Plasma insulin and all-cause, cardiovascular, and noncardiovascular mortality: the 22-year follow-up results of the Helsinki Policemen Study

OBJECTIVE: To investigate the association of plasma insulin with all-cause, cardiovascular, and noncardiovascular mortality. RESEARCH DESIGN AND METHODS: We studied 22-year mortality data from the Helsinki Policemen Study The study population comprised 970 men, 34-64 years of age, who were free of coronary heart disease, other cardiovascular disease, and diabetes. Area under the insulin response curve (AUC insulin) during an oral glucose tolerance test was used to reflect plasma insulin levels. RESULTS: During the follow-up period, 276 men died: 130 from cardiovascular and 146 from noncardiovascular causes. The hazard ratio (HR) for hyperinsulinemia (highest AUC insulin quintile vs. combined lower quintiles) with regard to all-cause mortality adjusting for age, was 1.94 (95% CI 1.20-3.13) during the first 10 years of the follow-up period and 1.51 (1.15-1.97) during the entire 22 years; adjusting for other risk factors, the HR was 1.88 (1.08-3.30) and 1.37 (1.00-1.87) during 10 and 22 years, respectively The corresponding HRs for cardiovascular mortality during 10 and 22 years were 2.67 (1.35-5.29) and 1.73 (1.19-2.53), respectively, for age-adjusted and 2.30 (1.03-5.12) and 1.39 (0.90-2.15), respectively, for multiple-adjusted HRs. A U-shaped association was observed between insulin and noncardiovascular mortality, multiple-adjusted HRs for lowest and highest versus middle AUC insulin quintiles were 1.85 (1.20-2.86) and 1.43 (0.91-2.24), respectively CONCLUSIONS: Hyperinsulinemia was associated with increased all-cause and cardiovascular mortality in Helsinki policemen independent of other risk factors, although these associations weakened with the lengthening of the follow-up period. The association of insulin with noncardiovascular mortality was U-shaped.     

Metabolic syndrome as a predictor of all-cause and cardiovascular mortality in type 2 diabetes: the Casale Monferrato Study

OBJECTIVE: The aim of this study was to assess in an 11-year survival follow-up of a population-based cohort of type 2 diabetes the predictive role of World Health Organization-defined metabolic syndrome, independent of conventional cardiovascular risk factors. RESEARCH DESIGN AND METHODS: During the follow-up (1991-2001), 1,565 patients were regularly examined with centralized measurements of HbA(1c). The independent role of the metabolic syndrome as a predictor of all-cause and cardiovascular mortality was assessed with multivariate Cox proportional hazards modeling. RESULTS: At baseline, the prevalence of the metabolic syndrome was 75.6% (95% CI 73.6-77.9). Results are based on 685 deaths (520 with the metabolic syndrome and 165 without it) in 10,890.2 person-years of observations. With respect to subjects without the metabolic syndrome, those with the metabolic syndrome had a similar hazard ratio (HR) of cardiovascular mortality after adjustment for age, sex, smoking, total cholesterol level, and coronary heart disease. In contrast, relative to subjects with diabetes only, the HR of subjects with only one component of the syndrome was 2.92 (1.16-7.33), independent of other risk factors. CONCLUSIONS: We found that 1) the prevalence of the metabolic syndrome in a population-based cohort of type 2 diabetes is high (75.6%); 2) the metabolic syndrome is not a predictor of 11-year all-cause and cardiovascular mortality; and 3) more than twofold higher cardiovascular risk, independent of conventional risk factors, is evident in diabetic subjects with only one component of the syndrome compared with those with diabetes only. Categorizing type 2 diabetic subjects as having or not having the metabolic syndrome does not provide further prediction compared with the knowledge of its single components.     

Red blood cell distribution width as an independent predictor of all-cause mortality in out of hospital cardiac arrest

Objective

Post-resuscitation period is characterized by high early mortality due to post-cardiac arrest syndrome. Recent studies found that elevated red cell distribution width (RDW) is a strong predictor of mortality in critically ill patients. We investigated the prognostic significance of RDW in out-of-hospital cardiac arrest (OHCA) victims.

