in one following CPR and defibrillation, and in the remaining four after additional advanced life support. CONCLUSIONS: In this community, EMS was involved in the majority of acute drug poisonings characterized by cardiovascular collapse and may potentially lower total mortality by approximately 4.5%. The results show that, in some survivors, return of spontaneous circulation may be achieved with CPR alone, suggesting a different pathophysiology in drug poisoning compared with cardiac arrest due to heart disease.

Adult↗
PubMed1992

Molecular genetics of cell death in the nematode Caenorhabditis elegans.

In C. elegans, cell death can be readily studied at the cellular, genetic, and molecular levels. Two types of death have been characterized in this nematode: (1) programmed cell death, which occurs as a normal component in development; and (2) pathological cell death, which occurs aberrantly as a consequence of mutation. Analysis of mutations that disrupt programmed cell death in various ways has defined a genetic pathway for programmed cell death which includes genes that perform such functions as the determination of which cells die, the execution of cell death, the engulfment of cell corpses, and the digestion of DNA from dead cells. Molecular analysis is providing insight into the nature of the molecules that function in these aspects of programmed cell death. Characterization of some genes that mutate to induce abnormal cell death has defined a novel gene family called degenerins that encode putative membrane proteins. Dominant alleles of at least two degenerin genes, mec-4 and deg-1, can cause cellular swelling and late onset neurodegeneration of specific groups of cells.

Animals↗
PubMed1984

Leading causes of death among children under 5 years of age in the various population groups of the RSA in 1970.

The mortality rates (MRs) of children under 5 years of age in the various population groups of the RSA were calculated as deaths/10(5) for various causes of death and groupings of causes of death as classified by the International Classification of Diseases. In 1970 the ten leading causes of death among Coloured and Black children under 5 years of age in the RSA were similar to those among children in developing countries. The rank order of causes of death (in MRs/10(5] among Coloured children was as follows: gastro-enteritis (1 733), pneumonia (725), immaturity (405), ill-defined causes of death (168), nutritional deficiencies (167), measles (126), anoxia (97), 'other bacterial diseases' (91), inflammatory diseases of the nervous system (55) and tuberculosis (48). The ten leading causes of death among White children in the RSA were characteristic of children in Western developed countries. The rank order (in MRs/10(5] was as follows: immaturity (144), anoxia (94), pneumonia (46), gastro-enteritis (41), congenital heart disease (32), other accidents (19), birth injury (19), ill-defined causes of death (12) and inflammatory diseases of the nervous system (11).

Canada↗
PubMed1990

Carbon monoxide and lethal arrhythmias.

The effect of acute exposure to carbon monoxide on ventricular arrhythmias was studied in a previously described chronically maintained animal model of sudden cardiac death. In 60 percent of dogs with a healed anterior myocardial infarction, the combination of mild exercise and acute myocardial ischemia induces ventricular fibrillation. The events in this model are highly reproducible, thus allowing study by internal control analysis. Dogs that develop ventricular fibrillation during the test of exercise and acute myocardial ischemia are considered at high risk for sudden death and are defined as "susceptible"; dogs that survive the test without a fatal arrhythmia are considered at low risk for sudden death and are defined as "resistant." In the current study, the effects of carboxyhemoglobin levels ranging from 5 to 15 percent were tested in resistant and susceptible dogs. A trend toward higher heart rates was observed at all levels of carboxyhemoglobin, although significant differences were observed only with 15 percent carboxyhemoglobin. This trend was observed at rest and during exercise in both resistant and susceptible dogs. In resistant animals, in which acute myocardial ischemia is typically associated with bradycardia even under the control condition, this reflex response occurred earlier and was augmented after exposure to carbon monoxide. This effect may depend on the increased hypoxic challenge caused by carbon monoxide, and thus on an augmentation of the neural reflex activation or a sensitization of the sinus node to acetylcholine induced by hypoxia. In both resistant and susceptible dogs, carbon monoxide exposure induced a worsening of ventricular arrhythmias in a minority of cases. This worsening was not reproducible in subsequent trials. These data indicate that acute exposure to carbon monoxide is seldom arrhythmogenic in dogs that have survived myocardial infarction. Nevertheless, the observation that carbon monoxide exposure increases heart rate at rest and during moderate exercise may have clinical implications relevant to patients with coronary artery disease.(ABSTRACT TRUNCATED AT 400 WORDS)

Analysis of Variance↗
PubMed1989

Classification of perinatal and late neonatal deaths in Iceland. A survey from a defined population.

