scholarly journals The U-Shape Relationship Between Glycated Hemoglobin Level and Long-Term All-Cause Mortality Among Patients With Coronary Artery Disease

2021 ◽  
Vol 8 ◽  
Author(s):  
Liwei Liu ◽  
Jianfeng Ye ◽  
Ming Ying ◽  
Qiang Li ◽  
Shiqun Chen ◽  
...  

Background: Although glycated hemoglobin (HbA1c) was considered as a prognostic factor in some subgroup of coronary artery disease (CAD), the specific relationship between HbA1c and the long-term all-cause death remains controversial in patients with CAD.Methods: The study enrolled 37,596 CAD patients and measured HbAlc at admission in Guangdong Provincial People's Hospital. The patients were divided into 4 groups according to HbAlc level (Quartile 1: HbA1c ≤ 5.7%; Quartile 2: 5.7% < HbA1c ≤ 6.1%; Quartile 3: 6.1% < HbA1c ≤ 6.7%; Quartile 4: HbA1c > 6.7%). The study endpoint was all-cause death. The restricted cubic splines and cox proportional hazards models were used to investigate the association between baseline HbAlc levels and long-term all-cause mortality.Results: The median follow-up was 4 years. The cox proportional hazards models revealed that HbAlc is an independent risk factor in the long-term all-cause mortality. We also found an approximate U-shape association between HbA1c and the risk of mortality, including increased risk of mortality when HbA1c ≤ 5.7% and HbA1c > 6.7% [Compared with Quartile 2, Quartile 1 (HbA1c ≤ 5.7), aHR = 1.13, 95% CI:1.01–1.26, P < 0.05; Quartile 3 (6.1% < HbA1c ≤ 6.7%), aHR = 1.04, 95% CI:0.93–1.17, P =0.49; Quartile 4 (HbA1c > 6.7%), aHR = 1.32, 95% CI:1.19–1.47, P < 0.05].Conclusions: Our study indicated a U-shape relationship between HbA1c and long-term all-cause mortality in CAD patients.

2013 ◽  
Vol 2013 ◽  
pp. 1-7 ◽  
Author(s):  
Dongfang Su ◽  
Zhongxia Li ◽  
Xinrui Li ◽  
Yuming Chen ◽  
Yuan Zhang ◽  
...  

Objectives. To evaluate whether serum interleukin-6 (IL-6) is associated with increased risk of mortality in coronary artery disease (CAD) patients.Methods. We performed a prospective cohort study of 718 CAD patients from the Guangzhou Cardiovascular Disease Cohort (GCDC) study. Multivariable-adjusted Cox proportional hazards regression analyses were used to examine the association between serum IL-6 with all-cause and cardiovascular mortality.Results. During the 1663 person-years of followup, the cumulative all-cause mortality and cardiovascular mortality were 6.5% (n=47) and 3.3% (n=24), respectively. The mean length of followup was2.32±0.81years. In the multivariable analyses, a one-SD increment in log-transformed serum IL-6 was positively associated with an increased risk of all-cause and cardiovascular mortality, with hazard ratios (HR) of 2.93 (95% CI, 2.11–4.08) and 2.04 (95% CI, 1.34–3.68) within the patients combined and 2.98 (95% CI, 2.12–4.18) and 3.10 (95% CI, 1.98–4.85) within males, respectively. Patients in the highest serum IL-6 tertile versus the lowest tertile were at higher risk of all-cause and cardiovascular mortality, with HR of 17.12 (95% CI 3.11–71.76) and 8.68 (95% CI, 1.88–37.51), respectively.Conclusions. In hospitalized patients with CAD, serum IL-6 is significantly associated with all-cause and cardiovascular mortality.


2021 ◽  
Vol 8 ◽  
Author(s):  
Bin Zhou ◽  
Xuerong Sun ◽  
Na Yu ◽  
Shuang Zhao ◽  
Keping Chen ◽  
...  