Methods

Analysis of emergency department OHCA registry extending from January 2007 to December 2010 was conducted. Patients with ROSC were assessed for Utstein predictors including sex, age, arrest location, presence of witness, bystander cardiopulmonary resuscitation, response time, initial rhythm and cause of arrest. RDW, hematocrit, white blood cell and platelet counts, blood urea nitrogen (BUN), creatinine and albumin were also obtained. Outcome variable was survival duration within 30 days. RDW was categorized in quartiles as <13.2%, 13.2% to 14.0%, 14.1% to 15.4% and >15.4%. Hazard ratios (HRs) were estimated using Cox-proportional hazard models in both univariate and multivariate analysis. All prognostic variables with their p value < 0.1 in univariate analysis were used in multivariate analysis for adjustment.

Results

Among 409 OHCA patients, 219 patients had ROSC. Highest RDW quartile (RDW > 15.4%), female sex, older age, non-shockable initial rhythm, increased BUN and creatinine and decreased albumin, hematocrit and platelet count were associated with increased mortality in univariate analysis. In multivariate analysis, the highest RDW quartile was independently associated with all-cause mortality (HR = 1.95; 95% CI 1.05–3.60; p = 0.034) during 30-day post-resuscitation period. Other significant variables were age, initial rhythm and serum albumin.

Conclusions

Initial RDW is an independent predictor of all-cause mortality in post-resuscitation patients.     

Red cell distribution width is an independent predictor of mortality in necrotizing fasciitis

Introduction

Necrotizing fasciitis (NF) is a rapidly progressing and potentially lethal infectious disease of the soft tissue. An elevated red blood cell distribution width (RDW) is associated with increased risk of death in patients with heart disease and infectious disease. We retrospectively assessed the association of elevated RDW with in-hospital mortality due to NF.

Methods

All patients had diagnoses of NF and were admitted to the emergency department of a single institution in Taiwan over a 4-year period. Demographics, comorbidities, clinical presentations, and laboratory parameters were retrospectively reviewed. Red blood cell distribution width was categorized as elevated (> 14.5%) or not elevated. Multivariate regression analysis was used to identify risk factors associated with mortality.

Results

A total of 98 patients were enrolled, and the mortality rate was 23%. Univariate analysis indicated that advanced age, initial hypotension, low hemoglobin level, and elevated RDW (69.6% vs 20%, OR = 9.14, P < .001) were significantly associated with mortality. Multivariate analysis indicated that RDW was a significant and independent predictor of mortality in enrolled patients.

Conclusions

Elevated RDW is a significant and independent predictor of in-hospital mortality for patients with NF.     

Chronic renal insufficiency is an independent predictor of mortality in implantable cardioverter-defibrillator recipients

BACKGROUND: Chronic renal insufficiency (CRI) has been associated with increased risk of cardiovascular morbidity and mortality. However, there is limited knowledge regarding this association and the effect of renal dysfunction on survival benefit in patients with implantable cardioverter-defibrillators (ICDs). METHODS: We investigated whether there was an association between CRI (defined as serum creatinine levels >or=1.5 mg/dL) and increased risk of mortality in ICD recipients. We retrospectively studied all patients (n = 336) followed within our ICD clinic in a 2.5-year period. CRI, ventricular tachycardia (VT), cardiomyopathy (CM), and mortality were recorded. Ischemic CM was defined as the presence of coronary artery disease (CAD) and left ventricular ejection fraction 相似文献   

Rapid progression of albumin excretion is an independent predictor of cardiovascular mortality in patients with type 2 diabetes and microalbuminuria.

