Analysis of Biological Aging and Risks of All-Cause and Cardiovascular Disease-Specific Death in Cancer Survivors.
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ABSTRACT:
SUBMITTER: Zhang D
PROVIDER: S-EPMC9218849 | biostudies-literature | 2022 Jun
REPOSITORIES: biostudies-literature
Publications
Analysis of Biological Aging and Risks of All-Cause and Cardiovascular Disease-Specific Death in Cancer Survivors.
Zhang Dongyu D Leeuwenburgh Christiaan C Zhou Daohong D Gong Yan Y Pahor Marco M Licht Jonathan D JD Braithwaite Dejana D
JAMA network open 20220601 6
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Project description:Background: Thyroid cancer is the most rapidly increasing cancer in the United States, affects a young population, has high survival, and is one of the most common cancers in people under age 40. The aim of this study was to examine the risks of aging-related diseases in a statewide sample of thyroid cancer survivors who were diagnosed <40 years compared with those diagnosed ≥40 and a cancer-free sample.Methods: Thyroid cancer survivors diagnosed 1997 to 2012 were matched to up to 5 cancer-free individuals on birth year, sex, birth state, using the statewide Utah Population Database. Medical records were used to identify disease diagnoses stratified over three time periods: 1 to 5, >5 to 10, and 10+ years after cancer diagnosis. Cox proportional hazards models were used to estimate hazard ratios with adjustment on matching factors, race, body mass index, and Charlson Comorbidity Index.Results: There were 3,706 thyroid cancer survivors and 15,587 matched cancer-free individuals (1,365 cases diagnosed <40 years old). Both age groups had increased risks for multiple circulatory health conditions 1 to 5 years after cancer diagnosis compared with cancer-free individuals. Survivors <40 had a higher risk of hypertension, cardiomyopathy, and nutritional deficiencies.Conclusions: Increased risks for diseases associated with aging were observed for both age groups, with younger thyroid cancer survivors having higher risks for select diseases.Impact: As thyroid cancer survivors in this study were found to have increased risks for aging-related diseases, future studies are needed to assess what can be done to reduce the increased risks of these long-term health effects. Cancer Epidemiol Biomarkers Prev; 26(12); 1695-704. ©2017 AACR.
| S-EPMC5903447 | biostudies-literature
Project description:Background and objectivesCKD is an important risk factor for cardiovascular disease (CVD) and death. We investigated whether select urine kidney injury biomarkers were associated with higher risk of heart failure (HF), CVD, and death in persons with CKD enrolled in the Chronic Renal Insufficiency Cohort (CRIC) Study.Design, setting, participants, & measurementsUrine kidney injury molecule-1 (KIM-1), neutrophil gelatinase-associated lipocalin, liver fatty acid-binding protein, and N-acetyl-β-d-glucosaminidase were measured in urine of a subset of CRIC participants (n=2466). We used Cox proportional hazards regression to examine associations between these biomarkers indexed to urinary creatinine (Cr) and (1) HF, (2) a composite of atherosclerotic CVD events (myocardial infarction, ischemic stroke, or peripheral artery disease), and (3) all-cause death.ResultsAt baseline, mean age of study participants was 59.5±10.8 years, 46% were women, and 34% had a self-reported history of any CVD. Median follow-up was 6.5 (interquartile range, 5.6-6.8) years. A total of 333 HF events, 282 atherosclerotic CVD events, and 440 deaths were observed during a median follow-up of 6.5 (interquartile range, 5.6-6.8) years. Those in the highest two quintiles of KIM-1/Cr levels had a higher risk of HF relative to the lowest quintile (quintile 5 versus quintile 1 adjusted hazard ratio [aHR] of 1.73 [95% confidence interval, 1.05 to 2.85]). N-acetyl-β-d-glucosaminidase/Cr was associated with HF in continuous analyses (aHR per log SD higher 1.18 [95% confidence interval, 1.01 to 1.38]). Only KIM-1/Cr was independently associated with atherosclerotic CVD events (aHR per log SD higher 1.21 [95% confidence interval, 1.02 to 1.41]), whereas both KIM-1/Cr (quintile 5 versus quintile 1 aHR of 1.56 [95% confidence interval, 1.06 to 2.31]) and neutrophil gelatinase-associated lipocalin/Cr (quintile 5 versus quintile 1 aHR of 1.82 [95% confidence interval, 1.19 to 2.8]) were associated with all-cause death.ConclusionsSelected urine kidney injury biomarkers were independently associated with higher risk of HF, CVD events, and death in CRIC. Among the biomarkers examined, only KIM-1/Cr was associated with each outcome. Further work is needed to determine the utility of these biomarkers to improve risk prediction for these adverse outcomes.
