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Digitoxin-associated mortality in acute myocardial infarction.

The use of digitalis in patients who have sustained an acute myocardial infarction has been controversial. A number of reports have suggested that the use of the glucoside actually can increase mortality. In all previous reports, digoxin has been the glucoside in use. In 620 patients admitted to Hamar Hospital from January 1, 1982 to December 31, 1984 with an acute myocardial infarction, 159 were using digitoxin at entry. Their survival until January 1, 1985 was compared with the rest of the population, not using digitoxin. The patients on digitoxin had a significantly higher mortality than those who were not, with a relative risk ratio of 2.33. However, major differences in baseline risk factors existed, and a multivariate Cox regression analysis was employed to adjust for the inequalities in baseline covariates. Only variables available at the entry of the index infarction were used for adjustment. Serum sodium, serum creatinine, age and no smoking were identified in a backward selection procedure as independently influencing mortality. By adjusting for these variables the relative risk ratio was reduced to 1.41, but digitoxin still exerted a significant influence on mortality. It is concluded that the results obtained with the use of digitoxin during a myocardial infarction is similar to previous reports with digoxin. Most of the excess mortality in the digitoxin group can be accounted for by inequalities in baseline characteristics. However, the possibility that a small excess in mortality is due to the digitalis glucoside cannot be excluded.

Aged↗

Effect of nosocomial vancomycin-resistant enterococcal bacteremia on mortality, length of stay, and costs.

OBJECTIVE: To determine the impact of vancomycin-resistant enterococcal bacteremia on patient outcomes and costs by assessing mortality, excess length of stay, and charges attributable to it. DESIGN: A population-based, matched, historical cohort study. SETTING: A 1,025-bed, university-based teaching facility and referral hospital. PATIENTS: Two hundred seventy-seven vancomycin-resistant enterococcal bacteremia case-patients and 277 matched control-patients identified between 1993 and 2000. RESULTS: The crude mortality rate was 50.2% and 19.9% for case-patients and control-patients, respectively, yielding a mortality rate of 30.3% attributable to vancomycin-resistant enterococcal bacteremia. The excess length of hospital stay attributable to vancomycin-resistant enterococcal bacteremia was 17 days, of which 12 days were spent in intensive care units. On average, dollars 77,558 in extra charges was attributable to each vancomycin-resistant enterococcal bacteremia. To adjust for severity of illness, 159 pairs of case-patients and control-patients, who had the same severity of illness (All Patient Refined-Diagnosis Related Group complexity level), were further analyzed. When patients were stratified by severity of illness, the crude mortality rate was 50.3% among case-patients compared with 27.7% among control-patients, accounting for an attributable mortality rate of 22.6%. Attributable excess length of stay and charges were 17 days and dollars 81,208, respectively. CONCLUSION: Vancomycin-resistant enterococcal bacteremia contributes significantly to excess mortality and economic loss, once severity of illness is considered. Efforts to prevent these infections will likely be cost-effective.

Adolescent↗

Nativity, race, and mortality: favorable impact of birth outside the United States on mortality in New York City.

To determine the association of birthplace (US-born vs. foreign-born) with mortality among blacks and whites in New York City, we examined death records for 5 years from 1988 to 1992 and the 1990 census data. Mortality rates by race and birthplace were compared for all causes of death and for specific causes. Although overall death rates for blacks generally exceeded those for whites (1224.8 per 100,000 inhabitants vs. 721.4 for males and 593.7 vs. 393.1 for females), foreign-born blacks had death rates (664.6 for males and 350.2 for females) slightly lower than those for whites. The most striking variation among blacks was among those aged 25 to 64 years. US-born black males were three times as likely (1588.9 vs. 525.2) and US-born black females were more than 2.5 times as likely (673.5 vs. 263.4) to die as were foreign-born blacks. Among US-born blacks AIDS, homicide, and cancer for males and AIDS, heart disease, and cancer for females were the most important determinants of excess deaths, defined as the difference between observed deaths and expected deaths; these causes of death account for about half of the excess deaths for each sex. Among whites natives generally had higher death rates than migrants, but less prominently and consistently so than for blacks. Excess mortality of blacks is largely explained by higher death rates of US-born compared with foreign-born Americans.

