A Lower Level of Forced Expiratory Volume in 1 Second Is a Risk Factor for All-Cause and Cardiovascular Mortality in a Japanese Population: The Takahata Study

Chronic obstructive pulmonary disease is a known risk factor for cardiovascular death in Western countries. Because Japan has a low cardiovascular death rate, the association between a lower level of forced expiratory volume in 1 s (FEV₁) and mortality in Japan’s general population is unknown. To clarify this, we conducted a community-based longitudinal study. This study included 3253 subjects, who received spirometry from 2004 to 2006 in Takahata, with a 7-year follow-up. The causes of death were assessed on the basis of the death certificate. In 338 subjects, airflow obstruction was observed by spirometry. A total of 127 subjects died. Cardiovascular death was the second highest cause of death in this population. The pulmonary functions of the deceased subjects were significantly lower than those of the subjects who were alive at the end of follow-up. The relative risk of death by all causes, respiratory failure, lung cancer, and cardiovascular disease was significantly increased with airflow obstruction. The Kaplan–Meier analysis showed that all-cause and cardiovascular mortality significantly increased with a worsening severity of airflow obstruction. After adjusting for possible factors that could influence prognosis, a Cox proportional hazard model analysis revealed that a lower level of FEV₁ was an independent risk factor for all-cause and cardiovascular mortality (per 10% increase; hazard ratio [HR], 0.89; 95% confidence interval [CI], 0.82–0.98; and HR, 0.72; 95% CI, 0.61–0.86, respectively). In conclusion, airflow obstruction is an independent risk factor for all-cause and cardiovascular death in the Japanese general population. Spirometry might be a useful test to evaluate the risk of cardiovascular death and detect the risk of respiratory death by lung cancer or respiratory failure in healthy Japanese individuals.     

Growth hormone and outcome in patients with intracerebral hemorrhage: a pilot study

Background: Endocrine alterations of the hypothalamic-pituitary-axis are one of the first measurable physiological changes in cerebral insults. During acute stress, human growth hormone (GH) is stimulated and has shown to have a prognostic value in various diseases. Within this pilot study, we evaluated the prognostic value of GH in patients with acute intracerebral hemorrhage (ICH).

Methods: In a prospective observational study in 40 consecutive patients with ICH, GH was measured on admission. The prognostic value of GH to predict 30-day mortality and 90-day functional outcome was assessed. Favorable functional outcome was defined as Barthel Index score >85 points and Modified Rankin Scale <3 points.

Results: GH levels were increased in patients who died within 30 days as compared to survivors (0.45 (IQR 0.20–1.51) vs. 1.51 (IQR 0.91–4.08) p?=?0.03), and in patients with an unfavorable functional outcome as compared to patients with a favorable functional outcome after 90 days 0.28 (IQR 0.16–0.61) vs. 0.78 (IQR 0.31–1.99) p?=?0.03). For mortality prediction, receiver-operating-characteristics revealed an area under the curve (AUC) on admission for GH of 0.78 (95% CI 0.60–0.96), which was in the range of the Glasgow Coma Score (GCS) (AUC 0.82 (95% CI 0.59–1.00) p?=?0.80). For functional outcome prediction, GH had an AUC of 0.71 (95% CI 0.54–0.87), which was statistically not different from the GCS (AUC 0.81 (95% CI 0.68–0.94) p?=?0.36).

Conclusions: In our small cohort of patients with acute ICH, elevated GH level were associated with increased mortality and worse outcome. If confirmed in a larger study, GH levels may be used as an additional prognostic factor in ICH patients. (ClincalTrials.gov number NCT00390962).     

A Low Serum Bicarbonate Concentration as a Risk Factor for Mortality in Peritoneal Dialysis Patients

Background and Aim

Metabolic acidosis is common in patients with chronic kidney disease and is associated with increased mortality in hemodialysis patients. However, this relationship has not yet been determined in peritoneal dialysis (PD) patients.

Methods

This prospective observational study included a total of 441 incident patients who started PD between January 2000 and December 2005. Using time-averaged serum bicarbonate (TA-Bic) levels, we aimed to investigate whether a low serum bicarbonate concentration can predict mortality in these patients.

