Natural History of Cardiac and Peripheral Vascular Death In ESKD: An Australian And New Zealand Data Linkage Study

IntroductionCardiovascular disease is a leading cause of death in patients with end-stage kidney disease (ESKD). However, ascertaining the impact of cardiovascular deaths has not been well characterised over long periods of follow-up and across different treatment states. Further insights into the lifetime risk of cardiovascular death are required to better inform clinical practice and economic planning. Objectives and ApproachWe performed a population-based cohort study on incident patients receiving ESKD treatment from the Australian and New Zealand Dialysis and Transplant registry (ANZDATA). Cardiac/vascular deaths were determined from ICD-10-AM codes listed in the underlying cause of death obtained via data linkage with the Australian National Death Index and New Zealand Mortality Collection database. We estimated mortality rates from cardiac/vascular death across time from ESKD treatment, and calculated probability of death and transplant status over time using multistate models. ResultsAcross 60,823 incident ESKD patients and 381,874 person-years of follow-up, 22% (7,551) of deaths were from cardiac/vascular disease. At 15 years from treatment, 15.6% of patients had died from cardiac/vascular causes, most of whom never received a transplant (13.6% vs 2.0% of cohort). Within the first year of dialysis, cardiac/vascular mortality was highest in the second month, at 3,632/100,000pys. Improvements in cardiac/vascular mortality with calendar year were only seen after 9 months of dialysis. Transplant recipients had consistently lower cardiac/vascular mortality rates (598/100,000 pys) compared to dialysis patients. However, comorbid cardiovascular disease was a risk factor for graft failure and death in transplant recipients (HR:1.52, 95% CI:1.42-1.62). Conclusion / ImplicationsDespite improvements in cardiac/vascular outcomes over time, cardiovascular death remains common in ESKD, particularly in the first few months of treatment. A greater focus on secondary prevention in earlier stages of chronic kidney disease may improve outcomes in new ESKD patients.

Increased Mean Platelet Volume (MPV) in Patients with ST Elevation Myocardial Infarction (STEMI) Compared to Non-ST Elevation Myocardial Infarction (NSTEMI) Patients

Platelets are known to have a role major in the pathogenesis of atherothrombosis. More giant and hyperreactive platelets accelerate the formation of an intracoronary thrombus. An increased MPV as an indicator of larger and more reactive platelets represents a risk factor for overall vascular mortality, including myocardial infarction. This study aimed to identify the increase of Mean Platelet Volume in Patients with Acute Coronary Syndromes, especially in ST-elevation myocardial infarction and Non-ST-elevation myocardial infarction. Thus this parameter can be used as consideration for diagnosis and treatment decisions. This research is an analytic observational with a cross-sectional method. The subjects were patients with STEMI and NSTEMI who were hospitalized in ICCU Dr.Sardjito Hospital Yogyakarta. Thirty-four subjects STEMI and NSTEMI patients at Dr. Sardjito Hospital, consisting of 28 males (82,35%) and six women (17,65%) with a mean age of 55,5 ± 10,3 years. The results showed that MPV in AMI was higher in patients with STEMI than NSTEMI, but this difference is not significant (p = 0,091). This study concludes that MPV to be higher in patients with STEMI compared to NSTEMI. MPV may be used as a marker of myocardial infarction in clinically appropriate situations.

Prevention of Venous Thromboembolism in 2020 and Beyond

Venous thromboembolism (VTE) is the third most common cause of vascular mortality worldwide and comprises deep-vein thrombosis (DVT) and pulmonary embolism (PE). In this review, we discuss how an understanding of VTE epidemiology and the results of thromboprophylaxis trials have shaped the current approach to VTE prevention. We will discuss modern thromboprophylaxis as it pertains to genetic risk factors, exogenous hormonal therapies, pregnancy, surgery, medical hospitalization, cancer, and what is known thus far about VTE in COVID-19 infection.