Adolescent↗

Postservice mortality among Vietnam veterans. The Centers for Disease Control Vietnam Experience Study.

The postservice mortality (through December 1983) of a cohort of 9324 US Army veterans who served in Vietnam was compared with that of 8989 Vietnam-era Army veterans who served in Korea, Germany, or the United States. Over the entire follow-up period, total mortality in Vietnam veterans was 17% higher than for other veterans. The excess mortality occurred mainly in the first five years after discharge from active duty (rate ratio, 1.45; 95% confidence interval, 1.08 to 1.96) and involved motor vehicle accidents, suicide, homicide, and accidental poisonings. Thereafter, mortality among Vietnam veterans was similar to that of other Vietnam-era veterans, except for drug-related deaths, which continued to be elevated. An unexpected finding was a deficit in deaths from diseases of the circulatory system among Vietnam veterans. The excess in postservice mortality due to external causes among Vietnam veterans is similar to that found among men returning from combat areas after World War II and the Korean War.

Centers for Disease Control and Prevention, U.S.↗

Predictive value of arterial blood pressure in old age. A ten-year prospective study of men and women born in 1897 and examined at the age of 70 and 80 years.

In a 10-year longitudinal study of men and women aged exactly 70 at entry and otherwise only selected according to geography, the predictive value of arterial blood pressure was evaluated concerning cardiovascular disease (CVD) at entry and CVD development or death during the following decade. At 70 the prevalence of arterial hypertension (greater than or equal to 160/95 mmHg) was 46% in men and 45% in women. At 80 these prevalences were 19 and 30%, respectively. In women, this fall could partly be explained by an association between high blood pressure and excess mortality. In both sexes it could partly be explained by an increasing part of the population being treated with antihypertensives/diuretics, partly by an association with myocardial degeneration. In a Cox's regression model for competing risks at 70, high systolic blood pressure had independent, predictive value for excess CVD mortality in the eighth decade in women alone, and for excess CVD development in both sexes. High diastolic blood pressure had no independent predictive value for any of these end points.

Aged↗

Non-invasively detected carotid stenosis and ischaemic heart disease in men with leg arteriosclerosis.

Since the excess mortality rate associated with an ankle-brachial blood-pressure index (ABPI) less than 0.9 was only partly explained by an excess cardiovascular mortality, we believe that leg artery disease should not only be regarded as a marker of generalised arteriosclerosis but also as a sign associated with an increased risk of premature death. 439 men who were part of a prospective population study in Malmö, Sweden, were, at 68 years of age, invited to a health examination including, ABPI, carotid-artery ultrasonography, and 24 h ambulatory electrocardiographic monitoring. Cause-specific mortality and incidence of myocardial infarction (MI) during 8 years of follow-up was compared in men with and without signs of arteriosclerotic disease. Of 60 men with an ABPI < 0.9, 20 (33%) had angina pectoris or previous MI. Another 11 (18%) had silent ST-segment depression (> or = 1 mm); 3 (5%) had a history of stroke; and 17 (28%) had symptom-free carotid stenosis (> 30% reduction of the cross-sectional diameter). Total mortality rate in men with no signs of arteriosclerotic disease was 19.6 per 1000 person-years and cardiac event rate (fatal and non-fatal MI and death from chronic ischaemic heart disease was 8.6 per 1000 person-years). Leg artery disease, carotid stenosis, and ischaemic heart disease were in a univariate analysis all associated with an increased cardiac event rate and an increased total mortality rate. In a multivariate analysis an ABPI less than 0.9 was associated with a 2.4 times higher total mortality (95% CI 1.5-3.9) and a 2.0 times higher cardiac event rate (1.1-3.9). Carotid stenosis and ischaemic heart disease contributed to the risk for MI (RR 2.1; 95% CI 1.2-3.8; and 2.1; 1.2-3.9, respectively), whereas no independent association with total mortality was found.

Aged↗

Role of social class in excess black stroke mortality.

