Association between cardiovascular diseases and osteoporosis-reappraisal.
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ABSTRACT:
SUBMITTER: Szulc P
PROVIDER: S-EPMC3727856 | biostudies-other | 2012
REPOSITORIES: biostudies-other
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Project description:Age was a modifier of the independent association between hyponatremia and osteoporosis (OP). Risk of OP was the highest in the youngest age group as compared to older patients. A longer duration of hyponatremia revealed a similar association with OP in all anatomical sites.Epidemiologic studies provide conflicting results on the relationship between hyponatremia and OP. Our aim is to test the modification effect of age on the relationship between hyponatremia and OP at various anatomical sites in a large patient population.This is a cross-sectional observation of consecutive patients with available bone densitometry, demographic, clinical, and laboratory data from 2001 to 2013 at a single center. OP was defined as a bone mineral density of ?2.5 standard deviations below the mean peak bone mass of young, healthy adults. Hyponatremia was defined as serum sodium ?135 mmol/L. Multiple logistic regressions were used to calculate adjusted odds ratio (OR).Overall, 24,784 patients were included. There were 4549 males (18.4 %). Hyponatremia was present in 703 patients (2.8 %), femoral neck OP in 2603 (10.5 %), total hip OP in 1885 (7.5 %), and lumbar OP in 4830 (19.5 %). Total hip OP occurred in 17.6 % (n?=?124) of patients with hyponatremia as compared to 6.6 % (n?=?880) of patients with sodium level of "140-145" mmol/L (P?<?0.001). After multivariable adjustments, hyponatremia was associated with 2.46-fold higher odds of total hip OP (95 % CI, 1.36 to 4.46) in age <55 years, 1.96-fold (1.13 to 3.41) in age 55 to 67 years, and 1.55-fold (1.13 to 2.12) in age >67 years (age-sodium category interaction P value?=?0.002).Age appeared as a modifier of the independent association between hyponatremia and OP. Risk of OP was the highest in the youngest age group as compared to older patients.
| S-EPMC4856473 | biostudies-literature
Project description:Observational studies have revealed that dental diseases such as periodontitis and dental caries increase the risk of cardiovascular diseases (CVDs). However, the causality between periodontal disease (PD) and CVDs is still not clarified. In the present study, two-sample Mendelian randomization (MR) studies were carried out to assess the association between genetic liability for periodontal diseases (dental caries and periodontitis) and major CVDs, including coronary artery disease (CAD), heart failure (HF), atrial fibrillation (AF), and stroke-including ischemic stroke as well as its three main subtypes-based on large-scale genome-wide association studies (GWASs). Our two-sample MR analyses did not provide evidence for dental caries and periodontitis as the causes of cardiovascular diseases; sensitivity analyses, including MR-Egger analysis and weighted median analysis, also supported this result. Gene functional annotation and pathway enrichment analyses indicated the common pathophysiology between cardiovascular diseases and periodontal diseases. The associations from observational studies may be explained by shared risk factors and comorbidities instead of direct consequences. This also suggests that addressing the common risk factors-such as reducing obesity and improving glucose tolerance-could benefit both conditions.
