327 results on '"Ukkola O"'
Search Results
2. Dietary sodium intake and prediction of cardiovascular events
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Aijala, M., Malo, E., Santaniemi, M., Bloigu, R., Silaste, M.-L., Kesaniemi, Y.A., and Ukkola, O.
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Sodium in the body ,Cardiovascular diseases ,Low density lipoproteins ,Food/cooking/nutrition ,Health - Abstract
BACKGROUND/OBJECTIVES: The association of dietary sodium and cardiovascular disease (CVD), as well as the reduction of sodium intake in the prevention of CVD, has been under debate. To study whether sodium consumption has a role as a risk factor for fatal and non-fatal CVD. SUBJECTS/METHODS: A well-defined population-based cohort of 1045 subjects collected between 1991 and 1993 (mean age 51.4 years) was used with approximately 19 years' follow-up. At the baseline, 716 subjects filled in a 1-week food follow-up diary, which was used to calculate the daily sodium intake (mg/1000 kcal). RESULTS: The baseline sodium intake correlated significantly with age ([r.sub.s] = 0.117, P = 0.002), BMI ([r.sub.s] = 0.216, P = 0.000), waist circumference ([r.sub.s] = 0.268, P = 0.000), smoking ([r.sub.s] = 0.144, P = 0.000), alcohol consumption ([r.sub.s] = 0.111, P = 0.003), systolic blood pressure ([r.sub.s] = 0.106, P = 0.005) and low-density lipoprotein (LDL) cholesterol ([r.sub.s] = 0.081, P = 0.033). Those who had cardiovascular events in the follow-up consumed more sodium at the baseline (mean 2010.4 mg/1000 kcal/day, s.d. 435.2, n =101) compared with the subjects without events (mean 1849.9 mg/1000 kcal/day, s.d. 361.2, n = 589;t-test;P = 0.001). The incidence of cardiovascular events was greater in the highest quartile (22.1%) than in the lower quartiles (first 11.0%, second 9.9% and third 15.6%; [X.sup.2] ; P = 0.005). Cox regression analysis showed that sodium intake as a continuous variable predicts CVD events (P = 0.031) independently when age, sex, smoking, alcohol consumption, systolic blood pressure, LDL cholesterol and waist circumference were added as covariates. This predictive role is seen especially in the group of subjects on hypertensive medication (P = 0.001). CONCLUSIONS: Dietary sodium intake is a significant independent predictor of cardiovascular events in the study population. European Journal of Clinical Nutrition (2015) 69, 1042-1047;doi: 10.1038/ejcn.2015.40;published online 25 March 2015, INTRODUCTION The relationship between salt and the cardiovascular system was observed by the ancient Chinese about 3000 years ago, and the first scientific paper on this subject, showing an association [...]
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- 2015
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3. Long-term metabolic fate and mortality in obesity without metabolic syndrome
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Käräjämäki, A. J. (Aki Juhani), Korkiakoski, A. (Arto), Hukkanen, J. (Janne), Kesäniemi, Y. A. (Y. Antero), and Ukkola, O. (Olavi)
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obesity ,cardiovascular disease ,atrial fibrillation ,metabolically healthy obesity ,Metabolic syndrome ,mortality - Abstract
Background: Obesity and metabolic syndrome (MetS) are known to expose to atrial fibrillation (AF), cardiovascular diseases (CVD) and mortality. Metabolically healthy obesity refers to obesity without MetS. This study aimed to investigate how obesity and MetS modify the risk of CVD, AF and mortality in very long-time follow-up. Methods: Finnish middle-aged subjects (n = 1045) were grouped into four subgroups according to the presence of obesity and MetS. CVD events and AF were followed for 24 years and total mortality for 30 years. Moreover, 600 available patients had a follow-up visit for metabolic examinations after approximately 22 years. Results: One-hundred and sixty-two (30%) subjects without obesity or MetS died during the follow-up. Ninety-two (17%) of the patients in this group had a CVD event and 58 (11%) were diagnosed with AF. As compared to them, obese subjects without MetS had similar metabolic fate and mortality (mortality 26 (38%), p = .143; CVD event 12 (18%), p = .858 and AF 7 (10%), p = .912, respectively), whereas subjects with obesity and MetS had greater mortality (102 (49%), p
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- 2022
4. One-hour post-load glucose improves the prediction of cardiovascular events in the OPERA study
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Saunajoki, A. (Anni), Auvinen, J. (Juha), Bloigu, A. (Aini), Ukkola, O. (Olavi), Keinänen-Kiukaanniemi, S. (Sirkka), and Timonen, M. (Markku)
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dysglycemia ,prediction ,oral glucose tolerance test ,cardiovascular outcomes - Abstract
Background: To estimate the ability of fasting, 1-h, and 2-h post-load glucose to predict cardiovascular outcomes. Methods: We examined a population-based study consisting of 977 middle-aged subjects who underwent an oral glucose tolerance test with glucose values measured at 0, 60, and 120 min. Participants were followed up to 24 years, and cardiovascular outcomes were collected from national registers. Predictive abilities of fasting, 1-h, and 2-h glucose were evaluated alone and in the prediction models with traditional cardiovascular risk factors using Cox proportional hazard models, the likelihood-ratio test, Harrell’s concordance index and integrated discrimination improvement. Results: Cardiovascular endpoint occurred in 222 (22.7%) participants during a median follow-up of 19.8 years. In the prognostic models, 1-h glucose (HR 1.67, 95%CI 1.10–2.53), but not fasting or 2-h glucose, predicted cardiovascular events statistically significantly. In addition, when adding glucose parameters into the model including traditional cardiovascular risk factors, only 1-h glucose improved the predictive ability (LR-test p=.046). Finally, 1-h glucose found slightly over 50% more cardiovascular endpoints that were not recognized by fasting or 2-h glucose levels. Conclusions: Our findings support the earlier ones suggesting that 1-h glucose would be a better long-term predictor of cardiovascular morbidity and mortality than fasting or 2-h glucose.