| S-EPMC5477212 | biostudies-literature
Project description:ObjectivesIndividuals with prior cancer diagnosis are more likely to have low muscle mass (LMM) than their cancer-free counterparts. Understanding the effects of LMM on the prognosis of cancer survivors can be clinically important. The aim of this study was to investigate whether risks for all-cause and cardiovascular disease (CVD)-specific mortality differ by status of LMM in cancer survivors and a matched cohort without cancer history.MethodsWe used cohort data from the 1999-2006 and 2011-2014 National Health and Nutrition Examination Survey. Participants included 946 adults surviving for ≥1 since cancer diagnosis and a matched cohort (by age, sex, and race) without cancer history (N = 1857). LMM was defined by appendicular lean mass and body height (men <7.26 kg/m2, women <5.45 kg/m2). Death was ascertained via the National Death Index and cause of death was assessed via International Classification of Diseases, Tenth Revision. Multivariable Cox proportional hazards models were used to estimate adjusted hazard ratio (aHR) and 95% confidence interval (CI) of LMM.ResultsThe mean age of cancer survivors and matched cohort was 60.6 y (SD 15) and 60.2 y (SD 14.9), respectively. The median follow-up was 10.5 y for survivors and 10.9 y for matched cohort. Overall, 22.2% of cancer survivors and 19.7% of the matched cohort had LMM, respectively. In all, 321 survivors (33.9%) and 495 participants (26.7%) in the matched cohort died during follow-up. CVD-specific deaths were identified in 58 survivors (6.1%) and 122 participants in the matched cohort (6.6%). The multivariable Cox model suggested that LMM was positively associated with all-cause (aHR, 1.73; 95% CI, 1.31-2.29) and CVD-specific (aHR, 2.13; 95% CI, 1.14-4.00) mortality in cancer survivors. The associations between LMM and risk for all-cause (aHR, 1.24; 95% CI, 0.98-1.56) and CVD-specific (aHR, 1.21; 95% CI, 0.75-1.93) mortality were not statistically significant in the matched cohort.ConclusionCancer survivors with LMM have an increased risk for all-cause and CVD-specific mortality. This increase appears to be larger than that in counterparts without cancer history.
| S-EPMC10753936 | biostudies-literature
Project description:BackgroundCancer survivors are at an increased risk of cardiovascular disease (CVD) compared with the general population. We sought to evaluate the impact of mosaic chromosomal alterations (mCA) on death of CVD causes, coronary artery disease (CAD) causes, and of any cause in patients with a cancer diagnosis.MethodsThe study was a prospective cohort analysis of 48,919 UK Biobank participants with a cancer diagnosis. mCAs were characterized using DNA genotyping array intensity data and long-range chromosomal phase inference. Multivariable Cox regression models were used to ascertain the associations of mCAs. Exploratory endpoints included various incident cardiovascular phenotypes.ResultsOverall, 10,070 individuals (20.6%) carried ≥ 1 mCA clone. In adjusted analyses, mCA was associated with an increased risk of death of CAD causes [HR, 1.37; 95% confidence interval (CI), 1.09-1.71; P = 0.006]. In sub-analyses, we found that carriers of mCAs diagnosed with kidney cancer had an increased risk of death of CVD causes (HR, 2.03; 95% CI, 1.11-3.72; P = 0.022) and CAD causes (HR, 3.57; 95% CI, 1.44-8.84; P = 0.006). Women diagnosed with breast cancer who carried a mCA also had a higher risk of death of CAD causes (HR, 2.46; 95% CI, 1.23-4.92; P = 0.011).ConclusionsAmong cancer survivors, carriers of any mCA are at an increased risk of CAD death compared with noncarriers. Mechanistic studies should be considered to better ascertain the biological mechanisms underneath the observed associations between mCAs and cardiovascular events for specific cancer types.ImpactThere may be clinical relevance in considering mCAs in patients diagnosed with cancer and undergoing treatment.