OBJECTIVE: In patients with type 2 diabetes, microalbuminuria is associated with an increase in predominantly cardiovascular mortality. Considerable interindividual variability in the rate of progression of microalbuminuria exists. The prognostic significance of rate of progression of microalbuminuria with regard to cardiovascular and renal clinical end points is, however, unknown. The purpose of this study was to determine the prognostic significance of rate of progression of microalbuminuria for cardiovascular end points and renal function. RESEARCH DESIGN AND METHODS: In a previous prospective cohort study, progression of microalbuminuria (expressed as mean yearly change in albumin-to-creatinine ratio) was assessed in 58 patients with type 2 diabetes. During a median follow-up of 7 years after progression of microalbuminuria was determined, we registered all-cause mortality and coronary heart disease mortality as primary end points and coronary heart disease (fatal or nonfatal), peripheral vascular disease, ischemic stroke, retinopathy, macroalbuminuria, and change in serum creatinine as secondary end points. RESULTS: Seven subjects died during the study; five of these subjects died of coronary heart disease. Cox's regression analysis identified progression of microalbuminuria as a significant predictor of all-cause mortality (hazard ratio 1.46 per point increase in albumin-to-creatinine ratio per year, P < 0.001), coronary heart disease mortality (hazard ratio 2.32, P = 0.006), and macroalbuminuria (hazard ratio 1.79, P < 0.001). Adjustment for multiple cardiovascular risk factors did not affect these results. Identical analyses for baseline level of microalbuminuria instead of progression rate of microalbuminuria did not show significant hazard ratios. In addition, progression of microalbuminuria significantly predicted an increase in serum creatinine (r = 0.29, P = 0.04). CONCLUSIONS: In patients with type 2 diabetes and microalbuminuria, the rate of progression of albumin excretion seems to be a powerful independent predictor of mortality caused mainly by coronary heart disease.     

Postprandial blood glucose predicts cardiovascular events and all-cause mortality in type 2 diabetes in a 14-year follow-up: lessons from the San Luigi Gonzaga Diabetes Study

OBJECTIVE

To evaluate whether postprandial blood glucose predicts cardiovascular events and all-cause mortality in type 2 diabetes in a long-term follow-up taking into account A1C and the main cardiovascular risk factors.

RESEARCH DESIGN AND METHODS

Consecutive type 2 diabetic patients (n = 505) followed up at our diabetes clinic were evaluated at baseline (1995) for the main cardiovascular risk factors and for five glycemic control parameters (fasting blood glucose, blood glucose 2 h after breakfast, blood glucose 2 h after lunch, blood glucose before dinner, and A1C); all-cause mortality and the first cardiovascular events occurring during the 14-year follow-up were measured.

RESULTS

We observed 172 cardiovascular events (34.1% of the population) and 147 deaths (29.1% of the population). Using the Cox analysis with the backward method, we categorized the variables according to the therapeutic targets of the American Diabetes Association. Our observations were as follows. When the five glycemic control parameters were considered together, the predictors were 1) for cardiovascular events, blood glucose 2 h after lunch (hazard ratio 1.507, P = 0.010) and A1C (1.792, P = 0.002); and 2) for mortality, blood glucose 2 h after lunch (1.885, P < 0.0001) and A1C (1.907, P = 0.002). When blood glucose 2 h after lunch and A1C were considered together with the main cardiovascular risk factors, the following glycemic control parameters were predictors: 1) for cardiovascular events, blood glucose 2 h after lunch (1.452, P = 0.021) and A1C (1.732, P = 0.004); and 2) for mortality, blood glucose 2 h after lunch (1.846, P = 0.001) and A1C (1.896, P = 0.004).

