Browsing by Subject "coronary heart disease"

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  • Vuori, Matti A.; Harald, Kennet; Jula, Antti; Valsta, Liisa; Laatikainen, Tiina; Salomaa, Veikko; Tuomilehto, Jaakko; Jousilahti, Pekka; Niiranen, Teemu J. (2020)
    Aims: The objective was to evaluate whether sodium intake, assessed with the gold standard 24-h urinary collections, was related to long-term incidence of death, cardiovascular disease (CVD) and diabetes mellitus (DM). Methods:A cohort of 4630 individuals aged 25-64 years collected 24-h urine samples in 1979-2002 and were followed up to 14 years for the incidence of any CVD, coronary heart disease (CHD), stroke, heart failure (HF) and DM event, and death. Cox proportional hazards models were used to estimate the association between the baseline salt intake and incident events and adjusted for baseline age, body mass index, serum cholesterol, prevalent DM, and stratified by sex and cohort baseline year. Results: During the follow-up, we observed 423 deaths, 424 CVD events (288 CHD events, 142 strokes, 139 HF events) and 161 DM events. Compared with the highest quartile of salt intake, persons in the lowest quartile had a lower incidence of CVD (hazard ratio [HR] 0.70; 95% confidence interval [CI], 0.51-0.95,p = .02), CHD (HR 0.63 [95% CI 0.42-0.94],p = .02) and DM (HR 0.52 [95% CI 0.31-0.87],p = .01). The results were non-significant for mortality, HF, and stroke. Conclusion: High sodium intake is associated with an increased incidence of CVD and DM.
  • Marjonen, Heidi; Marttila, Minttu; Paajanen, Teemu; Vornanen, Marleena; Brunfeldt, Minna; Joensuu, Anni; Halmesvaara, Otto; Aro, Kimmo; Alanne-Kinnunen, Mervi; Jousilahti, Pekka; Borodulin, Katja; Koskinen, Seppo; Tuomi, Tiinamaija; Ilanne-Parikka, Pirjo; Lindström, Jaana; Laine, Merja K.; Auro, Kirsi; Kääriäinen, Helena; Perola, Markus; Kristiansson, Kati (2021)
    We present a method for communicating personalized genetic risk information to citizens and their physicians using a secure web portal. We apply the method for 3,177 Finnish individuals in the P5 Study where estimates of genetic and absolute risk, based on genetic and clinical risk factors, of future disease are reported to study participants, allowing individuals to participate in managing their own health. Our method facilitates using polygenic risk score as a personalized tool to estimate a person's future disease risk while offering a way for health care professionals to utilize the polygenic risk scores as a preventive tool in patient care.
  • Tucker, Philip; Harma, Mikko; Ojajärvi, Anneli; Kivimäki, Mika; Leineweber, Constanze; Oksanen, Tuula; Salo, Paula; Vahtera, Jussi (2019)
    Objective This study examined the associations between shift work and use of antihypertensive, lipid-lowering, and antidiabetic medications. Methods Survey data from two cohorts of Finnish men (N=11998) and women (N=49 944) working in multiple occupations where shift work was used were linked to national Drug Prescription Register data, with up to 11 years of follow-up. In each cohort, age-stratified Cox proportional hazard regression models were computed to examine any incident use of prescription medication for each of the three medical conditions, separately comparing each of two groups of rotating shift workers (those whose schedules included night shifts. and those whose schedules did not include night shifts) with day workers who worked in a similar range of occupations. Results In the larger cohort, among participants aged 40-49 at baseline, shift work without night shifts was associated with increased use of type-2 diabetes medication after adjustments for sex, occupational status, marital status, alcohol consumption, smoking, and physical activity [hazard ratio (HR) 1.28, 95% confidence interval (CI) 1.01-1.62], while shift work with night shifts was associated with increased use of dyslipidemia medication after adjustments (HR 1.33, 95% CI 1.12-1.57). There were no such associations among younger and older shift workers. Also in the larger cohort, among those aged Conclusions There was mixed evidence regarding the use of medications for cardiovascular risk factors by shift workers. Selection effects may have affected the associations.
  • Vuorio, Alpo; Kovanen, Petri T. (2018)
    This review covers the current knowledge about plant stanol esters as a dietary treatment option for heterozygous familial hypercholesterolemia (he-FH) children. The current estimation of the prevalence of he-FH is about one out of 200-250 persons. In this autosomal dominant disease, the concentration of plasma low-density lipoprotein cholesterol (LDL-C) is strongly elevated since birth. Quantitative coronary angiography among he-FH patients has revealed that stenosing atherosclerotic plaques start to develop in he-FH males in their twenties and in he-FH females in their thirties, and that the magnitude of the plaque burden predicts future coronary events. The cumulative exposure of coronary arteries to the lifelong LDL-C elevation can be estimated by calculating the LDL-C burden (LDL-C level x years), and it can also be used to demonstrate the usefulness of dietary stanol ester treatment. Thus, when compared with untreated he-FH patients, the LDL-C burden of using statin from the age of 10 is 15% less, and if he-FH patients starts to use dietary stanol from six years onwards and a combination of statin and dietary stanol from 10 years onwards, the LDL-C burden is 21% less compared to non-treated he-FH patients. We consider dietary stanol treatment of he-FH children as a part of the LDL-C-lowering treatment package as safe and cost-effective, and particularly applicable for the family-centered care of the entire he-FH families.