| S-EPMC8775300 | biostudies-literature
Project description:ImportanceIt is uncertain whether depressive symptoms are independently associated with subsequent risk of cardiovascular diseases (CVDs).ObjectiveTo characterize the association between depressive symptoms and CVD incidence across the spectrum of lower mood.Design, setting, and participantsA pooled analysis of individual-participant data from the Emerging Risk Factors Collaboration (ERFC; 162 036 participants; 21 cohorts; baseline surveys, 1960-2008; latest follow-up, March 2020) and the UK Biobank (401 219 participants; baseline surveys, 2006-2010; latest follow-up, March 2020). Eligible participants had information about self-reported depressive symptoms and no CVD history at baseline.ExposuresDepressive symptoms were recorded using validated instruments. ERFC scores were harmonized across studies to a scale representative of the Center for Epidemiological Studies Depression (CES-D) scale (range, 0-60; ≥16 indicates possible depressive disorder). The UK Biobank recorded the 2-item Patient Health Questionnaire 2 (PHQ-2; range, 0-6; ≥3 indicates possible depressive disorder).Main outcomes and measuresPrimary outcomes were incident fatal or nonfatal coronary heart disease (CHD), stroke, and CVD (composite of the 2). Hazard ratios (HRs) per 1-SD higher log CES-D or PHQ-2 adjusted for age, sex, smoking, and diabetes were reported.ResultsAmong 162 036 participants from the ERFC (73%, women; mean age at baseline, 63 years [SD, 9 years]), 5078 CHD and 3932 stroke events were recorded (median follow-up, 9.5 years). Associations with CHD, stroke, and CVD were log linear. The HR per 1-SD higher depression score for CHD was 1.07 (95% CI, 1.03-1.11); stroke, 1.05 (95% CI, 1.01-1.10); and CVD, 1.06 (95% CI, 1.04-1.08). The corresponding incidence rates per 10 000 person-years of follow-up in the highest vs the lowest quintile of CES-D score (geometric mean CES-D score, 19 vs 1) were 36.3 vs 29.0 for CHD events, 28.0 vs 24.7 for stroke events, and 62.8 vs 53.5 for CVD events. Among 401 219 participants from the UK Biobank (55% were women, mean age at baseline, 56 years [SD, 8 years]), 4607 CHD and 3253 stroke events were recorded (median follow-up, 8.1 years). The HR per 1-SD higher depression score for CHD was 1.11 (95% CI, 1.08-1.14); stroke, 1.10 (95% CI, 1.06-1.14); and CVD, 1.10 (95% CI, 1.08-1.13). The corresponding incidence rates per 10 000 person-years of follow-up among individuals with PHQ-2 scores of 4 or higher vs 0 were 20.9 vs 14.2 for CHD events, 15.3 vs 10.2 for stroke events, and 36.2 vs 24.5 for CVD events. The magnitude and statistical significance of the HRs were not materially changed after adjustment for additional risk factors.Conclusions and relevanceIn a pooled analysis of 563 255 participants in 22 cohorts, baseline depressive symptoms were associated with CVD incidence, including at symptom levels lower than the threshold indicative of a depressive disorder. However, the magnitude of associations was modest.
| S-EPMC7739139 | biostudies-literature
Project description:Combinations of anabolic and antiresorptive agents have potential to improve bone density and bone strength more than either agent alone. A large number of relatively small clinical trials have been performed evaluating combinations of PTH1-34 or PTH1-84 with a variety of antiresorptives, including hormone/estrogen therapy, raloxifene, alendronate (Aln), risedronate, ibandronate, zoledronic acid and denosumab (Dmab). Most of the studies evaluate dual-X-ray densitometry outcomes, with a few trials reporting volumetric bone mineral density (BMD) by quantitative computed tomography followed by finite element modeling of bone strength. None of the studies has been powered to assess differences in fracture incidence between combination therapy and monotherapy. BMD outcomes vary depending on the timing of introduction of the anabolic agent (before, during or after antiresorptive treatment), as well as according to the specific anabolic and antiresorptive used. Furthermore, effects of combination therapies are site dependent. The most consistent effect of combining antiresorptive agents with parathyroid hormone (PTH) is a superior hip BMD outcome compared with PTH alone. This is most evident when PTH is combined with a bisphosphonate or Dmab. In contrast to findings in the hip, in the majority of studies there is no benefit to spine BMD with combination therapy when compared with monotherapy. The two exceptions to this are when PTH is combined with Dmab and when PTH is given as monotherapy first for 9 months followed by the addition of Aln and continuation of PTH as combination treatment. On the basis of what we now know, in patients on bisphosphonates who suffer hip fractures or who have very low hip BMD, strong consideration should be given to starting teriparatide and continuing a bisphosphonate (possibly switching to zoledronic acid or even Dmab) to maximize hip BMD and strength. Furthermore, in treatment-naive individuals with very severe osteoporosis, such as those with spine and hip fractures, combination therapy with PTH and Dmab or PTH followed by combination treatment with a potent bisphosphonate or Dmab should be considered to maximize early increases in BMD.