A retrospective case record analysis of all perinatal and late neonatal deaths in Iceland in the periods 1976-80 and 1981-85 was done and the causes of death classified according to the extended Aberdeen classification. There was a significant (p less than 0.0001) reduction in number of deaths between the two periods with perinatal mortality rates declining from 10.6/1000 in 1976-80 to 6.8/1000 in 1981-85. In 1976-80 there were 81 (33%) antepartum, 37 (15%) intrapartum and 128 (52%) neonatal deaths compared to 61 (38%) antepartum, 13 (8%) intrapartum and 86 (54%) neonatal deaths in 1981-85. Fetal abnormality was the most common cause of death in both periods followed by the category Low birthweight in 1976-80. In 1981-85 increased morphological detection of infection in infants of very low birthweight by placental examination and autopsies lead to a shift from the category Low birthweight to Maternal Disease, the second most common cause in that period. To achieve lower perinatal mortality rates efforts should be directed towards lowering antepartum losses near term and increasing survival of very low birthweight infants.

Congenital Abnormalities↗
PubMed1998

Randomised placebo-controlled trial of ritonavir in advanced HIV-1 disease. The Advanced HIV Disease Ritonavir Study Group.

BACKGROUND: Ritonavir is a potent, orally bioavailable inhibitor of HIV-1 protease. We undertook an international, multicentre, randomised, double-blind, placebo-controlled trial of ritonavir in patients with HIV-1 infection and CD4-lymphocyte counts of 100 cells/microL or less, who had previously been treated with antiretroviral drugs. METHODS: 1090 patients were randomly assigned twice-daily liquid oral ritonavir 600 mg (n = 543) or placebo (n = 547) while continuing treatment with up to two licensed nucleoside agents. The primary study outcome was any first new, or specified recurrent, AIDS-defining event or death. Open-label ritonavir was provided after 16 weeks in the study to any patient who had an AIDS defining event. FINDINGS: The baseline median CD4-lymphocyte count was 18 (IQR 10-43)/microL in the ritonavir group and 22 (10-47)/microL in the placebo group. Study medication was discontinued in 114 (21.1%) ritonavir-group patients and 45 (8.3%) placebo-group patients mainly because of initial adverse symptoms. Outcomes of AIDS-defining illness or death occurred in 119 (21.9%) ritonavir-group patients and 205 (37.5%) placebo-group patients (hazard ratio 0.53 [95% CI 0.42-0.66]; log-rank p < 0.0001) during median follow-up of 28.9 weeks, with loss to follow-up of 15 (1.4%) patients. Ritonavir was then offered to all patients; at median follow-up of 51 weeks, 87 (16%) ritonavir-group patients had died of any cause versus 126 (23%) placebo-group patients (hazard ratio 0.69 [95% CI 0.52-0.91], log-rank p = 0.0072). INTERPRETATION: Although earlier intervention with combination therapy may provide much more effective treatment, ritonavir in patients with advanced disease and extensive previous antiretroviral use is safe and effective, lowers the risk of AIDS complications, and prolongs survival.

Acquired Immunodeficiency Syndrome↗
PubMed2002

As individual as death itself: a focus group study of terminal care in nursing homes.

One in four Americans who reach the age of 65 will die in a nursing home, yet little research exists to define the end of life care needs of this population. We used focus groups with experienced nursing home staff and physicians to: (1) define a good death in a nursing home and (2) describe factors that promote or prevent good care for the dying in this setting. We audiotaped 11 focus groups with 77 participants. Discussions were structured around 3 questions: "How does someone die in the nursing home?" "What makes the difference between a good death and a bad death?," and "What can aides, nurses, or physicians do to help ensure that when someone dies it is a good death?" Participants described lack of training, regulatory emphasis on rehabilitation, and a resource-poor setting as important barriers to high quality care of the dying in nursing homes. They affirmed the value of their experience and personal relationships with residents as the basis for good care. Three major themes emerged to define a good death in a nursing home: highly individualized care based on continuity relationships with caregivers, effective teamwork by staff, physicians and family, and comprehensive advance care planning that addresses prognosis, emotional preparation, and appropriate use of medical treatments. The significance of these themes may be tested in the design of interventions to improve care of the dying in long-term care.