CONCLUSIONS

In type 2 diabetes, both postprandial blood glucose and A1C predict cardiovascular events and all-cause mortality in a long-term follow-up.The relationships between the parameters of blood glucose control, cardiovascular events, and all-cause mortality are controversial. The Diabetes Epidemiology Collaborative Analysis of Diagnostic Criteria in Europe (DECODE) reported that blood glucose concentrations at 2 h of an oral glucose tolerance test (OGTT) (i.e., postchallenge blood glucose) are better predictors of cardiovascular events and of all-cause mortality than fasting blood glucose (FBG) (1). Similarly, in the Framingham Offspring Study, 2-h postchallenge blood glucose predicted cardiovascular events better than did A1C (2).Furthermore, a meta-analysis of 38 prospective studies carried out in nondiabetic subjects confirmed a strong association between 2-h postchallenge blood glucose with fatal and nonfatal cardiovascular events (3), and a linear relationship between this parameter and the risk of cardiovascular death has been observed (4).In the studies mentioned above, the subjects were tested with an OGTT; the concern has been raised that OGTT is not a composite meal and that postchallenge hyperglycemia is only a surrogate marker of postmeal hyperglycemia. Thus, the last one should be directly measured to evaluate the risk conferred by postprandial hyperglycemia. A large body of evidence shows a relationship between postprandial hyperglycemia and factors causally related to atherosclerosis, such as oxidative stress (5), or markers of the atherosclerotic process, such as endothelial dysfunction (6) and carotid intima-media thickness (7). However, it has also been shown that mean blood glucose and A1C show stronger associations with cardiovascular risk factors than does postprandial blood glucose (8).Only two studies have investigated the predictive power of postprandial blood glucose on cardiovascular events: the Diabetes Intervention Study (DIS) (9) and the San Luigi Gonzaga Diabetes Study (10). The DIS (9) is a pioneering investigation carried out in relatively young, newly diagnosed type 2 diabetic patients followed up for 11 years; it showed for the first time that postprandial blood glucose predicts myocardial infarction and mortality, but the study did not consider A1C. Thus, as far as we know, the only results demonstrating the independent predictive power of postprandial blood glucose on cardiovascular events after correction for A1C are the 5-year follow-up of the San Luigi Gonzaga Diabetes Study (10). We carried out this investigation in patients attending our diabetes clinic with a mean diabetes duration of about 9 years; the short-term follow-up, however, did not allow us to draw conclusions about mortality (10). For this reason, we carried out a long-term follow-up of the same study to evaluate whether 1) the predictive role of postprandial blood glucose on cardiovascular events that we demonstrated after 5 years lasted up to 14 years; 2) postprandial blood glucose also predicts all-cause mortality, even when A1C and the main nonglycemic cardiovascular risk factors are taken into account; and 3) the predictive power of postprandial blood glucose and A1C could be demonstrated when these variables are categorized according to the therapeutic targets stated by the American Diabetes Association (11).     

New-onset diabetes and risk of all-cause and cardiovascular mortality: the Cardiovascular Health Study

OBJECTIVE: Cardiovascular risk associated with new-onset diabetes is not well characterized. We hypothesized that risk of all-cause and cardiovascular mortality would be similar among participants with and without new-onset diabetes in the first years of follow-up and rise over time for new-onset diabetes. RESEARCH DESIGN AND METHODS: The Cardiovascular Health Study (CHS) is a longitudinal study of cardiovascular risk factors in adults aged > or =65 years. We used CHS participants to define a cohort (n = 282) with new-onset diabetes during 11 years of follow-up. New-onset diabetes was defined by initiation of antidiabetes medication or by fasting plasma glucose >125 mg/dl among CHS participants without diabetes at study entry. Three CHS participants without diabetes were matched for age, sex, and race to each participant with new-onset diabetes at the time of diabetes identification (n = 837). Survival analysis provided adjusted hazard ratios (HRs) for all-cause and cardiovascular mortality. RESULTS: During a median of 5.9 years of follow-up, there were 352 deaths, of which 41% were cardiovascular. In adjusted analyses, new-onset diabetes was associated with an HR of 1.9 (95% CI 1.4-2.5) for all-cause and 2.2 (1.4-3.4) for cardiovascular mortality compared with no diabetes. Mortality risks were elevated within 2 years of onset, especially cardiovascular risk (4.3 [95% CI 1.7-10.8]), and did not increase over time. CONCLUSIONS: Our findings indicate that there may be a mortality differential soon after diabetes onset in older adults and suggest that long-term macrovascular damage from atherosclerosis may not be primarily responsible for increased risk.     

Handgrip strength is inversely associated with fatal cardiovascular and all-cause mortality events

Abstract

Purpose: We aimed to assess the associations of handgrip strength (HS) with cardiovascular and all-cause mortality and whether adding data on HS to cardiovascular disease (CVD) risk factors is associated with improvement in CVD mortality prediction.

Design: Handgrip strength was assessed in a population-based sample of 861 participants aged 61–74 years at baseline. Relative HS was obtained by dividing the absolute value by body weight.