Results

Among the baseline parameters, serum bicarbonate level was positively associated with hemoglobin level and residual glomerular filtration rate (GFR), while it was negatively associated with albumin, C-reactive protein (CRP) levels, peritoneal Kt/V urea, and normalized protein catabolic rate (nPCR) in a multivariable linear regression analysis. During a median follow-up of 34.8 months, 149 deaths were recorded. After adjustment for age, diabetes, coronary artery disease, serum albumin, ferritin, CRP, residual GFR, peritoneal Kt/V urea, nPCR, and percentage of lean body mass, TA-Bic level was associated with a significantly decreased risk of mortality (HR per 1 mEq/L increase, 0.83; 95% CI, 0.76-0.91; p < 0.001). In addition, compared to patients with a TA-Bic level of 24-26 mEq/L, those with a TA-Bic level < 22 and between 22-24 mEq/L conferred a 13.10- and 2.13-fold increased risk of death, respectively.

Conclusions

This study showed that a low serum bicarbonate concentration is an independent risk factor for mortality in PD patients. This relationship between low bicarbonate levels and adverse outcome could be related to enhanced inflammation and a more rapid loss of RRF associated with metabolic acidosis. Large randomized clinical trials to correct acidosis are warranted to confirm our findings.     

Effect of tailored use of tirofiban in patients with Non-ST-elevation acute coronary syndrome undergoing percutaneous coronary intervention: a randomized controlled trial

The association of sodium intake with the risk of cardiovascular morbidity and mortality is inconsistent. Thus, the present meta-analysis was conducted to summarize the strength of association between sodium intake and cardiovascular morbidity and mortality. PubMed, Embase, and the Cochrane Library were searched systematically to identify the relevant studies up to October 2017. The effect estimates for 100 mmol/day increase in sodium intake were calculated using 95% confidence intervals (CIs) of cardiac death, total mortality, stroke, or stroke mortality for low (< 3 g/d), moderate (3–5 g/d), or heavy (> 5 g/d) sodium intake, and minimal sodium intake comparison. A total of 16 prospective cohort studies reported data on 205,575 individuals. The results suggested that an increase in sodium intake by 100 mmol/d demonstrated little or no effect on the risk of cardiac death (P = 0.718) and total mortality (P = 0.720). However, the risk of stroke incidence (P = 0.029) and stroke mortality (P = 0.007) was increased significantly by 100 mmol/day increment of sodium intake. Furthermore, low sodium intake was associated with an increased risk of cardiac death (P = 0.003), while moderate (P < 0.001) or heavy (P = 0.001) sodium intake was associated with an increased risk of stroke mortality. These findings suggested that sodium intake by 100 mmol/d increment was associated with an increased risk of stroke incidence and stroke mortality. Furthermore, low sodium intake was related to an increased cardiac death risk, while moderate or heavy sodium intake was related to an increased risk of stroke mortality.     

Reverse causality and confounding and the associations of overweight and obesity with mortality

Objective: To examine the effect of reverse causality and confounding on the association of BMI with all‐cause and cause‐specific mortality. Research Methods and Procedures: Data from two large prospective studies were used. One (a community‐based cohort) included 8327 women and 7017 men who resided in two Scottish towns at the time of the baseline assessment in 1972–1976; the other (an occupational cohort) included 4016 men working in the central belt of Scotland at the time of the baseline assessment in 1970–1973. Participants in both cohorts were ages 45 to 64 years at baseline; the follow‐up period was 28 to 34 years. Results: In age‐adjusted analyses that did not take account of reverse causality or smoking, there was no association between being overweight (BMI 25 to <30 kg/m²) and mortality, and weak to modest associations between obesity (BMI ≥30 kg/m²) and mortality. There was a strong association between smoking and lower BMI in women and men in both cohorts (all p < 0.0001). Among never‐smokers and with the first 5 years of deaths removed, overweight was associated with an increase in all‐cause mortality (relative risk ranging from 1.12 to 1.38), and obesity was associated with a doubling of risk in men in both cohorts (relative risk, 2.10 and 1.96, respectively) and a 60% increase in women (relative risk, 1.56). In both never‐smokers and current smokers, being overweight or obese was associated with important increases in the risk of cardiovascular disease. Discussion: These findings demonstrate that with appropriate control for smoking and reverse causality, both overweight and obesity are associated with important increases in all‐cause and cause‐specific mortality, and in particular with cardiovascular disease mortality.     