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- 2021
5. Temporal variability of T-wave morphology and risk of sudden cardiac death in patients with coronary artery disease
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Rahola, J. T. (Janne T.), Kiviniemi, A. M. (Antti M.), Ukkola, O. H. (Olavi H.), Tulppo, M. P. (Mikko P.), Junttila, J. (Juhani), Huikuri, H. V. (Heikki V.), Kenttä, T. V. (Tuomas V.), and Perkiömäki, J. S. (Juha S.)
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T-wave morphology ,repolarization ,electrocardiography ,cardiovascular diseases ,T-wave ,sudden cardiac death - Abstract
Background: The possible relationship between temporal variability of electrocardiographic spatial heterogeneity of repolarization and the risk of sudden cardiac death (SCD) in patients with coronary artery disease (CAD) is not completely understood. Methods: The standard deviation of T-wave morphology dispersion (TMD-SD), of QRST angle (QRSTA-SD), and of T-wave area dispersion (TW-Ad-SD) were analyzed on beat-to-beat basis from 10 min period of the baseline electrocardiographic recording in ARTEMIS study patients with angiographically verified CAD. Results: After on average of 8.6 ± 2.3 years of follow-up, a total of 66 of the 1,678 present study subjects (3.9%) had experienced SCD or were resuscitated from sudden cardiac arrest (SCA). TMD-SD was most closely associated with the risk for SCD and was significantly higher in patients who had experienced SCD/SCA compared with those who remained alive (3.61 ± 2.83 vs. 2.64 ± 2.52, p = 0.008, respectively), but did not differ significantly between the patients who had experienced non-SCD (n = 71, 4.2%) and those who remained alive (3.20 ± 2.73 vs. 2.65 ± 2.53, p = 0.077, respectively) or between the patients who succumbed to non-cardiac death (n = 164, 9.8%) and those who stayed alive (2.64 ± 2.17 vs. 2.68 ± 2.58, p =0.853). After adjustments with relevant clinical risk indicators of SCD/SCA, TMD-SD still predicted SCD/SCA (HR 1.107, 95% CIs 1.035–1.185, p = 0.003). Conclusions: Temporal variability of electrocardiographic spatial heterogeneity of repolarization represented by TMD-SD independently predicts long-term risk of SCD/SCA in patients with CAD.
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- 2021
6. Prognostic value of heart rate variability in patients with coronary artery disease in the current treatment era
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Vuoti, A. O. (Antti O.), Tulppo, M. P. (Mikko P.), Ukkola, O. H. (Olavi H.), Junttila, M. J. (M. Juhani), Huikuri, H. V. (Heikki V.), Kiviniemi, A. M. (Antti M.), and Perkiömäki, J. S. (Juha S.)
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Coronary artery disease (CAD) mortality has declined substantially over the past decades thanks to advancing medical and interventional/surgical treatments; therefore, the prognostic value of the heart rate variability in CAD in the current treatment era is not well established. We evaluated the prognostic significance of baseline heart rate variability in 1,757 ARTEMIS study patients with angiographically verified CAD. During an average follow-up time of 8.7 ± 2.2 years, a total of 285 (16.2%) patients died. Of the patients, 63 (3.6%) suffered sudden cardiac death or were resuscitated from sudden cardiac arrest (SCD/SCA), 60 (3.4%) experienced non-sudden cardiac death (NSCD), and death attributable to non-cardiac causes (NCD) occurred in 162 (9.2%) patients. For every 10 ms decrease in standard deviation of normal to normal intervals the risk for SCD/SCA, NSCD and NCD increased significantly: HR 1.153 (95% CI 1.075–1.236, p
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- 2021
7. Nighttime ambulatory pulse pressure predicts cardiovascular and all-cause mortality among middle-aged participants in the 21-year follow-up
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Lempiäinen, P. A. (Päivi A.), Ylitalo, A. (Antti), Huikuri, H. (Heikki), Kesäniemi, Y. A. (Y. Antero), and Ukkola, O. H. (Olavi H.)