  • Kajantie, Mira (2007)
    Administrative registers provide an inexhaustible source of information that is exploited in growing trend by social researchers. Register based research differs in some ways from traditional ways of making research. The purpose of this study was to examine the possibilities that register data provides for equity in health care research and to illustrate how the project can be conducted in practise. The process of register based research was examined through actual research data. Study data was a part of the STAKES research data originally collected to identify and examine differences in treatment of coronary heart disease population in Finland in 1995-1998. Originally for other purposes compiled register data was reworked into retrospective cohort study setting. The purpose was to examine possible socioeconomic differences in treatment histories among patients that underwent their first revascularisation in 1995-1995. Statistical methods used in this study are commonly used in epidemiological research, including logistic and multinomial logistic regression, Poisson regression and Cox regression. Based on previous research it was known that higher socioeconomic groups received more revascularisations than those worse-off in 1990s. This study aimed to conclude whether patients in high socioeconomic groups received the operation in earlier stage of the disease based on their treatment history. According to the results, statistically significant differences that favoured those better-off existed in 1995-1998 in pathways to revascularisation. Patients from higher socioeconomic groups were operated sooner after being diagnosed and had less acute hospitalisations due to coronary heart disease in their treatment histories. The study used several graphic and statistical methods to gain a more detailed picture of the pathways to revascularisation.
  • Gregson, John M.; Freitag, Daniel F.; Surendran, Praveen; Stitziel, Nathan O.; Chowdhury, Rajiv; Burgess, Stephen; Kaptoge, Stephen; Gao, Pei; Staley, James R.; Willeit, Peter; Nielsen, Sune F.; Caslake, Muriel; Trompet, Stella; Polfus, Linda M.; Kuulasmaa, Kari; Kontto, Jukka; Perola, Markus; Blankenberg, Stefan; Veronesi, Giovanni; Gianfagna, Francesco; Mannisto, Satu; Kimura, Akinori; Lin, Honghuang; Reilly, Dermot F.; Gorski, Mathias; Mijatovic, Vladan; Munroe, Patricia B.; Ehret, Georg B.; Thompson, Alex; Uria-Nickelsen, Maria; Malarstig, Anders; Dehghan, Abbas; Vogt, Thomas F.; Sasaoka, Taishi; Takeuchi, Fumihiko; Kato, Norihiro; Yamada, Yoshiji; Kee, Frank; Mueller-Nurasyid, Martina; Ferrieres, Jean; Arveiler, Dominique; Amouyel, Philippe; Salomaa, Veikko; Boerwinkle, Eric; Thompson, Simon G.; Ford, Ian; Jukema, J. Wouter; Sattar, Naveed; Packard, Chris J.; Majumder, Abdulla al Shafi; CKDGen Consortium; Int Consortium Blood Pressure; CHARGE Inflammation Working Grp; MICAD Exome Consortium; EPIC-CVD Consortium; CHD Exome Consortium (2017)
    Aims: Darapladib, a potent inhibitor of lipoprotein-associated phospholipase A(2) (Lp-PLA(2)), has not reduced risk of cardiovascular disease outcomes in recent randomized trials. We aimed to test whether Lp-PLA(2) enzyme activity is causally relevant to coronary heart disease. Methods: In 72,657 patients with coronary heart disease and 110,218 controls in 23 epidemiological studies, we genotyped five functional variants: four rare loss-of-function mutations (c. 109+2T> C (rs142974898), Arg82His (rs144983904), Val279Phe (rs76863441), Gln287Ter (rs140020965)) and one common modest-impact variant (Val379Ala (rs1051931)) in PLA2G7, the gene encoding Lp-PLA(2). We supplemented de-novo genotyping with information on a further 45,823 coronary heart disease patients and 88,680 controls in publicly available databases and other previous studies. We conducted a systematic review of randomized trials to compare effects of darapladib treatment on soluble Lp-PLA(2) activity, conventional cardiovascular risk factors, and coronary heart disease risk with corresponding effects of Lp-PLA(2)-lowering alleles. Results: Lp-PLA(2) activity was decreased by 64% (p = 2.4 x 10 (-25)) with carriage of any of the four loss-of-function variants, by 45% (p<10 (-300)) for every allele inherited at Val279Phe, and by 2.7% (p = 1.9 x 10 (-12)) for every allele inherited at Val379Ala. Darapladib 160 mg once-daily reduced Lp-PLA(2) activity by 65% (p<10 (-300)). Causal risk ratios for coronary heart disease per 65% lower Lp-PLA(2) activity were: 0.95 (0.88-1.03) with Val279Phe; 0.92 (0.74-1.16) with carriage of any loss-of-function variant; 1.01 (0.68-1.51) with Val379Ala; and 0.95 (0.89-1.02) with darapladib treatment. Conclusions: In a large-scale human genetic study, none of a series of Lp-PLA(2)-lowering alleles was related to coronary heart disease risk, suggesting that Lp-PLA(2) is unlikely to be a causal risk factor.