Predictive value of plasma copeptin level for the risk and mortality of heart failure: a meta‐analysis

Epidemiologic studies are inconsistent regarding the association between plasma copeptin level and heart failure (HF). The aim of this study was to perform a meta‐analysis to determine whether high level of copeptin is correlated with incidence of HF and mortality in patients with HF. We searched PUBMED and EMBASE databases for studies conducted from 1966 through May 2016 to identify studies reporting hazard ratio (HR) estimates with 95% confidence intervals (CIs) for the association between plasma copeptin level and HF. A random‐effects model was used to combine study‐specific risk estimates. A total of 13 studies were included in the meta‐analysis, with five studies on the incidence of HF and eight studies on the mortality of patients with HF. For incidence of HF, the summary HR indicated a borderline positive association of high plasma copeptin level with HF risk (HR, 1.60; 95% CI, 0.90–2.85). Furthermore, an increase of 1 standard deviation in log copeptin level was associated with a 17% increase in the risk of incident HF (HR, 1.17; 95% CI, 1.02–1.33). For all‐cause mortality of patients with HF, we also found a significant association between elevated plasma copeptin level and increased mortality of HF (HR, 1.76; 95% CI, 1.33–2.33). Our dose–response analysis indicated that an increment in copeptin level of 1 pmol/l was associated with a 3% increase in all‐cause mortality (HR, 1.03; 95% CI, 1.01–1.05). In conclusion, our results suggest that elevated plasma copeptin level is associated with an increased risk of HF and all‐cause mortality in patients with HF.     

Glycosylated hemoglobin in relationship to cardiovascular outcomes and death in patients with type 2 diabetes: a systematic review and meta-analysis

Background

Chronic hyperglycemia in type 2 diabetes increases the risk of microvascular events. However, there is continuing uncertainty about its effect on macrovascular outcomes and death. We conducted a meta-analysis of prospective studies to estimate the association of glycosylated hemoglobin level with the risk of all-cause mortality and cardiovascular outcomes among patients with type 2 diabetes.

Methodology/Principal Findings

We systematically searched the MEDLINE database through April 2011 by using Medical Subject Heading search terms and a standardized protocol. We included prospective cohort studies that reported data of glycosylated hemoglobin level on the risk of incident cardiovascular events and all-cause mortality. Relative risk estimates (continuous and categorical variables) were derived or abstracted from each cohort study. Twenty six studies were included in this analysis with a mean follow-up rang of 2.2–16 years. The pooled relative risk associated with a 1% increase in glycosylated hemoglobin level among patients with type 2 diabetes was 1.15 (95% CI, 1.11 to 1.20) for all-cause mortality, 1.17 (95% CI, 1.12 to 1.23) for cardiovascular disease, 1.15 (95% CI, 1.10 to 1.20) for coronary heart disease, 1.11 (95% CI, 1.05 to 1.18) for heart failure, 1.11 (95% CI, 1.06 to 1.17) for stroke, and 1.29 (95% CI, 1.18 to 1.40) for peripheral arterial disease, respectively. In addition, a positive dose-response trend existed between glycosylated hemoglobin level and cardiovascular outcomes.

Conclusions/Significance

Chronic hyperglycemia is associated with an increased risk for cardiovascular outcomes and all-cause mortality among patients with type 2 diabetes, likely independently from other conventional risk factors.     