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nighttime pulse pressure ,cardiovascular mortality ,follow-up ,all-cause mortality ,ambulatory pulse pressure - Abstract
Office pulse pressure (PP) is a predictor for cardiovascular (CV) events and mortality. Our aim was to evaluate ambulatory PP as a long-term risk factor in a random cohort of middle-aged participants. The Opera study took place in years 1991–1993, with a 24-h ambulatory blood pressure measurement (ABPM) performed to 900 participants. The end-points were non-fatal and fatal CV events, and deaths of all-causes. Follow-up period, until the first event or until the end of the year 2014, was 21.1 years (mean). Of 900 participants, 22.6% died (29.6% of men/15.6% of women, p
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- 2021
8. Ghrelin and its promoter variant associated with cardiac hypertrophy
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Ukkola, O, Pääkkö, T, and Kesäniemi, Y A
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- 2012
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9. Cord Compression May Rapidly Influence the Expression of Placental Angiogenic Genes in Pre-Eclampsia
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Järvenpää, J., Vuoristo, J.T., Ukkola, O., Hirvikoski, P., Savolainen, E.-R., Raudaskoski, T., and Ryynänen, M.
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- 2008
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10. Plasma adiponectin concentration is associated with ambulatory daytime systolic blood pressure but not with the dipping status
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Vasunta, R L, Kesäniemi, Y A, and Ukkola, O
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- 2010
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11. Serum ghrelin and the prediction of the development of impaired glucose regulation and Type 2 diabetes in middle-aged subjects
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Vartiainen, J., Rajala, U., Jokelainen, J., Keinänen-Kiukaanniemi, S., Kesäniemi, Y. A., and Ukkola, O.
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- 2010
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12. Glomerular filtration rate is related to dipping pattern in ambulatory blood pressure monitoring—a cross-sectional population-based study
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Kastarinen, H, Vasunta, R-L, Ukkola, O, and Kesäniemi, Y A
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- 2010
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13. High plasma ghrelin protects from coronary heart disease and Leu72Leu polymorphism of ghrelin gene from cancer in healthy adults during the 19 years follow-up study
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Laurila, M., Santaniemi, M., Kesäniemi, Y. A., and Ukkola, O.
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- 2014
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14. ApoE phenotype is associated with inflammatory markers in middle-aged subjects
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Ukkola, O., Kunnari, A., Jokela, M., Päivänsalo, M., and Kesäniemi, Y. A.
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- 2009
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15. Adiponectin concentration and insulin indicators following overfeeding in identical twins
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Ukkola, O., Terán-García, M., Tremblay, A., Després, J.-P., and Bouchard, C.
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- 2008
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16. Leu7Pro polymorphism of PreproNPY associated with an increased risk for type II diabetes in middle-aged subjects
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Ukkola, O and Kesäniemi, Y A
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- 2007
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17. Increased beat-to-beat variability of T-wave heterogeneity measured from standard 12-lead electrocardiogram Is associated with sudden cardiac death:a case–control study
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Hekkanen, J. J. (Jenni J.), Kenttä, T. V. (Tuomas V.), Haukilahti, M. A. (Mira Anette E.), Rahola, J. T. (Janne T.), Holmström, L. (Lauri), Vähätalo, J. (Juha), Tulppo, M. P. (Mikko P.), Kiviniemi, A. M. (Antti M.), Pakanen, L. (Lasse), Ukkola, O. H. (Olavi H.), Junttila, M. J. (M. Juhani), Huikuri, H. V. (Heikki V.), and Perkiömäki, J. S. (Juha S.)
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T-wave morphology ,repolarization ,electrocardiography ,ventricular arrhythmias ,cardiovascular diseases ,T-wave ,sudden cardiac death - Abstract
Introduction: The prognostic significance of beat-to-beat variability of spatial heterogeneity of repolarization measured from standard 12-lead ECG is not well-understood. Methods: We measured the short-term variability of repolarization parameters, such as T-wave heterogeneity in leads V4–V6 (TWH) and QT interval (QT), from five consecutive beats of previously recorded standard 12-lead ECG in 200 victims of unexpected sudden cardiac death (SCD) confirmed to be due to complicated atherosclerotic coronary artery disease (CAD) in medico-legal autopsy and 200 age- and sex-matched controls with angiographically confirmed CAD. The short-term variability of repolarization heterogeneity was defined as the standard deviation (SD) of the measured repolarization parameters. All ECGs were in sinus rhythm, and no premature ventricular contractions were included in the measured segment. Results: TWH-SD and QT-SD were significantly higher in SCD victims than in subjects with CAD (6.9 ± 5.6 μV vs. 3.8 ± 2.6 μV, p = 1.8E-11; 8.3 ± 13.1 ms vs. 3.8 ± 7.1 ms, p = 0.00003, respectively). After adjusting in the multivariate clinical model with factors, such as diabetes, RR interval, and beta blocker medication, TWH-SD and QT-SD retained their significant power in discriminating between the victims of SCD and the patients with CAD (p = 0.00003, p = 0.006, respectively). TWH-SD outperformed QT-SD in identifying the SCD victims among the study subjects (area under the curve in the receiver operating characteristics curve 0.730 vs. 0.679, respectively). Conclusion: Increased short-term variability of repolarization heterogeneity measured from standard 12-lead ECG is associated with SCD.
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- 2020
18. Ghrelin and the metabolic balance
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Ukkola, O.
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- 2005
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19. The negative association between plasma ghrelin and IGF-I is modified by obesity, insulin resistance and type 2 diabetes
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Pöykkö, S. M., Ukkola, O., Kauma, H., Kellokoski, E., Hörkkö, S., and Kesäniemi, Y. A.