| S-EPMC4007166 | biostudies-other
Project description:BackgroundRecent studies have indicated that several critical illnesses are associated with an increased risk of cardiovascular diseases (CVDs). Nonetheless, studies of the association between heat-related illnesses (HRIs) and subsequent CVDs are still limited. We sought to evaluate whether heat stroke (HS) was associated with an increased CVD incidence.MethodsThe data from the nationwide, population-based, retrospective, cohort study described herein were obtained from the National Health Insurance Research Database in Taiwan. The outcome evaluated in this study was the cumulative incidence of CVDs, which was compared between patients with HS, patients with other HRIs and a control group during a 14-year follow-up period.ResultsOur analyses included 150 HS cases, 150 patients with other HRIs and 150 patients without HRIs. The HS patients had a significantly higher incidence of developing CVDs than the other HRI and control patients (32.67% vs. 23.33% vs. 16.67%, p = 0.005). Patients with HS had an increased incidence of acute myocardial infarction (AMI) compared with that of the controls (6% vs. 2.67%, p = 0.042) and an increased incidence of acute ischemic stroke (AIS) compared with those of the other HRI and control patients (12% vs. 6% vs. 4.67%, p = 0.038). An increased risk of chronic kidney disease (CKD) was also found in the patients with HS and other HRIs compared to that in the controls (17.33% vs. 14.67% vs. 6.67%, p = 0.016).ConclusionPrior HS was associated with an increased incidence of CVDs, particularly AMI and AIS, and an increased incidence of CKD.
| S-EPMC6373898 | biostudies-literature
Project description:Osteoporosis is the most common and serious age-related skeletal disorder, characterized by a low bone mass and bone microarchitectural deterioration, with a consequent increase in bone fragility and susceptibility to spontaneous fractures, and it represents a major worldwide health care problem with important implications for health care costs, morbidity and mortality. Today is well accepted that osteoporosis is a multifactorial disorder caused by the interaction between environment and genes that singularly exert modest effects on bone mass and other aspects of bone strength and fracture risk. The individuation of genetic factors responsible for osteoporosis predisposition and development is fundamental for the disease prevention and for the setting of novel therapies, before fracture occurrence. In the last decades the interest of the Scientific Community has been concentrated in the understanding the genetic bases of this disease but with controversial and/or inconclusive results. This review tries to summarize data on the most representative osteoporosis candidate genes. Moreover, since recently osteoporosis and cardiovascular diseases have shown to share common physiopathological mechanisms, this review also provides information on the current understanding of osteoporosis and cardiovascular diseases common genetic bases.
| S-EPMC2949079 | biostudies-literature
Project description:ObjectiveThis study aimed to investigate the associations between osteoporosis, biochemical indexes, bone mineral density (BMD), and cardiovascular disease.MethodsA cross-sectional study design was used to examine the relationships between these parameters. Logistic regression and correlation analyses were conducted to assess the associations between elevated levels of triglyceride, total cholesterol, low-density lipoprotein (LDL), high-density lipoprotein (HDL), homocysteine, and the presence of osteoporosis. Additionally, correlations between BMD and biochemical indexes were analyzed. The incidence of cardiovascular disease and its correlation with BMD were evaluated. Receiver operating characteristic (ROC) analysis was performed to determine the utility of BMD in identifying cardiovascular disease.ResultsThe results revealed that elevated triglyceride, total cholesterol, and LDL levels were positively associated with osteoporosis, while higher HDL levels and homocysteine were negatively associated. Correlation analysis demonstrated negative correlations between triglyceride levels and BMD, and positive correlations between total cholesterol and HDL levels with BMD. LDL levels showed a weak negative correlation, and homocysteine levels exhibited a strong negative correlation with BMD. The osteoporosis group had lower BMD and a higher incidence of cardiovascular disease compared to the non-osteoporosis group. Logistic regression analysis confirmed the correlation between lower BMD and increased risk of cardiovascular disease.ConclusionThis study provides evidence supporting the associations between osteoporosis, biochemical indexes, BMD, and cardiovascular disease. Aberrations in lipid profiles and homocysteine levels may contribute to osteoporosis development. Lower BMD, particularly in individuals with osteoporosis, appears to increase the risk of cardiovascular disease. BMD shows promise as a diagnostic tool for identifying individuals at risk of cardiovascular disease. Further research is needed to elucidate the underlying mechanisms and establish the clinical implications of these relationships. Future longitudinal studies are necessary to determine causality and long-term prognostic implications.