High-density lipoprotein lipid peroxidation as a molecular signature of the risk for developing cardiovascular disease: Results from MASHAD cohort

High-density lipoprotein (HDL) function rather than level may better predict cardiovascular disease (CVD). However, the contribution of the impaired antioxidant function of HDL that is associated with increased HDL lipid peroxidation (HDLox) to the development of clinical CVD remains unclear. We have investigated the association between serum HDLox with incident CVD outcomes in Mashhad cohort. Three-hundred and thirty individuals who had a median follow-up period of 7 years were recruited as part of the cohort. The primary end point was cardiovascular event, including myocardial infarction, stable angina, unstable angina, or coronary revascularization. In both univariate/multivariate analyses adjusted for traditional CVD risk factors, HDLox was an independent risk factor for CVD (odds ratio, 1.62; 95% confidence interval, 1.41–1.86; p < 0.001). For every increase in HDLox by 0.1 unit, there was an increase in CVD risk by 1.62-fold. In an adjusted analysis, there was a >2.5-fold increase in cardiovascular risk in individuals with HDLox higher than cutoff point of 1.06 compared to those with lower scores, suggesting HDLox > 1.06 is related to the impaired HDL oxidant function and in turn exposed to elevated risk of CVD outcomes (hazard ratio, 2.72; 95% CI, 1.88–3.94). Higher HDLox is a surrogate measure of reduced HDL antioxidant function that positively associated with cardiovascular events in a population-based cohort.     

Induction of oxidative DNA damage in human foreskin fibroblast Hs68 cells by oxidized β-carotene and lycopene

Two recent clinical trials suggest that β-carotene may be harmful to smokers. In this study we examined the hypothesis that β-carotene may become toxic when degradation occurs. β-Carotene (BC) and lycopene (LP) with or without prior heat treatment (60°C for 1h in open air) were incubated at 20 and 40 μM with calf thymus DNA or human fibroblasts Hs68 cells. The heat treatment resulted in ca. 80% and 35% bleaching of BC and LP, respectively. When Hs68 cells were incubated with the oxidized β-carotene (OBC) or oxidized lycopene (OLP) at 37°C for 20h, cell viability was significantly and dose-dependently decreased whereas cell viability was not affected by BC or LP. Cell death, which was already evident at 4h after incubation with OBC or OLP, was possibly attributable to apoptosis, as shown by the increased histone-associated DNA fragmentation. However, cell lysis, measured as release of lactate dehydrogenase, also occurred at 4h after incubation with OBC and OLP, although the extent was relatively small and was greater for OLP than for OBC. When calf thymus DNA was incubated with OBC or OLP at 37°C for 20h, the 8-hydroxy-2-deoxyguanosine (8-OH-dG) level was significantly and dose-dependently increased by OLP whereas the increase by OBC was only significant at 40 μM. When Hs68 cells were incubated with OBC and OLP for 20h, both compounds increased the 8-OH-dG level, but the effect was only significant for 40 μM OLP. Comet (single-cell gel electrophoresis) assay of DNA damage in Hs68 cells was determined at 2h after incubation with OBC or OLP because of its high sensitivity. Both OBC and OLP significantly and dose-dependently increased DNA breakage while BC and LP had no effect. Inclusion of BHT during incubation of cells with 40 μM OBC or OLP partially inhibited (ca. 40%, p<.05) the extent of comet formation. Intriguingly, OBC and OLP neither induce lipid peroxidation in Hs68 cells (measured as thiobarbituric acid-reactive substances released into the medium) nor increased the intracellular level of reactive oxygen species. Although it is presently unclear about what degradation products are formed, this study has demonstrated that, when oxidized, BC and LP lead to oxidative damage to both purified DNA and cellular DNA. The results suggest that such damage may contribute to the adverse effects of β-carotene reported in recent clinical studies and caution that it is important to prevent oxidation of BC and LP for human uses such as in supplemental studies.     

Summary of a Canadian Study of Smoking and Health

The object of this study was to investigate the relationship between residence, occupation and smoking habits, and mortality from chronic diseases, particularly lung cancer. It was a prospective study, initiated by a questionnaire sent to Canadian veteran pension recipients. The study was based on the replies of 78,000 males and 14,000 females, together with data on the deaths occurring among these respondents over a six-year follow-up period—July 1, 1956 to January 30, 1962.The outstanding finding of this study was that cigarette smokers compared to non-smokers had excessive mortality, particularly from heart and circulatory diseases, lung cancer, and bronchitis and emphysema. The mortality ratios for heart and circulatory diseases were elevated even for those who smoked cigarettes less than five years, and remained relatively constant as the duration of smoking increased. The mortality ratios for lung cancer increased markedly as the duration of smoking increased. A small excess in mortality was noted among urban residents. An association between cause of death and occupation was not evident in this study.Findings based on the data on smoking collected in this study were incorporated into the Report of the U.S. Surgeon-General''s Advisory Committee on Smoking and Health.     