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- 2005
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20. Role of candidate genes in the lipid responses to intensified treatment in Type 2 diabetes
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Ukkola, O., Salonen, J., and Kesäniemi, Y. Antero
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- 2005
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21. Two variants in the resistin gene and the response to long-term overfeeding
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Ukkola, O, Antero Kesäniemi, Y, Tremblay, A, and Bouchard, C
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- 2004
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22. Genetic variation at the adipsin locus and response to long-term overfeeding
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Ukkola, O, Chagnon, M, Tremblay, A, and Bouchard, C
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- 2003
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23. Ghrelin Arg51Gln mutation is a risk factor for Type 2 diabetes and hypertension in a random sample of middle-aged subjects
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Pöykkö, S., Ukkola, O., Kauma, H., Savolainen, M. J., and Kesäniemi, Y. A.
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- 2003
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24. Insulin-like growth factor 2 (IGF2 ) and IGF-binding protein 1 (IGFBP1) gene variants are associated with overfeeding-induced metabolic changes
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Ukkola, O., Sun, G., and Bouchard, C.
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- 2001
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25. Genetic variation at the uncoupling protein 1, 2 and 3 loci and the response to long-term overfeeding
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Ukkola, O, Tremblay, A, Sun, G, Chagnon, YC, and Bouchard, C
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- 2001
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26. Gastric bypass and glucose metabolism
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Ukkola, O.
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- 2009
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27. Early atherosclerosis and IgG2 to bacteria are associated with FcγRIIa genotype in non-smokers
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Sämpi, M., Ukkola, O., Päivänsalo, M., Kesäniemi, Y. A., and Hörkkö, S.
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- 2009
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28. Recovery of rate-pressure product and cardiac mortality in coronary artery disease patients with type 2 diabetes
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Kiviniemi, A. M. (Antti M.), Kenttä, T. V. (Tuomas V.), Lepojärvi, S. (Samuli), Perkiömäki, J. S. (Juha S.), Piira, O.-P. (Olli-Pekka), Ukkola, O. (Olavi), Huikuri, H. V. (Heikki V.), Junttila, M. J. (M. Juhani), and Tulppo, M. P. (Mikko P.)
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exercise testing ,autonomic nervous system ,ischemic heart disease ,sudden cardiac death - Abstract
Aims: To investigate prognostic significance of post-exercise recovery of rate-pressure product (RPP) in patients with stable coronary artery disease (CAD) and type 2 diabetes (T2D). Methods: Patients with angiographically documented CAD and T2D (n = 697) underwent symptom-limited bicycle exercise test. Exercise capacity (EC), heart rate, blood pressure and RPP responses to peak exercise and recovery (2′ and 5′ after cessation of exercise) were analyzed. Cardiac death was the primary and sudden cardiac death (SCD) secondary endpoint. Results: During a median follow-up of 76 months, 49 cardiac deaths (7.0%) and 28 SCDs (4.0%) were observed. The recovery of RPP at 5′ was the strongest univariate predictor of cardiac death (hazard ratio [HR]: 2.55 per SD decrease, 95%CI: 1.82–3.58, p
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- 2019
29. Prediabetes and risk for cardiac death among patients with coronary artery disease:the ARTEMIS study
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Kiviniemi, A. M. (Antti M.), Lepojärvi, E. S. (E. Samuli), Tulppo, M. P. (Mikko P.), Piira, O.-P. (Olli-Pekka), Kenttä, T. V. (Tuomas V.), Perkiömäki, J. S. (Juha S.), Ukkola, O. H. (Olavi H.), Myerburg, R. J. (Robert J.), Junttila, M. J. (M. Juhani), and Huikuri, H. V. (Heikki V.)
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cardiovascular diseases - Abstract
Objective: To compare cardiac mortality in patients with CAD and prediabetes with that in CAD patients with normal glycemic status and type 2 diabetes. Research design and methods: The Innovation to Reduce Cardiovascular Complications of Diabetes at the Intersection (ARTEMIS) study included patients with CAD after revascularization (79%), optimal medical therapy, or both. Patients had type 2 diabetes (n = 834), impaired glucose tolerance (IGT; n = 314), impaired fasting glucose (IFG; n = 103), or normal glycemic status (n = 697) as defined on the basis of the results of an oral glucose tolerance test. The primary end point was cardiac death. Major adverse cardiac event (MACE: cardiac death, heart failure, or acute coronary syndrome) and all-cause mortality were secondary end points. Results: During a mean ± SD follow-up of 6.3 ± 1.6 years, 101 cardiac deaths, 385 MACEs, and 208 deaths occurred. Patients with IGT tended to have 49% lower adjusted risk for cardiac death (P = 0.069), 32% lower adjusted risk for all-cause mortality (P = 0.076), and 36% lower adjusted risk for MACE (P = 0.011) than patients with type 2 diabetes. The patients with IFG had 82% lower adjusted risk for all-cause mortality (P = 0.015) than the patients with type 2 diabetes, whereas risks for cardiac death and MACE did not differ significantly between the two groups. The adjusted risks for cardiac death, MACE, and all-cause mortality among patients with IGT and IFG did not significantly differ from those risks among patients with normal glycemic status. Conclusions: Cardiac mortality or incidence of MACE in patients with CAD with prediabetes (i.e., IGT or IFG after revascularization, optimal medical therapy, or both) does not differ from those values in patients with normal glycemic status.
