Browsing by Subject "cardiovascular disease"

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  • Global Burden of Metabolic Risk Factors of Chronic D Collaborating Groupiseases; Asia-Pacific Cohort Studies Collaboration (APCSC); Diabetes Epidemiology: Collaborative analysis of Diagnostic criteria in Europe (DECODE); Emerging Risk Factor Collaboration (ERFC); Prospective Studies Collaboration (PSC); Miettinen, Tatu; Strandberg, Timo; Tilvis, Reijo (2013)
    BACKGROUND: The effects of systolic blood pressure (SBP), serum total cholesterol (TC), fasting plasma glucose (FPG), and body mass index (BMI) on the risk of cardiovascular diseases (CVD) have been established in epidemiological studies, but consistent estimates of effect sizes by age and sex are not available. METHODS: We reviewed large cohort pooling projects, evaluating effects of baseline or usual exposure to metabolic risks on ischemic heart disease (IHD), hypertensive heart disease (HHD), stroke, diabetes, and, as relevant selected other CVDs, after adjusting for important confounders. We pooled all data to estimate relative risks (RRs) for each risk factor and examined effect modification by age or other factors, using random effects models. RESULTS: Across all risk factors, an average of 123 cohorts provided data on 1.4 million individuals and 52,000 CVD events. Each metabolic risk factor was robustly related to CVD. At the baseline age of 55-64 years, the RR for 10 mmHg higher SBP was largest for HHD (2.16; 95% CI 2.09-2.24), followed by effects on both stroke subtypes (1.66; 1.39-1.98 for hemorrhagic stroke and 1.63; 1.57-1.69 for ischemic stroke). In the same age group, RRs for 1 mmol/L higher TC were 1.44 (1.29-1.61) for IHD and 1.20 (1.15-1.25) for ischemic stroke. The RRs for 5 kg/m(2) higher BMI for ages 55-64 ranged from 2.32 (2.04-2.63) for diabetes, to 1.44 (1.40-1.48) for IHD. For 1 mmol/L higher FPG, RRs in this age group were 1.18 (1.08-1.29) for IHD and 1.14 (1.01-1.29) for total stroke. For all risk factors, proportional effects declined with age, were generally consistent by sex, and differed by region in only a few age groups for certain risk factor-disease pairs. CONCLUSION: Our results provide robust, comparable and precise estimates of the effects of major metabolic risk factors on CVD and diabetes by age group.
  • Ji, Fuling; Ning, Feng; Duan, Haiping; Dong, Liyan; Yang, Feng; Liu, Zhisheng; Song, Xuyan; Zhang, Dongfeng; Wang, Shaojie; Pang, Zengchang; Kaprio, Jaakko; Silventoinen, Karri (2020)
    We explored the genetic architecture of metabolic risk factors of cardiovascular diseases (CVDs) and their clustering in Chinese boys and girls. Seven metabolic traits (body mass index [BMI], waist circumference [WC], systolic blood pressure [SBP], diastolic blood pressure [DBP], total cholesterol [TC], triglyceride [TG], and uric acid [UA]) were measured in a sample of 1016 twins between 8 and 17 years of age, recruited from the Qingdao Twin Registry. Cholesky, independent pathway, and common pathway models were used to identify the latent genetic structure behind the clustering of these metabolic traits. Genetic architecture of these metabolic traits was largely similar in boys and girls. The highest heritability was found for BMI (a(2) = 0.63) in boys and TC (a(2) = .69) in girls. Three heritable factors, adiposity (BMI and WC), blood pressure (SBP and DBP), and metabolite factors (TC, TG, and UA), which formed one higher-order latent phenotype, were identified. Latent genetic, common environmental, and unique environmental factors indirectly impacted the three factors through one single latent factor. Our results suggest that there is one latent factor influencing several metabolic traits, which are known risk factors of CVDs in young Chinese twins. Latent genetic, common environmental, and unique environmental factors indirectly imposed on them. These results inform strategies for gene pleiotropic discovery and intervening of CVD risk factors during childhood and adolescence.