BACKGROUND AND PURPOSE: It has been suggested that a substantial proportion of the excess stroke mortality among black Americans may be attributable to relatively lower socioeconomic status (SES) in this group. In this report we provide the first quantitative estimates of the proportion of excess black stroke mortality attributable to SES for a large population-based cohort. METHODS: We used data from the National Longitudinal Mortality Study for persons 45 years and older (73,400 white men, 87,528 white women, 6522 black men, and 8816 black women). Sex-specific proportional hazards model were used to estimate excess black stroke mortality with and without adjustment for education and income (measures of SES). The contribution of SES to the excess black stroke risk was estimated from the difference in regression coefficients for race in these models. RESULTS: In men, low SES was associated with increased stroke mortality (P < or = .0001) and accounted for 14% to 46% of the excess black stroke risk (P < .05). However, we could find no association between SES and stroke mortality in women, and SES did not account for a significant proportion of the excess stroke mortality in black women. CONCLUSIONS: Although SES proved to account for a statistically significant proportion of excess male black stroke mortality, overall SES explained less than one quarter of the observed excess between ages 45 and 65. In women, SES did not significantly reduce the estimated excess black stroke mortality. Although SES may be playing a role in excess black stroke mortality, a substantial proportion of the excess appears attributable to other sources, including cerebrovascular risk factors that are unrelated to SES, unmeasured lifestyle influences, social resources, and genetic factors.

Black or African American↗

Maternal determinants of child survival in a rural African community.

BACKGROUND: The aim was to determine maternal factors related to child survival in the rural area of Bwamanda, Northern Zaire. METHODS: A prospective study of 30-months mortality was carried out in a cohort of 776 children aged 0-3 months, obtained by random cluster sampling. Inclusion criteria were exclusive breastfeeding, no severe prematurity and absence of severe protein-energy malnutrition, diarrhoea or acute respiratory infection. Mortality was recorded by regular home visits and inspection of hospital and funeral registers. Maternal factors that remain stable during follow-up were studied. RESULTS: Factors associated with excess mortality in bivariate and multiple logistic regression analysis were: (i) mother has parity > 5 (relative risk [RR] = 1.5-4.2); (ii) distance from the health centre > 5 km (RR = 0.9-2.9); (iii) invaliding maternal diseases (RR = 1.2-9.0). Maternal school education (conditional odds ratio [OR] = 1.0-5.0) was significant in the multiple regression. In contrast to the other risk factors, mother-child separation or problems with breastfeeding were rare and did not significantly increase mortality. CONCLUSIONS: Chronic stress situations created by maternal invalidity, high parity and distance from health care facilities, increase child mortality. Acute stress in the mother-child dyad seemed to be efficiently compensated for. In subsistence economy areas, maternal school education can be a disadvantage.

Adolescent↗

Increased socioeconomic differences in mortality in eight Spanish provinces.

In Spain, the study of socioeconomic differences in mortality has been limited by the fact that death certificates often do not include complete information on occupation. In this study, we chose those geographic areas with the highest quality information on occupation of the deceased in order to study socioeconomic differences in mortality from various causes of death. We used information from the death certificates of males who died between 30 and 64 years of age in eight Spanish provinces to compare mortality from the leading causes of death in professionals and managers (group I) and in manual laborers (group II) in 1980-82 and 1988-90. In each period the standardized mortality ratios (SMRs) were higher in group II, except for ischaemic heart disease during the first period, and cancer of the colon and rectum in both, although in the latter case the differences were not statistically significant. The ratio between the SMR from all causes in group II and group I was 1.27 in 1980-82, and 1.72 in 1988-90; for cancer of the colon and rectum the ratio went from 0.98 to 0.84, and for ischaemic heart disease, from 0.80 to 1.31. Except for cancer of the colon and rectum, which resulted in higher mortality in occupational group I, the excess mortality in occupational group II increased between the first and second period. The relation between socioeconomic level and mortality for ischaemic heart disease was reversed, a phenomenon similar to that which took place in the 1960s and 1970s in the developed countries.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗

Dietary patterns and their associations with demographic, lifestyle and health variables in a random sample of British adults.