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- 2019
30. Insertion/deletion polymorphism in the angiotensin-converting enzyme gene associated with macroangiopathy and blood pressure in patients with non-insulin-dependent diabetes mellitus
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Ukkola, O., Savolainen, M. J., Salmela, P. I., von Dickhoff, K., Kiema, T., and Kesäniemi, Y. A.
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- 1995
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31. Peripheral regulation of food intake: New insights
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Ukkola, O.
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- 2004
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32. Plasma ghrelin concentrations are positively associated with carotid artery atherosclerosis in males
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PÖYKKÖ, S. M., KELLOKOSKI, E., UKKOLA, O., KAUMA, H., PÄIVÄNSALO, M., KESÄNIEMI, Y. A., and HÖRKKÖ, S.
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- 2006
33. Resistin polymorphisms are associated with cerebrovascular disease in Finnish Type 2 diabetic patients
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Kunnari, A., Ukkola, O., and Kesäniemi, Y. A.
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- 2005
34. Tyrosine phosphatase 1B and leptin receptor genes and their interaction in type 2 diabetes
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SANTANIEMI, M., UKKOLA, O., and KESÄNIEMI, Y. A.
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- 2004
35. Role of candidate genes in the responses to long-term overfeeding: review of findings
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Ukkola, O. and Bouchard, C.
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- 2004
36. Preproghrelin Leu72Met polymorphism in patients with type 2 diabetes mellitus
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UKKOLA, O. and KESÄNIEMI, Y. A.
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- 2003
37. Ghrelin and insulin metabolism
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Ukkola, O.
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- 2003
38. Interactions among the β2- and β3- adrenergic receptor genes and total body fat and abdominal fat level in the HERITAGE Family Study
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Ukkola, O, Rankinen, T, Rice, T, Gagnon, J, Leon, A S, Skinner, J S, Wilmore, J H, Rao, D C, and Bouchard, C
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- 2003
39. Protein tyrosine phosphatase 1B: a new target for the treatment of obesity and associated co-morbidities
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Ukkola, O and Santaniemi, M
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- 2002
40. Lipoprotein lipase polymorphisms and responses to long-term overfeeding
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UKKOLA, O, TREMBLAY, A, and BOUCHARD, C
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- 2002
41. Lack of association between polymorphisms of catalase, copper–zinc superoxide dismutase (SOD), extracellular SOD and endothelial nitric oxide synthase genes and macroangiopathy in patients with type 2 diabetes mellitus
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Ukkola, O., Erkkilä, P. H., Savolainen, M. J., and Kesäniemi, Y. A.
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- 2001
42. Leptin receptor Gln223Arg variant is associated with a cluster of metabolic abnormalities in response to long-term overfeeding
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Ukkola, O., Tremblay, A., Després, J.-P., Chagnon, Y. C., Campfield, L. A., and Bouchard, C.
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- 2000
43. Polymorphisms of the β 2-adrenergic receptor gene (ADRB2) in relation to cardiovascular risk factors in men
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Rosmond, R., Ukkola, O., Chagnon, M., Bouchard, C., and Björntorp, P.
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- 2000
44. Biomarkers as predictors of sudden cardiac death in coronary artery disease patients with preserved left ventricular function (ARTEMIS study)
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Lepojärvi, E. S. (E. Samuli), Huikuri, H. V. (Heikki V.), Piira, O.-P. (Olli-Pekka), Kiviniemi, A. M. (Antti M.), Miettinen, J. A. (Johanna A.), Kenttä, T. (Tuomas), Ukkola, O. (Olavi), Perkiömäki, J. S. (Juha S.), Tulppo, M. P. (Mikko P.), and Junttila, M. J. (M. Juhani)
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Aims: Biomarkers have shown promising results in risk assessment of cardiovascular events. Their role in predicting the risk of sudden cardiac death (SCD) is not well established. We tested the performance of several biomarkers in risk assessment for SCD in patients with coronary artery disease (CAD) and preserved left ventricular function. Methods and results: The study population consisted of 1,946 CAD patients (68% male; mean age 66.9±8.6 yrs; type 2 diabetes (T2D) 43%) enrolled in the ARTEMIS study. The study subjects underwent examinations with echocardiography and measurement of several biomarkers. The primary endpoint of the study was SCD. During the mean follow up of 76±20 months 50 patients experienced SCD. Elevated high sensitive CRP (hs-CRP, p = 0.001), soluble ST2 (sST2, p
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- 2018
45. Cardiac remodeling from middle age to senescence
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Möttönen, M. J. (Mikko J.), Ukkola, O. (Olavi), Lumme, J. (Jarmo), Kesäniemi, Y. A. (Y. Antero), Huikuri, H. V. (Heikki V.), and Perkiömäki, J. S. (Juha S.)