| S-EPMC10233351 | biostudies-literature
Project description:BackgroundWith continuous increases in survival rates following breast cancer (BC) diagnosis, the challenge of multiple primary cancers has become an issue. The data on familial risk of SPCs after BC diagnosis and the related mortality in BC patients are scarce.MethodsA total of 87 752 female BC patients were followed for SPC diagnoses and records of death. Relative risks (RRs) of SPC in BC patients who had first-degree relatives (parents or siblings) affected by the same cancer were compared to the patients without family history. Causes of death were compared between patients with and without SPC.ResultsAfter a median follow-up of 5 years, 14 952 BC patients developed SPCs, among which 10 280 (68.8%) had first-degree relatives diagnosed with cancer. Familial risks were significant for 14 site-specific SPCs, and the highest risk was for second ovarian cancer (RR = 6.28, 95%CI: 4.50-8.75), compared to those without family history (1.49, 1.34-1.65). In patients with SPC, SPC was the main cause of death, including diverse cancers and BC in approximately equal proportions.ConclusionsFamily history contributed to the excess number of patients with SPCs, and SPC was the leading cause of death in patients with SPC. Taking family history at diagnosis of BC may provide warning signs with regard to possible subsequent SPCs and may offer possibilities for counseling, intervention and management.
| S-EPMC6346247 | biostudies-literature
Project description:BackgroundDespite no sufficient evidence on benefits and harms of multivitamin use, cancer survivors use multivitamins as a self-care strategy to improve or maintain health. We examined if multivitamin use was associated with mortality in cancer survivors.Methods15,936 male and 7026 female cancer survivors in the NIH-AARP Diet and Health Study were included in the analysis. Types and frequency of multivitamin use at on average 4.6 years after cancer diagnosis were assessed. Multivariable-adjusted relative risks (RR) and 95% confidence intervals (CI) were estimated using Cox proportional hazards regression models.ResultsMultivitamin use was not associated with lower all-cause mortality risk in all female (RR = 0.94, 95% CI:0.87-1.01 daily vs. no use) or male cancer survivors (RR = 0.96, 95% CI:0.91-1.00); however, a modest inverse association for CVD mortality was observed in female survivors of reproductive cancers (RR = 0.75, 95% CI:0.61-0.92) and male survivors of non-reproductive cancers (RR = 0.81, 95% CI:0.70-0.94). Multivitamin use was also associated with a lower risk of cancer-specific mortality in survivors of skin (RR = 0.65, 95% CI:0.48-0.88) and breast (RR = 0.79, 95% CI:0.65-0.95) cancer.DiscussionMultivitamin use may provide a modest survival benefit to some cancer survivors. Cancer care providers should talk with cancer survivors about potential benefits and harms of multivitamin use.
| S-EPMC10781735 | biostudies-literature
Project description:BackgroundLife's Essential 8 (LE8), an indicator of cardiovascular health (CVH), can predict overall and cardiovascular mortality in the general population. Considering that cancer survivors have a higher risk of cardiovascular disease (CVD), our study aimed to investigate the association between LE8 and the prognosis of cancer survivors.MethodsA total of 2191 cancer survivors were included from the National Health and Nutrition Examination Survey (2005-2018). LE8 scores, derived from eight individual metrics, were categorized into three groups: low (0-49), moderate (50-79), and high (80-100). Cox regression analysis, nonlinear analysis, sensitivity analysis, and subgroup analysis were conducted to explore the association between LE8 scores and mortality risks, adjusting for potential confounders.ResultsDuring a median follow-up of six years, 479 deaths were recorded, including 118 CVD events and 156 cancer events. LE8 scores showed an inverse linear relationship with all-cause and cardiovascular mortality. A 10-point increase in LE8 scores was associated with a 25 % reduction in all-cause mortality (hazard ratio [HR], 0.75; 95 % CI, 0.66-0.85) and a 29 % reduction in cardiovascular mortality (HR, 0.71; 95 % CI, 0.57-0.89). Additionally, moderate CVH was linked to a lower risk of all-cause mortality (HR, 0.55; 95 % CI, 0.37-0.81), while high CVH was associated with an even lower risk (HR, 0.35; 95 % CI, 0.19-0.68). Similarly, moderate CVH demonstrated a decreased risk of cardiovascular mortality (HR, 0.31; 95 % CI, 0.15-0.63), with high CVH showing an even lower risk (HR, 0.23; 95 % CI, 0.09-0.58). However, LE8 scores was not associated with cancer-specific mortality.ConclusionsA higher LE8 score was independently associated with a decreased risk of both all-cause and cardiovascular mortality in cancer survivors, underscoring the significance of optimizing CVH during the survivorship phase of cancer care.