Results: During a median (interquartile range) follow-up of 17.3 (12.6–18.4) years, 116 fatal coronary heart diseases (CHDs), 195 fatal CVDs and 412 all-cause mortality events occurred. On adjustment for several risk factors, the hazard ratios (95% confidence intervals (CIs)) for fatal CHD, fatal CVD and all-cause mortality were 0.59 (0.37–0.95), 0.59 (0.41–0.86) and 0.66 (0.51–0.84), respectively, comparing extreme tertiles of relative HS. Adding relative HS to a CVD mortality risk prediction model containing established risk factors did not improve discrimination or reclassification using Harrell’s C-index (C-index change: 0.0034; p = .65), integrated-discrimination–improvement (0.0059; p = .20) and net-reclassification-improvement (–1.31%; p = .74); however, there was a significant difference in –2 log likelihood (p < .001).

Conclusions: Relative HS is inversely associated with CHD, CVD and all-cause mortality events. Adding relative HS to conventional risk factors improves CVD risk assessment using sensitive measures of discrimination.

• KEY MESSAGES

• Handgrip strength (HS) assessment is simple, inexpensive and it takes only a few minutes to measure in clinical practice; however, its prognostic role for fatal cardiovascular outcomes on top of traditional risk factors in apparently healthy populations is uncertain.

• In a population-based prospective cohort study, good HS adjusted for body weight was associated with lower risk of fatal cardiovascular outcomes and the associations remained consistent across several clinically relevant subgroups.

• Handgrip strength may be a useful prognostic tool for fatal CHD and CVD events, in the general population.

     

Independent associations of glucose status and arterial stiffness with left ventricular diastolic dysfunction: an 8-year follow-up of the Hoorn Study

OBJECTIVE

To investigate relative contributions of glucose status and arterial stiffness to markers of left ventricular (LV) systolic and diastolic dysfunction after 8 years of follow-up.

RESEARCH DESIGN AND METHODS

In the population-based prospective Hoorn Study, 394 individuals with preserved LV systolic and diastolic function participated, of whom 87 had impaired glucose metabolism and 128 had type 2 diabetes. Measurements including arterial ultrasound and echocardiography were performed according to standardized protocols.

RESULTS

The presence of type 2 diabetes was associated with more severe LV systolic and diastolic dysfunction 8 years later: LV ejection fraction was 2.98% (95% CI 0.46–5.51) lower, and left atrial (LA) volume index, LV mass index, and tissue Doppler-derived E/e′ were 3.71 mL/m² (1.20–6.22), 5.86 g/m^2.7 (2.94–8.78), and 1.64 units (0.95–2.33) higher, respectively. Furthermore, presence of impaired glucose metabolism or type 2 diabetes was associated with 8-year increases in LV mass index. More arterial stiffness (measured as a lower distensibility) was associated with LV diastolic dysfunction 8 years later: LA volume index, LV mass index, and E/e′ at follow-up were higher. Subsequent adjustments for baseline mean arterial pressure and/or LV diastolic dysfunction did not eliminate these associations. Associations of type 2 diabetes and arterial stiffness with markers of LV diastolic dysfunction were largely independent of each other.