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left ventricular walls ,fractional shortening ,aging ,left atrial diameter ,cardiac remodeling ,left ventricular mass ,left ventricular size - Abstract
Background: The data on cardiac remodeling outside the scope of myocardial infarction and heart failure are limited. Methods: A cohort of middle-aged hypertensive subjects with age- and gender-matched control subjects without hypertension (n = 1,045, aged 51 ± 6 years) were randomly selected for the OPERA study (Oulu Project Elucidating Risk of Atherosclerosis study). The majority of those who were still alive after more than 20 years of follow-up underwent thorough re-examinations. Results: Left ventricular mass index (LVMI) increased significantly from 106.5 ± 27.1 (mean ± SD) to 114.6 ± 29.1 g/m² (p < 0.001), the thickness of the left ventricular posterior wall (LVPW) from 10.0 ± 1.8 to 10.6 ± 1.7 mm (p < 0.001), fractional shortening (FS) from 35.0 ± 5.7 to 38.4 ± 7.2 % (p < 0.001), and left atrial diameter (LAD) from 38.8 ± 5.2 to 39.4 ± 6.7 mm (p = 0.028) during the 20-year follow-up. After multivariate adjustments, hypertension treated with antihypertensive medication and male gender predicted a smaller increase in the thickness of LVPW (p = 0.017 to
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- 2017
46. Presence of atrial fibrillation is associated with liver stiffness in an elderly Finnish population
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Käräjämäki, A. J. (Aki Juhani), Kettunen, O. (Olli), Lepojärvi, S. . (Samuli ), Koivurova, O.-P. (Olli-Pekka), Kesäniemi , Y. A. (Y. Antero), Huikuri, H. (Heikki), and Ukkola, O. (Olavi)
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cardiovascular system ,macromolecular substances - Abstract
Background: Chronic liver injury from different etiologies drives liver fibrosis. However, little is known about the associated factors, systemic factors in particular. Recently, non-alcoholic fatty liver disease (NAFLD) and atrial fibrillation have been shown to be associated with each other. Thereby, we aimed to study the association between atrial fibrillation and liver stiffness. Study: Extensive clinical measurements including echocardiography of the heart, transient elastography (TE) of the liver and the presence of atrial fibrillation were determined in elderly Finnish study subjects (n = 76, mean age 73 years) from OPERA (Oulu Project Elucidating the Risk of Atherosclerosis) study cohort. Half of the study subjects had non-alcoholic fatty liver disease, whereas others did not have any known hepatic morbidity. The present study was cross-sectional by nature. Results: The subjects with atrial fibrillation had higher TE values (with atrial fibrillation TE = 9.3kPa, without atrial fibrillation TE = 6.3kPa, p = 0.018). When the cohort was divided to four subgroups (those without NAFLD or atrial fibrillation, with NAFLD but without atrial fibrillation, with both conditions, and with atrial fibrillation but without NAFLD), the TE value was the highest in the subjects with both conditions (5.3kPa, 7.4kPa, 10.8kPa and 7.8kPa, respectively, p = 0.019). Moreover, the higher the TE value, the more prevalent atrial fibrillation was (the atrial fibrillation prevalence by tertiles of TE 27% / 36% / 77%, p = 0.001). Likewise, the greater the TE value, the greater the left atrial diameter, a collateral of atrial fibrillation (left atrial diameters by tertiles of TE 39mm / 45mm / 48mm, p"
- Published
- 2017
47. Ezetimibe added to statin therapy after acute coronary syndromes
- Author