Background: The results of studies on the obesity paradox in all-cause mortality are inconsistent in patients equipped with an implantable cardioverter-defibrillator (ICD). There is a lack of relevant studies on Chinese populations with large sample size. This study aimed to investigate whether the obesity paradox in all-cause mortality is present among the Chinese population with an ICD.Methods: We conducted a retrospective analysis of multicenter data from the Study of Home Monitoring System Safety and Efficacy in Cardiac Implantable Electronic Device–implanted Patients (SUMMIT) registry in China. The outcome was all-cause mortality. The Kaplan–Meier curves, Cox proportional hazards models, and smooth curve fitting were used to investigate the association between body mass index (BMI) and all-cause mortality.Results: After inclusion and exclusion criteria, 970 patients with an ICD were enrolled. After a median follow-up of 5 years (interquartile, 4.1–6.0 years), in 213 (22.0%) patients occurred all-cause mortality. According to the Kaplan–Meier curves and multivariate Cox proportional hazards models, BMI had no significant impact on all-cause mortality, whether as a continuous variable or a categorical variable classified by various BMI categorization criteria. The fully adjusted smoothed curve fit showed a linear relationship between BMI and all-cause mortality (p-value of 0.14 for the non-linearity test), with the curve showing no statistically significant association between BMI and all-cause mortality [per 1 kg/m2 increase in BMI, hazard ratio (HR) 0.97, 95% CI 0.93–1.02, p = 0.2644].Conclusions: The obesity paradox in all-cause mortality was absent in the Chinese patients with an ICD. Prospective studies are needed to further explore this phenomenon.


2022 ◽  
Vol 2022 ◽  
pp. 1-11
Author(s):  
Qiong Ma ◽  
Bo-Lin Li ◽  
Lei Yang ◽  
Miao Zhang ◽  
Xin-Xin Feng ◽  
...  

Background. Chronological age (CA) is not a perfect proxy for the true biological aging status of the body. A new biological aging measure, phenotypic age (PhenoAge), has been shown to capture morbidity and mortality risk in the general US population and diverse subpopulations. This study was aimed at evaluating the association between PhenoAge and long-term outcome of patients with multivessel coronary artery disease (CAD). Methods. A total of 609 multivessel CAD patients who received PCI attempt and with follow-up were enrolled. The clinical outcome was all-cause mortality on follow-up. PhenoAge was calculated using an equation constructed from CA and 9 clinical biomarkers. Cox proportional hazards regression models and receiver operating characteristic (ROC) curves were performed to evaluate the association between PhenoAge and mortality. Results. Overall, patients with more diseases had older PhenoAge and phenotypic age acceleration (PhenoAgeAccel). After a median follow-up of 33.5 months, those with positive PhenoAgeAccel had a significantly higher incidence of all-cause mortality ( P = 0.001 ). After adjusting for CA, Cox proportional hazards models showed that both PhenoAge and PhenoAgeAccel were significantly associated with all-cause mortality. Even after further adjusting for confounding factors, each 10-year increase in PhenoAge was also associated with a 51% increased mortality risk. ROC curves revealed that PhenoAge, with an area under the curve of 0.705, significantly outperformed CA, the individual clinical chemistry measure, and other risk factors. When reexamining the ROC curves using various combinations of variables, we found that PhenoAge provides additional predictive power to all models. Conclusions. In conclusion, PhenoAge was strongly associated with all-cause mortality even after adjusting for CA. Our findings suggest that PhenoAge measure may be complementary in predicting mortality risk for patients with multivessel CAD.


Author(s):  
Jong‐Young Lee ◽  
Seung‐Jae Lee ◽  
Seung‐Whan Lee ◽  
Tae Oh Kim ◽  
Yujin Yang ◽  
...  

Background The long‐term impact of newly discovered, asymptomatic abnormal ankle–brachial index (ABI) in patients with significant coronary artery disease is limited. Methods and Results Between January 2006 and December 2009, ABI was evaluated in 2424 consecutive patients with no history of claudication or peripheral artery disease who had significant coronary artery disease. We previously reported a 3‐year result; therefore, the follow‐up period was extended. The primary end point was a composite of all‐cause death, myocardial infarction (MI), and stroke over 7 years. Of the 2424 patients with significant coronary artery disease, 385 had an abnormal ABI (ABI ≤0.9 or ≥1.4). During the follow‐up period, the rate of the primary outcome was significantly higher in the abnormal ABI group than in the normal ABI group ( P <0.001). The abnormal ABI group had a significantly higher risk of composite of all‐cause death/MI/stroke than the normal ABI group, after adjustment with multivariable Cox proportional hazards regression analysis (hazard ratio [HR], 2.07; 95% CI, 1.67–2.57; P <0.001) and propensity score–matched analysis (HR, 1.97; 95% CI, 1.49–2.60; P <0.001). In addition, an abnormal ABI was associated with a higher risk of all‐cause death, MI, and stroke, but not repeat revascularization. Conclusions Among patients with significant coronary artery disease, asymptomatic abnormal ABI was associated with sustained and increased incidence of composite of all‐cause death/MI/stroke, all‐cause death, MI, and stroke during extended follow‐up over 7 years.