The Effect of Obesity and Weight Loss on Aortic Pulse Wave Velocity as Assessed by Magnetic Resonance Imaging

Obesity is an escalating global health problem associated with both an increased risk of death and an increased risk of cardiovascular events. Our goal was to use magnetic resonance imaging (MRI) to determine the effect of obesity and weight loss, in the absence of the traditional cardiovascular risk factors, on aortic pulse wave velocity (PWV) a reliable, reproducible, and accurate clinical measure of aortic stiffness linked to increased mortality. Fifty obese (BMI 38.3 ± 6.8 kg/m²) and eighteen normal‐weight controls (BMI 22.0 ± 1.7 kg/m²) with no identifiable cardiovascular risk factors underwent vascular MRI to assess PWV between the ascending aorta at the level of the pulmonary artery and the abdominal aorta (AA). Twenty‐eight subjects underwent repeat imaging after a 1‐year period of weight loss. Both groups were well matched for age, systolic blood pressure, fasting glucose, and total cholesterol. Obesity was associated with a 14% increase in PWV (P = 0.021), and with elevated C‐reactive protein (CRP) (P < 0.01) and leptin levels (P < 0.001) factors known to cause increase arterial stiffness. Weight loss (average 50% excess weight) was associated with a 14% improvement in PWV (P = 0.03), and with reductions in serum leptin levels (P < 0.01). Obesity, in the absence of the traditional cardiovascular risk factors, is associated with increased aortic PWV, a noninvasive clinical measure of aortic stiffness independently predictive of cardiovascular mortality. Significant weight loss results in improvements in aortic PWV. This may provide a potential link between both obesity and increased mortality, and the reduction in mortality that occurs with weight loss.     

Radon and risk of death from cancer and cardiovascular diseases in the German uranium miners cohort study: follow-up 1946–2003

Data from the German uranium miners cohort study were analyzed to investigate the radon-related risk of mortality from cancer and cardiovascular diseases. The Wismut cohort includes 58,987 men who were employed for at least 6 months from 1946 to 1989 at the former Wismut uranium mining company in Eastern Germany. By the end of 2003, a total of 3,016 lung cancer deaths, 3,355 deaths from extrapulmonary cancers, 5,141 deaths from heart diseases and 1,742 deaths from cerebrovascular diseases were observed. Although a number of studies have already been published on various endpoints in the Wismut cohort, the aim of the present analyses is to provide a direct comparison of the magnitude of radon-related risk for different cancer sites and cardiovascular diseases using the same data set, the same follow-up period and the same statistical methods. A specific focus on a group of cancers of the extrathoracic airways is also made here, due to the assumed high organ doses from absorbed radon progeny. Internal Poisson regression was used to estimate the excess relative risk (ERR) per unit of cumulative exposure to radon in working level months (WLM) and its 95% confidence limits (CI). There was a statistically significant increase in the risk of lung cancer with increasing radon exposure (ERR/WLM = 0.19%; 95% CI: 0.17%; 0.22%). A smaller, but also statistically significant excess was found for cancers of the extrathoracic airways and trachea (ERR/WLM = 0.062%; 95% CI: 0.002%; 0.121%). Most of the remaining nonrespiratory cancer sites showed a positive relationship with increasing radon exposure, which, however, did not reach statistical significance. No increase in risk was noted for coronary heart diseases (ERR/WLM = 0.0003%) and cerebrovascular diseases (ERR/WLM = 0.001%). The present data provide clear evidence of an increased radon-related risk of death from lung cancer, some evidence for an increased radon-related risk of death from cancers of the extrathoracic airways and some other extrapulmonary cancers, and no evidence for mortality from cardiovascular diseases. These findings are consistent with the results of other miner studies and dosimetric calculations for radon-related organ doses.     