  • Boren, Jan; Packard, Chris J.; Taskinen, Marja-Riitta (2020)
    Cardiovascular disease (CVD) is the leading cause of death globally. It is well-established based on evidence accrued during the last three decades that high plasma concentrations of cholesterol-rich atherogenic lipoproteins are causatively linked to CVD, and that lowering these reduces atherosclerotic cardiovascular events in humans (1-9). Historically, most attention has been on low-density lipoproteins (LDL) since these are the most abundant atherogenic lipoproteins in the circulation, and thus the main carrier of cholesterol into the artery wall. However, with the rise of obesity and insulin resistance in many populations, there is increasing interest in the role of triglyceride-rich lipoproteins (TRLs) and their metabolic remnants, with accumulating evidence showing they too are causatively linked to CVD. Plasma triglyceride, measured either in the fasting or non-fasting state, is a useful index of the abundance of TRLs and recent research into the biology and genetics of triglyceride heritability has provided new insight into the causal relationship of TRLs with CVD. Of the genetic factors known to influence plasma triglyceride levels variation inAPOC3- the gene for apolipoprotein (apo) C-III - has emerged as being particularly important as a regulator of triglyceride transport and a novel therapeutic target to reduce dyslipidaemia and CVD risk (10).
  • Helve, Salla; Nieminen, Tuomo; Helanterä, Ilkka; Finne, Patrik; Rajala, Helena; Sinisalo, Juha; Laine, Mika (2020)
    Abstract The value of myocardial single-photon emission computed tomography (SPECT) in pre-transplant evaluation of kidney transplant recipients is controversial. We assessed whether myocardial SPECT predicts major adverse cardiac events (MACE) and determined whether SPECT findings affected transplant recipients? medical and invasive treatment. We analyzed 301 patients referred for myocardial SPECT before kidney transplantation and combined the results with information from patient files and the Transplantation registry. During the median follow-up time of 96 months (IQR 70.75-118.25 months), the incidence of MACE was higher in patients (n=37) with severely abnormal SPECT (>10 % reversible perfusion defect) than in patients (n=35) with mildly abnormal or normal SPECT (51.4%, 29.4% and 27.0%, respectively, p=0.011). Severely abnormal SPECT findings predicted long-term MACE in a univariable analysis but not after adjusting for other risk factors. Following SPECT, 29 patients (9.6%) underwent coronary angiography and 14 (4.6%) were revascularized. New antithrombotic or statin medication was prescribed to 7.3% of patients with ischemia in SPECT. Kidney transplantation patients are at high long-term risk of MACE even with normal preoperative myocardial SPECT. Abnormal SPECT did not predict MACE when adjusted for other risk factors. Minority of the patients underwent coronary revascularization or had changes in preventive medication before transplantation.
  • FIELD investigators; Cao, Jacob Y.; Waldman, Boris; O’Connell, Rachel; Taskinen, Marja-Riitta; Keech, Anthony C. (2020)
    Aim To explore the relationship between baseline uric acid (UA) levels and long-term cardiovascular events in adults with type 2 diabetes (T2D) and to determine whether the cardioprotective effects of fenofibrate are partly mediated through its UA-lowering effects. Methods Data from the Fenofibrate Intervention and Event Lowering in Diabetes (FIELD) trial were utilized, comprising 9795 adults with T2D randomly allocated to treatment with fenofibrate or matching placebo. Plasma UA was measured before and after a 6-week, active fenofibrate run-in phase in all participants. Cox proportional hazards models were used to explore the relationships between baseline UA, pre-to-post run-in reductions in UA and long-term cardiovascular outcomes. Results Mean baseline plasma UA was 0.33 mmol/L (SD 0.08). Baseline UA was a significant predictor of long-term cardiovascular events, with every 0.1 mmol/L higher UA conferring a 21% increase in event rate (HR 1.21, 95% CI 1.13-1.29, P <.001). This remained significant after adjustment for treatment allocation, cardiovascular risk factors and renal function. The extent of UA reduction during fenofibrate run-in was also a significant predictor of long-term cardiovascular events, with every 0.1 mmol/L greater reduction conferring a 14% lower long-term risk (HR 0.86, 95% CI 0.76-0.97, P = .015). This effect was not modified by treatment allocation (P-interaction = .77). Conclusions UA is a strong independent predictor of long-term cardiovascular risk in adults with T2D. Although greater reduction in UA on fenofibrate is predictive of lower cardiovascular risk, this does not appear to mediate the cardioprotective effects of fenofibrate.