| S-EPMC10712301 | biostudies-literature
Project description:Objectives:This study assessed whether the physical component summary score of the RAND-36 health-related quality-of-life survey was associated with incidence of coronary heart disease, stroke, congestive heart failure, angina, or peripheral arterial disease, and whether baseline chronic conditions modified these associations. Methods:Analysis was limited to 69,155 postmenopausal women (50-79?years) in the Women's Health Initiative Study who had complete data on the RAND-36, the outcomes, and covariates. Chronic conditions were defined as blood pressure ?140/90?mm or self-reported heart disease, diabetes, hypertension, arthritis, asthma, emphysema, cancer, and/or cholesterol-reducing medication use. Outcomes data were ascertained during follow-up (1993-2005) with medical records. Results:There were 2451 coronary heart disease, 1896 stroke, 1533 congestive heart failure, 1957 angina, and 502 peripheral arterial disease events during follow-up (median 8.2?years). Participants in the lowest physical component summary quintile, compared to the highest, had a significantly higher risk of developing coronary heart disease (hazard ratio (95% confidence interval) 2.0 (1.7, 2.3)), stroke (1.8 (1.5, 2.2)), angina (2.4(2.0, 2.9)), and peripheral arterial disease (3.0 (2.0, 4.4)), irrespective of chronic conditions. Interactions between physical component summary and existing chronic conditions were not significant for any outcome except congestive heart failure (p?=?0.005); after adjustment, participants in the lowest physical component summary quintile and with any chronic condition had nearly a twofold higher risk of congestive heart failure (Yes?=?4.4 (3.3, 5.8) vs No?=?2.4 (1.2, 4.3)). Conclusion:We found a low physical component summary score was a significant risk factor for individual cardiovascular disease incidence in postmenopausal women.
| S-EPMC6041849 | biostudies-literature
Project description:Background Cardiovascular diseases (CVD), including coronary heart disease (CHD), heart failure, ischemic heart disease (IHD), and atrial fibrillation, are prevalent in the aged. However, the influence of CVD on ED is less investigated. This study was performed to clarify the causal association between CVD and ED. Materials and methods Genome-wide association studies (GWAS) datasets targeting CHD, heart failure, IHD, and atrial fibrillation were downloaded to retrieve single nucleotide polymorphisms (SNPs). Further, single-variable Mendelian randomization and multivariable Mendelian randomization (MVMR) were adopted to explore the causal association between CVD and ED. Results Genetically predicted CHD and heart failure were found to increase the risks of ED (OR = 1.09, P < 0.05 and OR = 1.36, P < 0.05, respectively). However, no causal association was disclosed among IHD, atrial fibrillation and ED (all P > 0.05). These findings remained consistent in sensitivity analyses. After controlling for body mass index, alcohol, low density lipoprotein, smoking and total cholesterol levels, the results of MVMR support the causal role of CHD on ED (P < 0.05). Similarly, the direct causal effect estimates of heart failure on ED were significant in MVMR analyses (P < 0.05). Conclusion Using genetic data, this study revealed that genetically predicted CHD and heart failure may predict better ED compared with atrial fibrillation and IHD. The results should be interpreted with caution and the insignificant causal inference of IHD still needs further verification in future studies.
| S-EPMC9947236 | biostudies-literature
Project description:BackgroundExcessive daytime sleepiness (EDS), experienced in 10% to 20% of the population, has been associated with cardiovascular disease and death. However, the condition is heterogeneous and is prevalent in individuals having short and long sleep duration. We sought to clarify the relationship between sleep duration subtypes of EDS with cardiovascular outcomes, accounting for these subtypes.Methods and resultsWe defined 3 sleep duration subtypes of excessive daytime sleepiness: normal (6-9 hours), short (<6 hours), and long (>9 hours), and compared these with a nonsleepy, normal-sleep-duration reference group. We analyzed their associations with incident myocardial infarction (MI) and stroke using medical records of 355 901 UK Biobank participants and performed 2-sample Mendelian randomization for each outcome. Compared with healthy sleep, long-sleep EDS was associated with an 83% increased rate of MI (hazard ratio, 1.83 [95% CI, 1.21-2.77]) during 8.2-year median follow-up, adjusting for multiple health and sociodemographic factors. Mendelian randomization analysis provided supporting evidence of a causal role for a genetic long-sleep EDS subtype in MI (inverse-variance weighted β=1.995, P=0.001). In contrast, we did not find evidence that other subtypes of EDS were associated with incident MI or any associations with stroke (P>0.05).ConclusionsOur study suggests the previous evidence linking EDS with increased cardiovascular disease risk may be primarily driven by the effect of its long-sleep subtype on higher risk of MI. Underlying mechanisms remain to be investigated but may involve sleep irregularity and circadian disruption, suggesting a need for novel interventions in this population.
| S-EPMC10863774 | biostudies-literature