The present study aimed to identify dietary patterns, from the frequency of consumption of food items and some semi-quantitative data, in a random sample of 9003 British adults, and to examine the associations of the main dietary patterns with demographic factors, lifestyle habits, measures of self-reported health and mortality. Principal component analysis was used to identify four main dietary patterns, and analysis of variance employed to examine the characteristics associated with them. The four components explained, respectively, 10.2, 7.3, 5.1 and 4.9% of the total dietary variation. Component 1, frequent fruit, salad and vegetable consumption with infrequent consumption of high-fat foods, was associated with middle age, non-manual socio-economic groups, non- and ex-smokers, 'sensible' drinkers, small households, the south of the country, and self-assessed 'excellent' or 'good' health. Component 2, frequent consumption of high-starch foods, most vegetables and meat, was popular with young men, older men and women, large households, non-smokers, non-drinkers and those who viewed themselves as healthy. Component 3, frequent consumption of high-fat foods, was predominantly consumed by young people, smoking women, 'high-risk' drinkers, and men reporting many illness and/or malaise symptoms. Component 4, high positive loadings for sweets, biscuits and cakes, with negative weightings for vegetables, was most favoured by students, the elderly, those living alone, residents in Scotland, but not those in central England, and those who did not smoke. For women only the first component was associated with low all-cause mortality, and the third component with excess mortality.

Adult↗

Alcohol-related deaths contribute to socioeconomic differentials in mortality in Sweden.

BACKGROUND: This study aims at estimating the contribution of alcohol to socioeconomic mortality differentials in Sweden. METHODS: Data were obtained from a Census-linked Deaths Registry. Participants in the 1980 and 1990 censuses were included with a follow-up of mortality 1990-1995. Socioeconomic status was assigned from occupation in 1990 or 1980. Alcohol-related deaths were defined from underlying or contributory causes. Poison regressions were applied to compute age-adjusted mortality rate ratios for all-causes, alcohol-related and other causes among 30-79-year-olds. The contribution of alcohol to mortality differentials was calculated from absolute differences. RESULTS: Around 5% (9,547) of all deaths were alcohol-related (30-79 years). For both sexes, manual workers, lower nonmanuals, entrepreneurs and unclassifiable groups had significantly higher alcohol-related mortality than did upper nonmanuals. Male farmers had significantly lower such mortality. The contribution of alcohol to excess mortality over that of upper nonmanuals was greatest among middle-aged (40-59 years) men who were manual workers or who belonged to a group of 'unclassifiable & others' (25-35%). It was of considerable size also for middle-aged lower nonmanuals (both sexes), male entrepreneurs, female manual workers and 'unclassifiable & others'. Among men, the total contribution of alcohol (30-79 years) was estimated at 16% for manual workers, 10% for lower nonmanuals and 7% for entrepreneurs; and among women, 6% (manual workers, lower nonmanuals) and 3% (entrepreneurs). CONCLUSION: Although deaths related to alcohol were probably underreported (e.g. accidents), alcohol clearly contributes to socioeconomic mortality differentials in Sweden. The size of this contribution depends strongly on age (peak among the middle-aged) and gender (greatest among men).

Adult↗

An indirect estimate of the incidence of non-insulin-dependent diabetes mellitus.

Our goal was to estimate non-insulin-dependent diabetes mellitus incidence in the Netherlands in the absence of equivocal empirical data. Incidence can be expressed as a function of age, sex, prevalence, and mortality. We obtained prevalence data from a study that pooled existing prevalence estimates. We calculated diabetes-related mortality using relative risks on all-cause mortality. Sensitivity for the rate of excess mortality was determined using the 95% confidence intervals (95% CI) of the relative risks. The estimated incidence increases exponentially with age, with a doubling time of 10 years for men and 9 years for women. The rate increases from 8.1 per 10,000 (95% CI = 7.7-8.8) for men ages 40-44 years and 7.0 (95% CI = 6.8-8.0) for women to 79.7 per 10,000 (95% CI = 69.5-90.9) for men ages 75-79 years and 85.8 (95% CI = 80.6-91.0) for women. When empirical estimates of incidence are largely lacking, the methodology described offers a useful alternative, in particular for the assessment of potential intervention effects.

Adolescent↗

Dangers of growth hormone therapy in critically ill patients.