2019 ◽  
Vol 189 (3) ◽  
pp. 224-234
Author(s):  
Jamie M Madden ◽  
Finbarr P Leacy ◽  
Lina Zgaga ◽  
Kathleen Bennett

Abstract Studies have shown that accounting for time-varying confounding through time-dependent Cox proportional hazards models may provide biased estimates of the causal effect of treatment when the confounder is also a mediator. We explore 2 alternative approaches to addressing this problem while examining the association between vitamin D supplementation initiated after breast cancer diagnosis and all-cause mortality. Women aged 50–80 years were identified in the National Cancer Registry Ireland (n = 5,417) between 2001 and 2011. Vitamin D use was identified from linked prescription data (n = 2,570). We sought to account for the time-varying nature of vitamin D use and time-varying confounding by bisphosphonate use using 1) marginal structural models (MSMs) and 2) G-estimation of structural nested accelerated failure-time models (SNAFTMs). Using standard adjusted Cox proportional hazards models, we found a reduction in all-cause mortality in de novo vitamin D users compared with nonusers (hazard ratio (HR) = 0.84, 95% confidence interval (CI): 0.73, 0.99). Additional adjustment for vitamin D and bisphosphonate use in the previous month reduced the hazard ratio (HR = 0.45, 95% CI: 0.33, 0.63). Results derived from MSMs (HR = 0.44, 95% CI: 0.32, 0.61) and SNAFTMs (HR = 0.45, 95% CI: 0.34, 0.52) were similar. Utilizing MSMs and SNAFTMs to account for time-varying bisphosphonate use did not alter conclusions in this example.


PLoS ONE ◽  
2020 ◽  
Vol 15 (12) ◽  
pp. e0243290
Author(s):  
David Teye Doku ◽  
Subas Neupane ◽  
Henrik Dobewall ◽  
Arja Rimpelä

Background and aim Bereavement affects the health of the bereaved both emotionally and physically. Bereavement resulting from alcohol-related death of the previous generation (parents-first generation) may increase the risk of alcohol abuse and consequently alcohol-related mortality as well as all-cause mortality in the next generation (offspring-second generation). Furthermore, these associations can be bi-directional. However, there is no conclusive evidence of these effects, and studies exploring these intergenerational effects are rare. This study investigates these associations. Methods A longitudinal data were constructed by linking participants from the Adolescent Health and Lifestyle Surveys (AHLS) from 1979 to 1997 with census and registry-based data from Statistics Finland containing the socioeconomic status of the survey participants and their parents (N = 78610) to investigate these associations. Multivariate Cox proportional hazards models were used to calculate hazard ratios with 95% confidence intervals to determine the effect of bereavement with alcohol-related mortality and all-cause mortality. Results The findings suggest that bereavement following the death of an offspring increases the risk of both alcohol-related and all-cause mortality among both parents. The magnitude of the risk of mortality following the death of an offspring is higher for mothers than for fathers. There were no clear associations of a parent’s death with an offspring’s alcohol-related or all-cause mortality. However, generally, a father’s death seems to be protective of the risk of mortality among the offspring while a mother’s alcohol-related death slightly increased the risk of alcohol-related mortality among their offspring. Conclusions These findings emphasise the role of bereavement, particularly resulting from the death of an offspring, on alcohol-related and all-cause mortality and therefore inequalities in mortality. Furthermore, the findings highlighting the need for alcohol abuse intervention and emotional support for bereaved persons following the death of an offspring.


2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Marc N. Jarczok ◽  
Julian Koenig ◽  
Julian F. Thayer

AbstractIn recent clinical practice, a biomarker of vagal neuroimmunomodulation (NIM), namely the ratio of vagally-mediated heart rate variability (vmHRV) and CRP, was proposed to index the functionality of the cholinergic anti-inflammatory pathway. This study aims to transfer and extend the previous findings to two general population-based samples to explore the hypothesis that NIM-ratio is associated with all-cause mortality. Two large population studies (MIDUS 2: N = 1255 and Whitehall II wave 5: N = 7870) with complete data from a total of N = 3860 participants (36.1% females; average age = 56.3 years; 11.1% deaths, last exit 18.1 years post inclusion) were available. NIM indices were calculated using the vagally-mediated HRV measure RMSSD divided by measures of CRP (NIMCRP) or IL-6 (NIMIL6). The NIM-ratios were quartiled and entered into age, ethnicity and body mass index adjusted Cox proportional hazards models. For NIMIL6 the lowest quartile was 45% more likely to die during the observed period (max. 18 years follow-up) compared to the highest quartile (HR = 0.55 CI 0.41–0.73; p < .0001). NIMCRP parallel these results. Here we show that an easily computable index of IL-6 inhibition is associated with all-cause mortality in two large general population samples. These results suggest that this index might be useful for risk stratification and warrant further examination.