  • Mehta, Neil K.; Abrams, Leah R.; Myrskylä, Mikko (2020)
    After decades of robust growth, the rise in US life expectancy stalled after 2010. Explanations for the stall have focused on rising drug-related deaths. Here we show that a stagnating decline in cardiovascular disease (CVD) mortality was the main culprit, outpacing and overshadowing the effects of all other causes of death. The CVD stagnation held back the increase of US life expectancy at age 25 y by 1.14 y in women and men, between 2010 and 2017. Rising drug-related deaths had a much smaller effect: 0.1 y in women and 0.4 y in men. Comparisons with other high-income countries reveal that the US CVD stagnation is unusually strong, contributing to a stark mortality divergence between the US and peer nations. Without the aid of CVD mortality declines, future US life expectancy gains must come from other causes—a monumental task given the enormity of earlier declines in CVD death rates. Reversal of the drug overdose epidemic will be beneficial, but insufficient for achieving pre-2010 pace of life expectancy growth.
  • Paige, Ellie; Barrett, Jessica; Pennells, Lisa; Sweeting, Michael; Willeit, Peter; Di Angelantonio, Emanuele; Gudnason, Vilmundur; Nordestgaard, Borge G.; Psaty, Bruce M.; Goldbourt, Uri; Best, Lyle G.; Assmann, Gerd; Salonen, Jukka T.; Nietert, Paul J.; Verschuren, W. M. Monique; Brunner, Eric J.; Kronmal, Richard A.; Salomaa, Veikko; Bakker, Stephan J. L.; Dagenais, Gilles R.; Sato, Shinichi; Jansson, Jan-Hakan; Willeit, Johann; Onat, Altan; de la Camara, Agustin Gomez; Roussel, Ronan; Volzke, Henry; Dankner, Rachel; Tipping, Robert W.; Meade, Tom W.; Donfrancesco, Chiara; Kuller, Lewis H.; Peters, Annette; Gallacher, John; Kromhout, Daan; Iso, Hiroyasu; Knuiman, Matthew; Casiglia, Edoardo; Kavousi, Maryam; Palmieri, Luigi; Sundstrom, Johan; Davis, Barry R.; Njolstad, Inger; Couper, David; Danesh, John; Thompson, Simon G.; Wood, Angela (2017)
    The added value of incorporating information from repeated blood pressure and cholesterol measurements to predict cardiovascular disease (CVD) risk has not been rigorously assessed. We used data on 191,445 adults from the Emerging Risk Factors Collaboration (38 cohorts from 17 countries with data encompassing 1962-2014) with more than 1 million measurements of systolic blood pressure, total cholesterol, and high-density lipoprotein cholesterol. Over a median 12 years of follow-up, 21,170 CVD events occurred. Risk prediction models using cumulative mean values of repeated measurements and summary measures from longitudinal modeling of the repeated measurements were compared with models using measurements from a single time point. Risk discrimination (C-index) and net reclassification were calculated, and changes in C-indices were meta-analyzed across studies. Compared with the single-time-point model, the cumulative means and longitudinal models increased the C-index by 0.0040 (95% confidence interval (CI): 0.0023, 0.0057) and 0.0023 (95% CI: 0.0005, 0.0042), respectively. Reclassification was also improved in both models; compared with the single-time-point model, overall net reclassification improvements were 0.0369 (95% CI: 0.0303, 0.0436) for the cumulative-means model and 0.0177 (95% CI: 0.0110, 0.0243) for the longitudinal model. In conclusion, incorporating repeated measurements of blood pressure and cholesterol into CVD risk prediction models slightly improves risk prediction.
  • Snell, Karoliina; Helén, Ilpo (2020)
    This article presents results from a Finnish focus group's study conducted among participants of a project called GeneRISK, in which the participants received a personal risk score for having a cardiovascular event based on genetic analysis, lifestyle and laboratory results. In the discussions, interpretations of the genetic risk score and its meaning were incorporated into personal narratives of health and illness. We argue that instead of serving as an explanation for health and illness, which can help guide people's lives and choices, the genetic risk information became an object of explanation. Therefore, the risk information did not create new conceptions of personal risk, nor did it generate enough power to push people to change their lifestyles. Instead, the risk information was used to strengthen the existing impression of personal risk and the narrative of personal health and illness.