Aged↗
PubMed2006

[Quality of Mortality statistics in Chile, 1997-2003].

BACKGROUND: Death certification is the basis for the study of mortality patterns and the identification of leading causes of death. These data are used for planning health policies and prevention programs. AIM: To evaluate the quality of mortality statistics in Chile from 1997 and 2003. MATERIAL AND METHODS: Mortality data from 1997 to 2003 available at the Chilean Ministry of Health was used. Quality of information was evaluated using the percentage of certifications done by physicians and ill-defined causes of death according to rural or urban residence, medical services, age and gender. RESULTS: Death certification done by physicians increased from 97.6% to 99.0% in the studied period. The greatest increase was observed in rural areas, from 89.9% to 94,8%. There was a steady reduction in the percentage of ill-defined causes of deaths, from 4.7% in 1997 to 2.8% in 2003. The percentage of ill-defined causes had a great variation among the different medical services. The variation went from 1.5% in Magallanes to 13.7% in Araucania Sur. There was an inverse linear correlation between death certification by physicians and ill-defined conditions. CONCLUSIONS: Quality of Chilean mortality statistics has improved over time. Nevertheless, there is still space for enhancement for the appropriate use of this information.

Cause of Death↗
PubMed1998

Depression and risk of coronary heart disease in elderly men and women: New Haven EPESE, 1982-1991. Established Populations for the Epidemiologic Studies of the Elderly.

BACKGROUND: Results of several recent studies suggest that depression is predictive of incident coronary disease. However, few studies have examined this relationship in the elderly, the age at which most coronary heart disease (CHD) becomes clinically manifest. METHODS AND RESULTS: Data are from the New Haven, Conn, cohort (N = 2812) of the Established Populations for the Epidemiologic Studies of the Elderly project. Baseline information on depressive symptoms and CHD risk factors was collected during an in-person interview in 1982. Nonfatal myocardial infarctions were identified through monitoring of admissions to local hospitals and were validated by medical chart review. Cause of death was obtained from death certificates for all deceased participants. Outcomes were defined as CHD deaths (n = 255) and total incident CHD events (n = 391) between January 1, 1982, and December 31, 1991. There was no association between depressive symptoms and CHD outcomes in men. Among women, depressive symptoms were associated with an age-adjusted relative risk of 1.03 (per unit increase on the symptom scale) for CHD mortality (P=.001) and total CHD incidence (P=.002). These associations were largely unaffected by adjustment for established CHD risk factors but were reduced to nonsignificant levels after additional adjustment for impaired physical function. Additional analysis showed a significant association for depressive symptoms among women who had no physical function impairments or who survived at least 3 years without an event. CONCLUSION: Depressive symptoms may not be independent risk factors for CHD outcomes in elderly populations in general but may increase risk among relatively healthy older women.

Activities of Daily Living↗
PubMed1998

Role of nitric oxide in mediation of macrophage cytotoxicity and apoptosis.

Macrophages can recognize and eliminate tumor cells. To this effect, these cells use a variety of cytotoxic effectors. Recent work has paid particular attention to nitric oxide (NO) and its metabolic by-products in mediating macrophage tumor cytotoxicity. Moreover, work from this and other laboratories have indicated that macrophage-dependent, NO mediated tumor cell death meets the morphologic and molecular criteria that define apoptotic cell death. This review will initially discuss the characteristics of macrophage tumor cytotoxicity and the potential mechanisms by which NO can induce apoptosis in tumor cells. In addition, observations of spontaneous and acquired resistance to NO will be analyzed. Lastly, the relevance of results obtained using animal cells to the biology of the human macrophage will be considered.

Animals↗