1,721,150 research outputs found
Lipoprotein alterations and reduced growth hormone secretion: relationships with obesity and cardiovascular risk
No full textCardiotoxicity and cancer therapy
No full textA fundamental concept of treatment is to do no harm. However, with cancer treatment this is not always possible.
Chemotherapy is associated with cardiovascular (CV) complications.1,2 This risk is even greater in the elderly patients and patients with established CV disease. More specifically, tachyarrhythmias (eg, cisplatin), bradyarrythmias (eg, paclitaxel), or QT prolongation (eg, dasatinib) have been reported. Furthermore, myocardial necrosis, coronary vaso-occlusion or vasospasm, pericardial disease (eg, cytarabine), endocardial fibrosis (eg, busulfan), and heart failure can occur. Hypotension (eg, fludarabine) or hypertension (eg, vinca alkaloids) has also been reported.1,2 Cardiotoxicity, endothelial injury, and Takotsubo syndrome have been reported in patients treated with 5-fluorouracil (5-FU).3⇓–5 Cardiotoxicity to 5-FU was reported 35 years ago.3⇓–5 Cardiotoxicity of chemotherapy has been reported in patients ranging from children through adults (eg, with anthracyclines or cisplatin).6 Adriamycin-induced myocyte damage has been attributed to the production of toxic oxygen free radicals.7 This can cause lipid peroxidation of membranes resulting in vacuolation, irreversible damage, and myocyte replacement by fibrous tissue.7
The use of angiogenesis inhibitors in cancer therapy is expanding as are the associated adverse CV effects (eg, hypertension, thromboembolism, left ventricular dysfunction, and QTc prolongation).2,8 Vascular endothelial growth factor (VEGF) plays a role in maintaining vascular homeostasis via the production of the vasodilator nitric oxide (NO) and decreased vascular resistance through the generation of new blood vessels.2,8 Therefore, it is not surprising that inhibition of VEGF signaling (eg, …
[Full Text of this Article
Associations of serum uric acid with total and cause-specific mortality: Findings from individuals and pooling prospective studies
No full textBackground and aims: There is considerable controversy regarding the link between serum uric acid (SUA) and mortality. We prospectively evaluated the association between SUA and risk of total and cause specific (coronary heart disease [CHD], cerebrovascular and cancer) mortality by using the National Health and Nutrition Examination Surveys (NHANES, 1999-2010). Furthermore, a systematic review and meta-analysis of cohort studies was performed to investigate pooled associations of SUA with all-cause and cause-specific mortality.
Methods: Vital status through December 31, 2011 was ascertained. PubMed-Medline, SCOPUS, Web of Science and Google Scholar databases were searched (up to April 2018). Adjusted Cox proportional hazard regression models were used to determine the association between SUA and mortality. The DerSimonian-Laird method and generic inverse variance methods were used for quantitative data synthesis.
Results: Overall, 21,025 individuals were included (mean age = 47.6 years, 48.7% men) and 3520 deaths occurred during the 144 months of follow-up. In adjusted models, individuals in the highest quartile of SUA had 10 and 8% greater risk of CHD and stroke mortality, whereas there was no link between SUA, all-cause and cancer mortality. The associations of CHD and stroke mortality with SUA were more pronounced in women and, among women, in those aged >50 years. Furthermore, all-cause mortality was positively and significantly related to SUA concentrations only in women. In the meta-analysis, SUA was shown to predict the risk of total (21%), CHD (24%) and stroke (29%) mortality. Furthermore, participants with a higher level of central adiposity had a greater risk of mortality from CHD and stroke for the same level of SUA.
Conclusions: Our results highlight the adverse impact of SUA on mortality, particularity in older (>50 years) women. The clinical implications of these findings remain to be established in future trials
Platelet activation, gamma-glutamyltransferase and stent restenosis - Comment on the article by Ulus et al
No full text
Effect of Dietary Insulinemia on All-Cause and Cause-Specific Mortality
No full textBackground: Insulin response to diet might predict the risk of mortality; however, the evidence is limited. We prospectively evaluated the link between the dietary hyperinsulinemia index (DHI) and dietary insulin resistance index (DIRI) with all-cause and cause-specific (cardiovascular disease [CVD] and cancer) mortality.Methods: The National Health and Nutrition Examination Survey (1999-2010) database was used. Vital status through December 31, 2011, was ascertained. Stepwise linear regression models consisted of 39 macro/micronutrients applied, and fasting plasma C-peptide for the DHI and triglyceride/high-density lipoprotein cholesterol ratio (TG/HDL-C) for the DIRI were used. Adjusted Cox regression (followed by propensity score matching) was performed to determine the hazard ratios (HRs) and 95% confidence interval (95% CIs).Results: Overall, 22,246 participants were included (mean age = 47.8 years; 48.9% men). There was a significant increasing risk of mortality across the quartiles of DHI, i.e., participants with a highest score of DHI (Q4) had a greater risk of all-cause (HR: 1.21, 95% CI: 1.17-1.26), CVD (HR: 1.17, 95% CI: 1.07-1.29), and cancer (HR: 1.15, 95% CI: 1.08-1.23) mortality compared with the first quartile (Q1; p < 0.001 for all comparisons). Similarly, participants in the highest DIRI quartile (Q4) had 23% and 31% higher risk of all-cause and CVD mortality, respectively, compared with Q1, while the association between cancer mortality and DIRI was non-significant (HR: 0.88, 95% CI: 0.35-2.61).Conclusions: These findings highlight, for the first time, the detrimental role (association) of insulinemia and insulin resistance potential of diet on all-cause and cause-specific mortality. Our findings support the role of C-peptide and TG/HDL-C ratio as cost-effective and practical biomarkers in clinical settings. These results need to be confirmed to establish their implications
- …