CONCLUSIONS

Both glucose status and arterial distensibility are independently associated with more severe LV diastolic dysfunction 8 years later and with deterioration of LV diastolic dysfunction. Therefore, type 2 diabetes and arterial stiffness may relate to LV diastolic dysfunction through different pathways.Metabolic disturbances and arterial stiffness are both recognized contributors to left ventricular (LV) stiffness and LV systolic and diastolic dysfunction. The most frequent comorbid conditions of heart failure with normal LV ejection fraction (HFNEF) (mainly characterized by LV diastolic dysfunction) are hypertension, type 2 diabetes, and obesity (1). Moreover, a recent review of medical records revealed that even after exclusion of heart failure patients, 23% of individuals with type 2 diabetes had LV diastolic dysfunction (2). Data from the MONICA (Monitoring of Trends and Determinations in Cardiovascular Disease) registry have shown that hypertension and obesity—both associated with type 2 diabetes and arterial stiffness—independently predicted left atrial (LA) enlargement, a sensitive indicator of an elevated LV preload (3).HFNEF patients were shown to display combined stiffening of arteries and the LV, which was not ascribable to age, body weight, or arterial pressure (4). Data from Olmsted County confirm that arterial stiffness is increased in HFNEF patients and in hypertensive patients without heart failure (5). Arterial stiffness is hypothesized to lead to increased arterial wave reflections, which in turn lead to an increased cardiac afterload and myocardial oxygen demand and simultaneously to a decreasing diastolic coronary perfusion pressure (6). These direct effects of arterial stiffening are thought to contribute to both systolic and diastolic LV dysfunction but predominantly to the former (7,8). Besides these mechanisms, there may also be indirect effects due to shared underlying pathways that lead to stiffening of both arterial and LV walls (9). As previously shown in our cohort, individuals with type 2 diabetes commonly have stiffer arteries (10). Both arterial and LV stiffness in type 2 diabetes have been related to deposition of advanced glycation end products, fibrosis, and an elevated myocyte resting tension (11,12). These effects might predominantly contribute to LV diastolic dysfunction and might underlie both type 2 diabetes– and arterial stiffness–related LV diastolic dysfunction. In the current study, we investigated whether glucose status and arterial stiffness were prospectively associated with (changes in) LV systolic and diastolic dysfunction. Secondly, we assessed whether these associations were independent of each other.     

Impact of diabetes duration and cardiovascular risk factors on mortality in type 2 diabetes: the Hoorn Study

BACKGROUND: Several studies have reported differences in the mortality risk between diabetic subjects detected by screening and known diabetic patients. We studied mortality in relation to diabetes duration, and the contribution of other cardiovascular risk factors to the elevated risk. MATERIALS AND METHODS: Participants were type 2 diabetic subjects (n = 174) of a population-based cohort study. Of these, 95 were diagnosed by screening. Known diabetic subjects were grouped into two categories of diabetes duration, with a median duration of 2.4 and 11.2 years, respectively. We assessed the contribution of classical cardiovascular risk factors (dyslipidaemia, hypertension, and prior myocardial infarction), and of new cardiovascular risk factors (microalbuminuria, von Willebrand factor, sVCAM-1 and C-reactive protein) to the mortality risk during nearly 10 years of follow up. Cox's proportional hazards model was used to study the association of diabetes duration and mortality. RESULTS: The age- and sex-adjusted relative risks of mortality were 2.06 (95% C.I. 1.04-4.10) and 3.19 (1.64-6.20) for the patients with short- and long-term diabetes compared with the screening-detected diabetic subjects, respectively. Adjustment for cardiovascular risk factors resulted in a reduction of mortality risk in both groups: 1.13 (0.51-2.50) and 2.39 (1.18-4.83), respectively. Mortality risk significantly increased with increasing diabetes duration, even after multiple adjustment (P-value for trend ranged from < 0.001-0.018). CONCLUSIONS: Mortality risk increased with increasing diabetes duration. In subjects with short diabetes duration the mortality risk could largely be attributed to other risk factors. In subjects with a longer diabetes duration, however, the elevated mortality risk was independent of these cardiovascular risk factors.     

HIV is an independent predictor of aortic stiffness

Background

Patients with treated Human Immunodeficiency Virus-1 (HIV) infection are at increased risk of cardiovascular events. Traditionally much of this risk has been attributed to metabolic and anthropometric abnormalities associated with HIV, which are similar to the metabolic syndrome (MS), an established risk factor for cardiovascular mortality. It remains unclear whether treated HIV infection is itself associated with increased risk, via increase vascular stiffness.

Methods

226 subjects (90 with HIV) were divided into 4 groups based on HIV and MS status: 1) HIV-ve/MS-ve, 2) HIV-ve/MS + ve, 3) HIV + ve/MS-ve and 4)HIV + ve/MS + ve. CMR was used to determine aortic pulse wave velocity (PWV) and regional aortic distensibility (AD).