Prolonged length of stay is the major challenge for modern intensive care because of the associated morbidity and the impact on resource utilization. Severe trauma or infection is associated with a catabolic response, which is characterized by increased protein turnover and negative nitrogen balance. Severe catabolism leads to end-organ dysfunction and muscular weakness, prolonging the need for mechanical ventilation. Catabolism cannot be prevented with standard parenteral or enteral nutritional formulas. In order to prevent the complications of catabolism in intensive care patients, recombinant growth hormone has been applied as an experimental therapy for two decades in patients requiring parenteral nutrition and in patients with respiratory failure. Administration of recombinant growth hormone has resulted in positive nitrogen balance, and studies in mechanically ventilated patients suggest that it may shorten the need for ventilatory support. In contrast to the results of these relatively small studies, a recent multinational randomized controlled trial revealed that the administration of recombinant growth hormone (with doses 10-20 times higher than used for replacement therapy) increases mortality of critically ill patients. The excessive mortality in patients treated with recombinant growth hormone was related to infections and development of multiple organ failure, leading to the conclusion that administration of high doses of recombinant growth hormone cannot be recommended for critically ill patients. This review reinforces that conclusion.

Critical Illness↗

Pneumonia caused by oxacillin-resistant Staphylococcus aureus treated with glycopeptides.

OBJECTIVE: To determine whether ventilator-associated pneumonia caused by oxacillin-resistant Staphylococcus aureus (VAP-ORSA) treated with glycopeptides is associated with an increased mortality rate. DESIGN: Retrospective matched cohort study. SETTING: Four intensive care units in teaching hospitals. PATIENTS: Seventy-five patients were matched to 75 controls. INTERVENTIONS: None. MEASUREMENTS AND MAIN RESULTS: All adult intensive care unit patients with microbiologically documented VAP-ORSA were matched to intubated controls who did not develop VAP-ORSA, based on disease severity (Acute Physiology and Chronic Health Evaluation II score) at admission (+/-3 points), diagnostic category, and length of stay before pneumonia onset. Population characteristics and intensive care unit mortality rates of patients with VAP-ORSA and their controls without pneumonia were compared. Attributable mortality was determined by subtracting the crude mortality rate of controls from the crude mortality rate of VAP-ORSA patients. Thirty-six of the 75 matched VAP-ORSA patients died, representing a crude mortality rate of 48%, whereas 19 of the 75 controls died, a crude mortality rate of 25.3% (p < .01). Excess mortality was estimated to be 22.7% (95% confidence interval, 2.4-42.9%). Median length of intensive care unit stay in the surviving pairs was 33 days (interquartile range, 25-75%: 25-45 days) for VAP-ORSA patients and 21 days (interquartile range, 25-75%: 15-34.75 days) days for controls (p = .054). CONCLUSIONS: Despite appropriate glycopeptide therapy, there is an increased attributable mortality for pneumonia by ORSA, after careful adjustment for disease severity and diagnostic category.

APACHE↗

Phagocytosis of small carbon particles (PM10) by alveolar macrophages stimulates the release of polymorphonuclear leukocytes from bone marrow.

Recent studies have shown that an increased concentration of ambient particulate matter (PM10) is related to decreased pulmonary function and respiratory and cardiovascular mortality. The mechanisms responsible for this excess mortality are unknown and the relationship between the level of PM10 and the circulating leukocyte counts has not been previously investigated. We postulated that the deposition of PM10 in the peripheral lung stimulates alveolar macrophages (AM), which results in polymorphonuclear leukocyte (PMN) release from bone marrow (BM). To test this hypothesis, either colloidal carbon (CC) (n = 3) or saline (n = 4) was instilled into the lungs of rabbits and PMN release from BM was evaluated by using 5'-bromo-2'-deoxyuridine (BrdU). CC instillation in the lung shortened the transit time of PMN through the BM to 71.0 +/- 6.9 h compared with the saline controls (85.5 +/- 2.8 h, p < 0.01). The role of AM in this response was further investigated by incubating isolated AM in tissue culture medium either with or without the presence of CC, and measuring the effect of the supernatants on the release of PMN from the BM. The supernatant of AM incubated with CC shortened the PMN transit time through the BM to 74.9 +/- 3.7 h (p < 0.05) compared with the supernatant from the unstimulated AM (98.6 +/- 1.9 h) and medium alone (94.3 +/- 3.7 h). We conclude that the phagocytosis of CC by AM releases mediators (cytokines) that stimulate the BM to release PMN. We speculate that these newly released PMN may play an important role in the decline in lung function and high mortality seen in populations exposed to high concentrations of atmospheric PM10.

Animals↗

Respiratory risk factors and mortality: longitudinal studies in Washington County, Maryland.