Pre-procedural elevated cardiac troponin predict risk of long-term all-cause mortality after transcatheter aortic valve replacement: a meta-analysis of prospective studies

Abstract

Background: The purpose of this meta-analysis was to evaluate the relationship between elevated cardiac troponin pre-transcatheter aortic valve replacement (TAVR) and long-term all-cause mortality.

Methods: Prospective studies with the endpoint of all-cause mortality were included. We primarily used the fixed-effect model weighted by inverse variance. Meta-regression and subgroup analyses were conducted to explore the potential sources of heterogeneity by specified study characteristics.

Results: Seven prospective studies comprising of 3049 subjects were included in our meta-analysis. Pre-procedural elevated cardiac troponin was associated with increased risk of long-term mortality post TAVR [hazard ratio (HR) 2.25, 95% CI 1.83–2.78, p?=?0.000, I² = 30.3%, p for heterogeneity 0.197]. In addition, subgroup analyses have shown that the group with an younger age (<82?y) seemed to have a higher risk of all-cause mortality than the group with older age (≥82?y) [HR 4.08 (2.41 to 6.89) VS 2.01 (1.60 to 2.53), p?=?0.016 for subgroup difference].

Conclusions: Pre-procedural elevated cardiac troponin was associated with increased long-term all-cause mortality in patients undergoing TAVR.     

Evaluation of Potential Factors Predisposing Livestock to Predation by Jaguars

ABSTRACT Depredation of livestock by large carnivores is an important but poorly understood source of human-carnivore conflict. We examined patterns of livestock depredation by jaguars (Panthera onca) and pumas (Puma concolor) on a ranch-wildlife reserve in western Brazil to assess factors contributing to prey mortality. We predicted jaguars would kill a greater proportion of calves than yearling and adult cattle and that proximity to suitable habitat would increase mortality risk. We further speculated that exposure to predation risk would promote livestock grouping and increased movement distance. We recorded 169 cattle mortality incidents during 2003–2004, of which 19% were due to predation by jaguars and pumas. This level of mortality represented 0.2–0.3% of the total livestock holdings on the ranch. Jaguars caused most (69%) cattle predation events, and survival in allotments was lower for calves than for other age classes. Forest proximity was the only variable we found to explain patterns of livestock mortality, with predation risk increasing as distance to forest cover declined. Due to low predation risk, cattle movement patterns and grouping behavior did not vary relative to level of spatial overlap with radiocollared jaguars. The overall effect of predation on cattle was low and livestock likely constituted an alternative prey for large cats in our study area. However, selection of calves over other age cohorts and higher predation risk among cattle in proximity to forest cover is suggestive of selection of substandard individuals. Cattle ranchers in the Pantanal region may reduce cattle mortality rates by concentrating on losses due to nonpredation causes that could be more easily controlled.     

Gastric dilatation and intestinal obstruction mimicking acute coronary syndrome with dynamic electrocardiographic changes

Background

Hyperuricemia may be associated with an increased risk of coronary heart disease (CHD) mortality; however, the results from prospective studies are conflicting. The objective of this study was to assess the association between hyperuricemia and risk of CHD mortality by performing a meta-analysis.

Methods

Pubmed and Embase were searched for relevant prospective cohort studies published until July 2015. Studies were included only if they reported data on CHD mortality related to hyperuricemia in a general population. The pooled adjusted relative risk (RR) was calculated using a random-effects model.

Results

A total of 14 studies involving 341 389 adults were identified. Hyperuricemia was associated with an increased risk of CHD mortality (RR: 1.14; 95 % CI: 1.06–1.23) and all-cause mortality (RR: 1.20; 95 % CI: 1.13–1.28). For each increase of 1 mg/dl of serum uric acid (SUA), the overall risks of CHD and all-cause mortality increased by 20 and 9 %, respectively. According to the gender subgroup analyses, hyperuricemia increased the risk of CHD mortality in women (RR: 1.47; 95 % CI: 1.21–1.73) compared to men (RR: 1.10; 95 % CI: 1.00–1.19). The risk of all-cause mortality was greater in women.