Results

PWV was 11% higher and regional AD up to 14% lower in the HIV + ve/MS-ve group when compared to HIV-ve/MS-ve (p < 0.01 all analyses). PWV and AD in the HIV + ve/MS-ve group was similar to that observed in the HIV-ve/MS + ve group (p > 0.99 all analyses). The HIV + ve/MS + ve group had 32% higher PWV and 30-34% lower AD than the HIV-ve/MS-ve group (all p < 0.001), and 19% higher PWV and up to 31% lower AD than HIV + ve/MS-ve subjects (all p < 0.05). On multivariable regression, age, systolic blood pressure and treated HIV infection were all independent predictors of both PWV and regional AD.

Conclusion

Across multiple measures, treated HIV infection is associated with increased aortic stiffness and is also an independent predictor of both PWV and regional AD. The magnitude of the effect of treated HIV and MS are similar, with additive detrimental effects on central vascular elasticity.     

Associations of prediabetes with all-cause and cardiovascular mortality: A meta-analysis

Abstract

Background. Reports on the association of prediabetes with all-cause mortality and cardiovascular mortality are inconsistent.

Objective. To evaluate the risk of all-cause and cardiovascular mortality in association with impaired fasting glucose (IFG) and impaired glucose tolerance (IGT).

Methods. Prospective cohort studies with data on prediabetes and mortality were included. The relative risks (RRs) of all-cause and cardiovascular mortality were calculated and reported with 95% confidence intervals (95% CIs).

Results. Twenty-six studies were included. The risks of all-cause and cardiovascular mortality were increased in participants with prediabetes defined as IFG of 110–125 mg/dL (IFG 110) (RR 1.12, 95% CI 1.05–1.20; and RR 1.19, 95% CI 1.05–1.35, respectively), IGT (RR 1.33, 95% CI 1.24–1.42; RR 1.23, 95% CI 1.11–1.36, respectively), or combined IFG 110 and/or IGT (RR 1.21, 95% CI 1.11–1.32; RR 1.21, 95% CI 1.07–1.36, respectively), but not when IFG was defined as 100–125 mg/dL (RR 1.07, 95% CI 0.92–1.26; and RR 1.16, 95% CI 0.94–1.42, respectively).

Conclusions. Prediabetes, defined as IFG 110, IGT, or combined IFG 110 and/or IGT, was associated with increased all-cause and cardiovascular mortality.     

Red blood cell distribution width is an independent predictor of mortality in patients with gram-negative bacteremia

Red blood cell distribution width (RDW) is known to be a predictor of severe morbidity and mortality in some chronic diseases such as congestive heart failure. However, to our knowledge, little is known about RDW as a predictor of mortality in patients with Gram-negative bacteremia, a major nosocomial cause of intra-abdominal infections, urinary tract infections, and primary bacteremia. Therefore, we investigated whether RDW is an independent predictor of mortality in patients with Gram-negative bacteremia. Clinical characteristics, laboratory parameters, and outcomes of 161 patients with Gram-negative bacteremia from November 2010 to March 2011 diagnosed at Severance Hospital, Yonsei University College of Medicine, Seoul, Korea, were retrospectively analyzed. The main outcome measure was 28-day all-cause mortality. The 28-day mortality rate was significantly higher in the increased RDW group compared with the normal RDW group (P < 0.001). According to multivariate Cox proportional hazard analysis, RDW levels at the onset of bacteremia (per 1% increase, P = 0.036), the Charlson index (per 1-point increase, P < 0.001), and the Sequential Organ Failure Assessment score (per 1-point increase, P = 0.001) were independent risk factors for 28-day mortality. Moreover, the nonsurvivor group had significantly higher RDW levels 72 h after the onset of bacteremia than did the survivor group (P = 0.001). In addition, the area under the curve of RDW at the onset of bacteremia, the 72-h RDW, and the Sequential Organ Failure Assessment score for 28-day mortality were 0.764 (P = 0.001), 0.802 (P < 0.001), and 0.703 (P = 0.008), respectively. Red blood cell distribution width at the onset of bacteremia was an independent predictor of mortality in patients with Gram-negative bacteremia. Also, 72-h RDW could be a predictor for all-cause mortality in patients with Gram-negative bacteremia.