2015 ◽  
Vol 35 (5) ◽  
pp. 566-575 ◽  
Author(s):  
Fenfen Peng ◽  
Xi Xia ◽  
Feng He ◽  
Zhijian Li ◽  
Fengxian Huang ◽  
...  

Objective To explore the effect of glycated hemoglobin (HbA1c) and albumin-corrected glycated serum proteins (Alb-GSP) on the mortality of diabetic patients receiving continuous peritoneal dialysis (PD). Methods In this single-center retrospective cohort study, incident diabetic PD patients from January 1, 2006, to December 31, 2010, were recruited, and followed up until December 31, 2011. The effect of HbA1c and Alb-GSP on mortality was evaluated by Cox proportional hazards models. Results A total of 200 patients (60% male, mean age 60.3 ± 10.6 years) with a mean follow-up of 29.0 months (range: 4.3 - 71.5 months) were recruited. Sixty-four patients died during the follow-up period, of whom 21 died of cardiovascular disease (CVD). Mean values for HbA1c, GSP and Alb-GSP were 6.7% (range: 4.1 - 12.5%), 202 μmol/L (range: 69 - 459 μmol/L), and 5.78 μmol/g (range: 2.16 - 14.98 μmol/g), respectively. The concentrations of GSP and Alb-GSP were closely correlated with HbA1c ( r = 0.41, p < 0.001 and r = 0.45, p < 0.001, respectively). In multivariate Cox proportional hazards models, patients with HbA1c ≥8% were associated with increased risk of all-cause mortality (hazard ratio [HR] = 2.29, 95% confidence interval [CI]: 1.06 - 4.96, p = 0.04), but no increased mortality in patients with 6.0% ≤ HbA1c ≤ 7.9%. Patients with Alb-GSP ≤ 4.50 μmol/g had increased all-cause and non-cardiovascular mortality (HR = 2.42, 95% CI: 1.13 - 5.19, p = 0.02; and HR = 2.98, 95% CI: 1.05 - 8.48, p = 0.04 respectively). Conclusions Increased HbA1c and decreased Alb-GSP may be associated with poorer survival in diabetic PD patients, with a non-significant trend observed for poorer survival with the highest level of Alb-GSP.


Circulation ◽  
2013 ◽  
Vol 127 (suppl_12) ◽  
Author(s):  
Ashim Hajra ◽  
Yan Li ◽  
Stanton Siu ◽  
Natalia Udaltsova ◽  
Mary Anne Armstrong ◽  
...  

INTRODUCTION: The number of Asian Americans (Asians) has increased substantially in recent decades, yet prospective data about their risk for coronary artery disease (CAD) remain sparse. We hypothesized significant disparities of CAD risk among Asians. METHODS: A multi-ethnic population of 126,088 adults in Northern California supplied baseline data from 1978-1985. Self-classified ethnicity yielded 13,448 (10.6%) Asians including 5,951 Chinese (CH), 1,676 Japanese (JA), 4,236 Filipinos (FI), 689 South Asians (SA) (mostly Asian Indians), and 896 Other Asians (OA). Persons with incident CAD hospitalizations through 2008 numbered 7,658, including 700 Asians. Analyses used Cox proportional hazards models which included age, sex, ethnicity, smoking, alcohol, body mass index, education, marital status, and a composite of possible baseline CAD history/symptoms/risk factors. Models with various referents enabled comparison of all Asian groups to each other as well as to whites, blacks, or Hispanics. These models yielded hazard ratios (HR) and 95% confidence intervals (CI). RESULTS: With whites as referent the adjusted HR (CI) for all Asians was 1.0 (0.9-1.0). In a separate model the HRs were: CH = 0.8 (0.7-0.9, p<0.001), JA = 0.9 (0.7-1.1), FI = 1.2 (1.0-1.3, p=0.02); SA = 2.4 (1.9-3.2, p<0.001), and OA = 0.8 (0.5-1.1). Addition of blood pressure, total cholesterol, blood glucose, or leukocyte count to the models had minimal effect on the magnitude of these HRs. SAs were at substantially higher risk than whites, blacks, Hispanics, and each other Asian group with HRs ranging from 2.2 to 3.3 (all p values < 0.001). FI were at a higher risk than all groups except for SA, with HRs ranging from 1.3-1.7 (all p values <0.04). The table gives HRs for Asian groups vs. CH. CONCLUSION: Disparities in CAD risk among Asian American ethnic groups are marked, indicating the need to study disease outcomes separately for the groups. The high risks of SAs and FIs mandate further investigation into causes and targeted public health measures.


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