| S-EPMC11401234 | biostudies-literature
Project description:In both cardiovascular disease and cancer, there are established sex-based differences in prevalence and outcomes. Males and females may also differ in terms of risk of cardiotoxicity following cancer therapy, including heart failure, cardiomyopathy, atherosclerosis, thromboembolism, arrhythmias, and myocarditis. Here, we describe sex-based differences in the epidemiology and pathophysiology of cardiotoxicity associated with anthracyclines, hematopoietic stem cell transplant (HCT), hormone therapy and immune therapy. Relative to males, the risk of anthracycline-induced cardiotoxicity is higher in prepubertal females, lower in premenopausal females, and similar in postmenopausal females. For autologous hematopoietic cell transplant, several studies suggest an increased risk of late heart failure in female lymphoma patients, but sex-based differences have not been shown for allogeneic hematopoietic cell transplant. Hormone therapies including GnRH (gonadotropin-releasing hormone) modulators, androgen receptor antagonists, selective estrogen receptor modulators, and aromatase inhibitors are associated with cardiotoxicity, including arrhythmia and venous thromboembolism. However, sex-based differences have not yet been elucidated. Evaluation of sex differences in cardiotoxicity related to immune therapy is limited, in part, due to low participation of females in relevant clinical trials. However, some studies suggest that females are at increased risk of immune checkpoint inhibitor myocarditis, although this has not been consistently demonstrated. For each of the aforementioned cancer therapies, we consider sex-based differences according to cardiotoxicity management. We identify knowledge gaps to guide future mechanistic and prospective clinical studies. Furthering our understanding of sex-based differences in cancer therapy cardiotoxicity can advance the development of targeted preventive and therapeutic cardioprotective strategies.
| S-EPMC8915444 | biostudies-literature
Project description:BackgroundIndividual unhealthy sleep behaviours have been associated with increased risks of all-cause mortality and deaths due to cardiovascular disease (CVD) or cancer. The evidence regarding the association of sleep patterns with these risks is limited.ObjectiveTo examine the associations of sleep patterns with all-cause, CVD and cancer mortality in a large prospective cohort.MethodsThis prospective cohort study included 283,443 adults from UK Biobank without CVD and cancer at baseline. We created a healthy sleep score and sleep patterns combining five individual sleep behaviours.ResultsDuring a mean (standard deviation) of 8.9 (1.1) years (2.5 million person-years) of follow up, a total of 7936 all-cause deaths, 762 CVD-caused deaths, and 4540 cancer-caused deaths occurred during follow up. One point increase of the healthy sleep score was associated with a 4-11% lower risk of all-cause mortality (Hazard Ratio [HR], 0.94; 95% CI, 0.92-0.96), CVD mortality (HR, 0.89; 95% CI, 0.83-0.95) and cancer mortality (HR, 0.96; 95% CI, 0.93-0.99), with adjustment for age, sex, assessment centres, smoking status, alcohol intake status, socioeconomic status and physical activity. Compared with participants with an unfavourable sleep pattern, those with a favourable sleep pattern had 24-42% lower risks of all-cause and CVD mortality. The association with all-cause mortality tended to be stronger among underweight participants and those with insufficient physical activity.ConclusionsA healthy sleep pattern was associated with lower risks of all-cause mortality and mortality from CVD and cancer. Our findings highlight the importance of improving overall sleep behaviours in lowering mortality.
| S-EPMC8688171 | biostudies-literature
Project description:IntroductionYoung cancer survivors may be at increased risk of early-onset chronic health conditions. The aim of this population-based study is to estimate cardiovascular disease (CVD) risk among younger versus older B-cell non-Hodgkin's lymphoma (B-NHL) survivors compared with their respective general population cohorts.MethodsB-NHL survivors diagnosed from 1997 to 2015 in the Utah Cancer Registry were matched with up to five cancer-free individuals on birth year, sex, and birth state, using the statewide Utah Population Database. Electronic medical records and statewide health care facility data were used to identify disease outcomes ≥5 years after cancer diagnosis. Cox Proportional Hazards models were used to estimate hazard ratios for B-NHL survivors diagnosed at <65 years and ≥65 years old.ResultsYounger B-NHL survivors had higher relative risks than older cancer survivors of chronic rheumatic disease of the heart valves (HR = 4.14, 99% CI = 2.17-7.89; P valueheterogeneity = 0.004); peri-, endo-, and myocarditis (HR = 2.43, 99% CI = 1.38-4.28; P valueheterogeneity = 0.016); diseases of the arteries (HR = 1.63, 99% CI = 1.21-2.21; P valueheterogeneity = 0.044); and hypotension (HR = 2.44, 99% CI = 1.58-3.75; P valueheterogeneity = 0.048). B-NHL survivors of both age groups had elevated relative risks of heart disease overall and congestive heart failure.ConclusionYounger B-NHL survivors had higher risks than older B-NHL survivors of specific cardiovascular diseases compared to their respective general population cohorts.
| S-EPMC8209610 | biostudies-literature