  • Martikainen, Pekka; Korhonen, Kaarina; Jelenkovic, Aline; Lahtinen, Hannu; Havulinna, Aki; Ripatti, Samuli; Borodulin, Katja; Salomaa, Veikko; Smith, George Davey; Silventoinen, Karri (2021)
    Background Genetic vulnerability to coronary heart disease (CHD) is well established, but little is known whether these effects are mediated or modified by equally well-established social determinants of CHD. We estimate the joint associations of the polygenetic risk score (PRS) for CHD and education on CHD events. Methods The data are from the 1992, 1997, 2002, 2007 and 2012 surveys of the population-based FINRISK Study including measures of social, behavioural and metabolic factors and genome-wide genotypes (N=26 203). Follow-up of fatal and non-fatal incident CHD events (N=2063) was based on nationwide registers. Results Allowing for age, sex, study year, region of residence, study batch and principal components, those in the highest quartile of PRS for CHD had strongly increased risk of CHD events compared with the lowest quartile (HR=2.26; 95% CI: 1.97 to 2.59); associations were also observed for low education (HR=1.58; 95% CI: 1.32 to 1.89). These effects were largely independent of each other. Adjustment for baseline smoking, alcohol use, body mass index, igh-density lipoprotein (HDL) and total cholesterol, blood pressure and diabetes attenuated the PRS associations by 10% and the education associations by 50%. We do not find strong evidence of interactions between PRS and education. Conclusions PRS and education predict CHD events, and these associations are independent of each other. Both can improve CHD prediction beyond behavioural risks. The results imply that observational studies that do not have information on genetic risk factors for CHD do not provide confounded estimates for the association between education and CHD.
  • Ripatti, Pietari (Helsingfors universitet, 2016)
    Familial combined hyperlipidemia (FCH) is a complex and common familial dyslipidemia characterized by elevated total cholesterol and/or triglyceride levels with over five-fold risk of coronary heart disease. The genetic architecture and contribution of rare Mendelian and common variants to FCH susceptibility is unknown. In 53 Finnish FCH families, we genotyped and imputed nine million variants in 715 family members with DNA available. We studied the enrichment of variants previously implicated with monogenic dyslipidemias and/or lipid levels in the general population by comparing allele frequencies between the FCH families and population samples. We also constructed weighted polygenic scores using 212 lipid-associated SNPs and estimated the relative contributions of Mendelian variants and polygenic scores to the risk of FCH in the families. We identified, across the whole allele frequency spectrum, an enrichment of variants known to elevate, and a deficiency of variants known to lower LDL-C and/or TG levels among both probands and FCH affecteds. The score based on TG associated SNPs was particularly high among affected individuals compared to non-affected family members. Out of 234 FCH affecteds across the families, seven (3 %) carried Mendelian variants and 83 (35 %) showed high accumulation of either known LDL-C or TG elevating variants by having either polygenic score over the 90th percentile in the population. There was large between-family variation in how much the polygenic scores contributed to the FCH phenotype. FCH is highly polygenic, supporting the hypothesis that variants across the whole allele frequency spectrum contribute to this complex familial trait. This reinforces the clinical tenet that FCH is a cluster of overlapping genetic defects instead of an etiologically homogenous disease entity.
  • Cruise, Sharon; Hughes, John; Bennett, Kathleen; Kouvonen, Anne Maria; Kee, Frank (2019)
    Objective: The aim of this study is to examine the prevalence of coronary heart disease (CHD)–related disability (hereafter also “disability”) and the impact of CHD risk factors on disability in older adults in the Republic of Ireland (ROI) and Northern Ireland (NI). Method: Population attributable fractions were calculated using risk factor relative risks and disability prevalence derived from The Irish Longitudinal Study on Ageing and the Northern Ireland Health Survey. Results: Disability was significantly lower in ROI (4.1% vs. 8.8%). Smoking and diabetes prevalence rates, and the fraction of disability that could be attributed to smoking (ROI: 6.6%; NI: 6.1%), obesity (ROI: 13.8%; NI: 11.3%), and diabetes (ROI: 6.2%; NI: 7.2%), were comparable in both countries. Physical inactivity (31.3% vs. 54.8%) and depression (10.2% vs. 17.6%) were lower in ROI. Disability attributable to depression (ROI: 16.3%; NI: 25.2%) and physical inactivity (ROI: 27.5%; NI: 39.9%) was lower in ROI. Discussion: Country-specific similarities and differences in the prevalence of disability and associated risk factors will inform public health and social care policy in both countries.