Risk factors for temporal changes in chronic respiratory disease mortality were evaluated from two studies conducted in Washington County, Maryland. The first examined the mortality of a private census population (greater than 35,000 whites) enumerated in 1963 over two subsequent time periods by age, sex, and initial smoking status. The second examined the 10-yr mortality of a subset of the 1963 census (884 men who had undergone spirometry). We observed a fall in age-adjusted mortality from all causes and from arteriosclerotic heart disease (ASHD), but an increase in COPD mortality. However, the increase in these chronic pulmonary deaths is essentially confined to persons who were smoking cigarettes at the beginning of the study period. Furthermore, while smokers showed an increased mortality risk for all causes, the excess mortality risk did not fall uniformly across cigarette smokers. It is a major observation of this study that all-cause and cardiovascular (as well as pulmonary) mortality are significantly more often found among subjects with ventilatory impairment (independent of smoking status). Reasons for the association of ASHD mortality with impaired forced expiration are discussed. Thus, men at increased risk for three (ASHD, lung cancer, COPD) of the five leading causes of death (three of eight for women) may be identified by spirometry. Perhaps it is time that this test was more generally applied.

Adult↗

GH strongly affects serum concentrations of mannan-binding lectin: evidence for a new IGF-I independent immunomodulatory effect of GH.

Studies in animals and humans indicate that GH and IGF-I modulate immune function. Recently, it was reported that GH therapy increased the mortality in critically ill patients. The excessive mortality was almost entirely attributable to septic shock or multiorgan failure, suggesting that a GH-induced modulation of immune function was involved. In the present study, we examined whether GH or IGF-I influences the serum concentrations of mannan-binding lectin (MBL). MBL is a plasma protein of the innate immune system that initiates the complement cascade and activates inflammation after binding to carbohydrate structures on microbial surfaces. We performed a cross-over study of 16 healthy men examined during a control period, and during treatment with either GH or IGF-I for 6 d. The levels of MBL were more than doubled during GH treatment, whereas no changes were observed in the IGF-I group or during the control period (P < 0.001). IGF-I levels were elevated similarly during treatment with GH and IGF-I. Subsequently, we studied 30 healthy persons and 25 GH-deficient (GHD) patients randomized to treatment with GH or placebo in a double-blinded manner, and further included samples from 23 patients with active acromegaly examined before and after treatment with octreotide or the GH-receptor antagonist pegvisomant for 3 months. Baseline concentrations of MBL were lower in GHD patients and higher in acromegalic patients than in healthy subjects (P < 0.02). Treatment with GH doubled the MBL concentrations in healthy subjects and almost quadrupled the concentrations in GHD patients; whereas in acromegalic patients, the levels of MBL were reduced to approximately two thirds of the initial values during treatment with octreotide or pegvisomant. Our results demonstrate that treatment with GH, but not IGF-I, significantly increases MBL concentrations. The clinical consequences of this new link between the endocrine and the immune system remain to be elucidated.

Acromegaly↗

Estimating the independent effects of multiple pollutants in the presence of measurement error: an application of a measurement-error-resistant technique.

Misclassification of exposure usually leads to biased estimates of exposure-response associations. This is particularly an issue in cases with multiple correlated exposures, where the direction of bias is uncertain. It is necessary to address this problem when considering associations with important public health implications such as the one between mortality and air pollution, because biased exposure effects can result in biased risk assessments. The National Morbidity and Mortality Air Pollution Study (NMMAPS) recently reported results from an assessment of multiple pollutants and daily mortality in 90 U.S. cities. That study assessed the independent associations of the selected pollutants with daily mortality in two-pollutant models. Excess mortality was associated with particulate matter of aerodynamic diameter less than or equal to 10 microm/m3 (PM10), but not with other pollutants, in these two pollutant models. The extent of bias due to measurement error in these reported results is unclear. Schwartz and Coull recently proposed a method that deals with multiple exposures and, under certain conditions, is resistant to measurement error. We applied this method to reanalyze the data from NMMAPS. For PM10, we found results similar to those reported previously from NMMAPS (0.24% increase in deaths per 10-microg/m3) increase in PM10). In addition, we report an important effect of carbon monoxide that had not been observed previously.

Air Pollutants↗