Association between C reactive protein and all-cause mortality in the ELSA-Brasil cohort

BackgroundHigh-sensitivity C reactive protein (hsCRP) has been proposed as a marker of incident cardiovascular disease and vascular mortality, and may also be a marker of non-vascular mortality. However, most evidence comes from either North American or European cohorts. The present proposal aims to investigate the association of hsCRP with the risk of all-cause mortality in a multiethnic Brazilian population.MethodsBaseline data (2008–2010) of a cohort of 14 238 subjects participating in the Brazilian Longitudinal Study of Adult Health were used. hsCRP was assayed with immunochemistry. The association of baseline covariates with all-cause mortality was calculated by Cox regression for univariate model and adjusted for different confounders after a mean follow-up of 8.0±1.1 years. The final model was adjusted for age, sex, self-rated race/ethnicity, schooling, health behaviours and prevalent chronic disease.ResultsThe risk of death increased steadily by quartiles of hsCRP, from 1.45 (95% CI 1.05 to 2.01) in quartile 2 to 1.95 (95% CI 1.42 to 2.69) in quartile 4, compared with quartile 1. Furthermore, the persistence of a significant graded association after the exclusion of deaths in the first year of follow-up suggests that these results are unlikely to be due to reverse causality. Finally, the HR was unaffected by the exclusion of participants who had self-reported medical history of diabetes, cancer and chronic obstructive pulmonary disease.ConclusionsOur study shows that hsCRP level is associated with mortality in a highly admixed population, independent of a large set of lifestyle and clinical variables.

Sleep-related breathing disorders

Obstructive sleep apnoea and other sleep-related breathing problems significantly impair the functioning of about 0.5–1% of the population. Obstructive sleep apnoea in adults is usually caused by obesity and fat deposits in the neck area (typically collar size of 17 inches (43 cm) or more), when the withdrawal of postural muscle tone during sleep allows the pharyngeal dilators to be overwhelmed, leading to excessive narrowing or collapse of the airway, with consequent apnoea and sleep fragmentation. Mild symptoms may resolve with lifestyle changes such as losing weight; learning to sleep on the side and avoiding sleeping on the back; no alcohol after 18.00 h; no sedatives; stopping smoking; keeping the nose as clear as possible. There is only one fully effective therapy for moderate to severe obstructive sleep apnoea—continuous positive airway pressure. Vascular mortality is higher than average, although recent data have questioned this link.

Prediction of individual life-years gained without cardiovascular events from lipid, blood pressure, glucose, and aspirin treatment based on data of more than 500 000 patients with Type 2 diabetes mellitus

Aims Although group-level effectiveness of lipid, blood pressure, glucose, and aspirin treatment for prevention of cardiovascular disease (CVD) has been proven by trials, important differences in absolute effectiveness exist between individuals. We aim to develop and validate a prediction tool for individualizing lifelong CVD prevention in people with Type 2 diabetes mellitus (T2DM) predicting life-years gained without myocardial infarction or stroke. Methods and results We developed and validated the Diabetes Lifetime-perspective prediction (DIAL) model, consisting of two complementary competing risk adjusted Cox proportional hazards functions using data from people with T2DM registered in the Swedish National Diabetes Registry (n = 389 366). Competing outcomes were (i) CVD events (vascular mortality, myocardial infarction, or stroke) and (ii) non-vascular mortality. Predictors were age, sex, smoking, systolic blood pressure, body mass index, haemoglobin A1c, estimated glomerular filtration rate, non- high-density lipoprotein cholesterol, albuminuria, T2DM duration, insulin treatment, and history of CVD. External validation was performed using data from the ADVANCE, ACCORD, ASCOT and ALLHAT-LLT-trials, the SMART and EPIC-NL cohorts, and the Scottish diabetes register (total n = 197 785). Predicted and observed CVD-free survival showed good agreement in all validation sets. C-statistics for prediction of CVD were 0.83 (95% confidence interval: 0.83–0.84) and 0.64–0.65 for internal and external validation, respectively. We provide an interactive calculator at www.U-Prevent.com that combines model predictions with relative treatment effects from trials to predict individual benefit from preventive treatment. Conclusion Cardiovascular disease-free life expectancy and effects of lifelong prevention in terms of CVD-free life-years gained can be estimated for people with T2DM using readily available clinical characteristics. Predictions of individual-level treatment effects facilitate translation of trial results to individual patients.