Conclusions

Hyperuricemia may modestly increase the risk of CHD and all-cause mortality. Future research is needed to determine whether urate–lowering therapy has beneficial effects for reducing CHD mortality.

     

Interleukin-6, but not soluble adhesion molecules, predicts a subsequent mortality from cardiovascular disease in patients with acute ST-segment elevation myocardial infarction

Inflammatory responses are an important element in the atherosclerotic process. Therefore, inflammatory markers can potentially serve as predictors of cardiovascular risk. However, the existing data are limited and controversial. We conducted a prospective cohort study with 263 patients with first acute ST-segment elevation myocardial infarction (STEMI) who were admitted to our Hospital within 6 h after the symptoms onset. Clinical data were recorded and serum admission levels of interleukin-6 (IL-6), soluble intercellular adhesion molecule-1 (sICAM-1), soluble vascular cell adhesion molecule-1 (sVCAM-1), and soluble P-selectin (sP-selectin) were determined. The patients were then followed up for 3 years to document cardiovascular mortality. During the follow-up, 34 patients died from cardiovascular causes. The admission levels of IL-6 were significantly higher in these patients, whereas sICAM-1, sVCAM-1, and sP-selectin were comparable between these and the survived patients. The Kaplan–Meier plots revealed a significant increase in cardiovascular mortality with increasing levels of IL-6 (P = 0.0002, χ² test). The logistic regression analysis indicated that IL-6 was an independent predictor for cardiovascular mortality. To conclude, our findings indicate that elevated admission levels of IL-6, but not soluble adhesion molecules, provide valuable information for risk assessment of long-term cardiovascular mortality in patients with STEMI.     

BMI and Mortality: Results From a National Longitudinal Study of Canadian Adults

Although a clear risk of mortality is associated with obesity, the risk of mortality associated with overweight is equivocal. The objective of this study is to estimate the relationship between BMI and all‐cause mortality in a nationally representative sample of Canadian adults. A sample of 11,326 respondents aged ≥25 in the 1994/1995 National Population Health Survey (Canada) was studied using Cox proportional hazards models. A significant increased risk of mortality over the 12 years of follow‐up was observed for underweight (BMI <18.5; relative risk (RR) = 1.73, P < 0.001) and obesity class II+ (BMI >35; RR = 1.36, P <0.05). Overweight (BMI 25 to <30) was associated with a significantly decreased risk of death (RR = 0.83, P < 0.05). The RR was close to one for obesity class I (BMI 30–35; RR = 0.95, P >0.05). Our results are similar to those from other recent studies, confirming that underweight and obesity class II+ are clear risk factors for mortality, and showing that when compared to the acceptable BMI category, overweight appears to be protective against mortality. Obesity class I was not associated with an increased risk of mortality.     

Utility of the Plasma Level of suPAR in Monitoring Risk of Mortality during TB Treatment

Objective

To investigate whether changes in the plasma level of soluble urokinase plasminogen activator receptor (suPAR) can be used to monitor tuberculosis (TB) treatment efficacy.

Design

This prospective cohort study included 278 patients diagnosed with active pulmonary TB and followed throughout the 8-month treatment period.

Results

Mortality during treatment was higher in the highest inclusion quartile of suPAR (23%) compared to the lowest three quartiles (7%), the risk ratio being 3.1 (95% CI 1.65–6.07). No association between early smear conversion and subsequent mortality or inclusion suPAR was observed. After 1 and 2 months of treatment, an increase in suPAR compared to at diagnosis was associated with a Mortality Rate Ratio (MRR) of 4.5 (95%CI: 1.45–14.1) and 2.1 (95%CI 0.62–6.82), respectively, for the remaining treatment period.

Conclusions

The present study confirmed that elevated suPAR level at time of initiation of TB treatment is associated with increased risk of mortality. Furthermore, increased suPAR levels after one month of treatment was associated with increased risk of mortality during the remaining 7-month treatment period.