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Cannon, Christopher P., Blazing, Michael A., Giugliano, Robert P., Mccagg, Amy, White, Jennifer A., Theroux, Pierre, Darius, Harald, Lewis, Basil S., Ophuis, Ton Oude, Jukema, J. 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E., Cullen, T., Eisenberg, S., Chronos, N., Allen, R.P., Erickson, B., Mahon, K., Kirby, A., Siegel, C., Stroud, L., Johnson, J., Panchal, V., Pearson, A., Abell, T., De Gregorio, M., Boomer, L., Vahdat, O., VanNatta, B., Long, P., Chalavarya, G., Skatrud, L., Carey, C., Wright, W., Mechem, C., Matthews, B., Adams, A., Vora, K., Wead, J., Koren, M., Gregory, D., El Khadra, M., Peacock, G., Kieval, J., Barron, M., Lewis, D., Grice, R., Bobek, M., Moore, C., Nygaard, T., Fischell, T., Salman, W., Schneider, C., Muhlestein, B., Peeler, D., Chang, D., Todd, A., Chilakamarri, V., Hanley, P., Gelormini, J., Iacona, M.A., Effron, B., Mazzurco, S., Mazzella, M., Wyman, P., Orchard, R., Battin, D., Rezkalla, S., Bishop, C., Sharp, S., Gredler, F., Knap, P., Fadel, M., Saucedo, J., Keng, A., Imburgia, M., Blank, E., Effat, M., Khoury, S., Mardis, R., Baldari, D., Tafuri, L., Mascolo, R., Taylor, D., Mandviwala, M., Khan, W., Mumford, T., Mayer, N., Mitchell, B., Oliver, T., Lombardi, W., Zimmerman, T., Rohrbeck, S., Cooke, L., Craig, M., Mego, D., Griffin, B., Perez, J., LeClerc, K., Addington, J., Aboufakher, R., Ahmed, A., Westecott, B., Steel, K., Hawkins, K., Shah, A., Ward, U., McGreevy, M., Goldberg, R., Prashad, R., McDonough, C., Silver, K., Josephson, R., Witsaman, S., Labib, S., Woodhead, G., Schrank, J., Bell, K., Chandna, H., Holly, D., Bethea, C., Fife, B., Gruberg, L., Singer, A., Ramgadoo, M., Lalonde, T., Morin, R., French, W., Barillas, O., Gradner, G., Kahn, Z., Gress, J., Rocco, D., Thew, S., Stifter, W., Fisher, M., McNamara, J., Kupfer, J., Agocha, A., Cush, S., Jones, S., Whitaker, T., Stover, T., Kumkumian, G., Kent, K., Greenberg, A., Pandey, P., Pytlewski, G., Matsumura, M., Kai, W., Sameshima, S., Thomas, J., MacNicholas, D., Pillai, K., Jones, D., Navas, J.P., Laskoe, B., Patel, P., Fini, G., Minor, S., Shipwash, T., Cabrera-Santamaria, A., Rivera, E., Mincher, L., Jafar, M., Yen, M., Finkle, C., Rahimtoola, A., Severson, L., Labroo, A., Jinich, D., Tam, K., Vogel, C., Aggarwal, R., Zakhary, B., Curtis, S., Lyster, M., Humphrey, K., Lavine, P., Fujise, K., Birnbaum, Y., Allen, J., Kesselbrenner, M., Michel, K., Staniloae, C., Liu, M., Sonel, A., Macioce-Caffas, A., Amidon, T., Leggett, J., Yedinak, S., Gudmundsson, G., Sabharwal, J., Dagefoerde, N., Wu, W., Meyerrose, G., Roongsritong, C., Jenkins, L., Lieberman, S., Sokol, S., Gutierrez, C., Nelson, C., Barrett, J., Hotchkiss, D., Farley, A., Atassi, K., Christy, L., Baig, M., Di Fazio, J., Meengs, M., Thomas, K., Surmitis, J., DeVault, S., Farhat, N., Hulyalkar, A., Riddell, L., Rivera, W., Sheynberg, B., Kobayashi, J., Katsaropoulos, J., Jan, M., Krucoff, M., Paterno, C., Chandrasekaran, S., Curry, R., Cassavar, D., Wheeler, M., McGarvey, J., Schwarz, L., Miller, E., Andrea, B., Carswell, B.S., Lurie, M., Patti, J., Bowden, W., Vasiliauskas, T., Latham, R., Schwartz, B., Bradford, L., Mattleman, S., Wertheimer, J., Goulden, D., Khan, M., Hawkins, B., Ostfeld, R., Mueller, H., Ash, Y., Wilson, V., Bayer, M., Marshall, J., Dobies, D., Dawson, G., Osman, A., Saba, F., Costello, T., Fuentes, F., Underwood, C., Vijay, N., Washam, M., Dietz, W., Glasgow, B., Mukherjee, S., Hinchion, N., Speirs, S., Thornley, A., Lee, K., Movahed, M., Strootman, D., Chernick, R., Parrott, C., Flock, C., Marques, V., Syzmanski, E., Rama, P., Domingo, D., Wu, L., Bauer, B., Dionisopoulos, P., Aggarwal, A., Holcomb, R., Foster, R., Hancock, T., Hargrove, J., Fletcher, A., Stine, R., Bullivant, M., Adams, K., Lohman, J., Klepper, V., Kabour, A., Neidhardt, J., Phillips, W., Tardiff, S., Aji, J., Corut, S., Foster, G., Firek, C., St Goar, F., Sumner, R., Davis, T., Schneider, R., Schneider, W., Villa, A., Desai, V., Chhabra, A., Banks, K., Herzog, W., Burley, T., Quyyumi, A., Smiley, W., Manocha, P., Fishbein, G., Weller, C., Coffman, A., Kim, C., Kedia, A., Firth, B., Rizvi, M., Dahiya, R., Foster, B., Balcells, E., Metzger, D.C., Lester, J., Bissett, J., Fahdi, I., Sides, E.A., Azrin, M., Martin, C., Quick, A., Conaway, D., Garg, M., Schallert, G., Lancaster, L., Mckissick, S., Atieh, M., Garbarino, J., Eisenberg, D., Uusinarkaus, K., Wirtemburg, P., Ellis, J., Cristaldi, J., Berglund, R., Negus, B., Pappas, J., Rocha, R., Nguyen, T., Stone, J., Janosik, D., Labovitz, A., Elmore, N., Dave, R., Loffredo, K., Gabriel, G., Snyder, C., Ahmed, O., Stone, H., Kelley, M., Diffenback, M., Friedman, B., Zirkle, J., Severa, L., Sample, S., Dignen, K., Raisinghani, A., Ben-Yehuda, O., Ghannadian, B., Moscoso, R., Mankowski, J., Boliek, W., Rukavina, M., Davis, W., Ledbetter, S., Handel, F., Mastouri, R., Mahenthiran, J., Foltz, J., Malhotra, V., Jonas, J., Berk, M., Singh, V., Nelson, M., Elsner, G., Gall, J., Kondo, N., Frank, S., Chandraratna, P., Ranasinghe, S., Ebrahimi, R., Treadwell, M., Walters, B., Hughes, L., Kramer, J., Kumar, K., Mente, T., Lachterman, B., Schifferdecker, B., Munshi, K., Sease, D., Waldo, D., Chandler, G., Manns, D., Nahhas, A., Kamalesh, M., Williams, V., Reich, D., Desalca, M., Sharma, S., Liston, M., Gupta, K., Costa, M., Altschuller, A., Lemmertz, K., Shanes, J., Hansen, C., Therrien, M., Mendelson, R., Ramnarine, R., Myers, G., Donovan, C., Klein, M., Fine, D., Owens, S., Murray, C., Ketroser, R., Heifetz, S., Darnell, Z., Touchon, R., Taghizadeh, B., Bohle, D., Norwood, D., Forrest, T., Jackson, S., Shumate, K., Bayles, A., Masroor, M., North, W.K., Fishberg, R., Merveil-Ceneus, B., Butcher, R., Menapace, F., Kilbride, S., Ramabadran, R.S., Loukinen, K., Khalil, J., Ramabadran, R., Walsh, S., Gill, S., Cyncar, R., McLachlan, J., Surakanti, V., Rusterholtz, L., Shoukfeh, F., Stephenson, L., Tsang, M., Nolan, V., Gilchrist, I., Jefferson, D., Feldman, T., Reyes, L., Santos, R., Little, W., Wesley, D., Gharib, W., Mendell, A., Esham, G., Kakavas, P., Whitcomb, C., Book, K., Bazzi, A., Alvarez, J., Cohen, Y., Ayres, T., Rhule, V., Labib, A., Schuler, P., Zughaib, M., Telck, K., Bikkina, M., Turnbull, K., Sharma, T., Orosz, S., Shah, R., Petrino, M., Hughes, M., Hershey, J., Hudock, D., Hui, P., Von Bakonyi, A., Arnold, A., Kappel, D., Pennock, G., Cloud, B., Tucker, K., Harp, L., Hoover, C., Eisenhauer, M., Roth, J., Young, C., Thai, H., Escalante, A., Bautista, J., Gazmuri, R., Nyland, J., Cubeddu, L., DeFranco, A., Dias, D., Fielding, M., Reeves, R., Hermany, P., Meissner-Dengler, S., Evans, M., Flores, E., Tannenbaum, A., McGarr, K., Moran, J., Stout, E., Allred, S., Henderson, D., Crandall, L., Strote, J., Voyles, W., Robeson, D., Bedoya, R., Omar, B., Pettyjohn, F., Revere, C., Coy, K., Margolis, J., Sotolongo, C., Scheffel, M., Munir, A., Shirwany, A., Douglas, L., Girala, R., Humphreys, R., Agarwal, J., Bankowski, D., Watson, R., Bishop, B., Klementowicz, P., Blais, D., Cohen, B., Lobur, E., Dimenna, J., Dempsey, K., Izzo, M., Bondi, L., Carell, E., Eaton, C., Saltiel, F., Grewal, G., Connolly, T., Little, T., Wiegman, P., Gips, S., Held, J., Paraschos, A., Quesada, R., Goudreau, E., Sears, M., Istfan, P., Holt, S., McClung, J., Nguyen, N., Quintana, O., Gottlieb, D., Knutson, T., Barringhaus, K., Lester, F., Sullivan, P., Rodriguez-Ospina, L., Cannon, Cp, Blazing, Ma, Giugliano, Rp, Mccagg, A, White, Ja, Theroux, P, Darius, H, Lewis, B, Ophuis, To, Jukema, Jw, De Ferrari, Gm, Ruzyllo, W, De Lucca, P, Im, K, Bohula, Ea, Reist, C, Wiviott, Sd, Tershakovec, Am, Musliner, Ta, Braunwald, E, Califf, Rm, for the IMPROVE-IT, Investigator, Cianflone, D, Cardiovascular Division (SZG), Brigham and Women's Hospital [Boston], College of Information Science and Engineering, Ritsumeikan University, Montreal Heart Institute (MONTREAL HEART INSTITUTE), Laboratoire des Micro-algues toxiques, Institut Louis Malardé [Papeete] (ILM), Institut de Recherche pour le Développement (IRD)-Institut de Recherche pour le Développement (IRD), Interuniversity Cardiology Institute Netherlands, Institute of Cardiology (WARSAW - Cardiology), Institute of Cardiology, Merck Sharp & Dohme Corp., Merck & Co. Inc, DIPARTIMENTO DI MEDICINA SPECIALISTICA, DIAGNOSTICA E SPERIMENTALE, Facolta' di MEDICINA e CHIRURGIA, AREA MIN. 06 - Scienze mediche, Cannon, C.P., Blazing, M.A., Giugliano, R.P., Mccagg, A., White, J.A., Lewis, B.S., Jukema, J.W., De Lucca, P., Im, K., Bohula, E.A., Reist, C., Wiviott, S.D., Tershakovec, A.M., Musliner, T.A., Braunwald, E., Califf, R.M., for the IMPROVE-IT Investigators [.., C. Rapezzi, ], Other departments, Cannon, Christopher P, Blazing, Michael A., Giugliano, Robert P., Mccagg, Amy, White, Jennifer A., Theroux, Pierre, Darius, Harald, Lewis, Basil S., Ophuis, Ton Oude, Jukema, J. Wouter, De Ferrari, Gaetano M., Ruzyllo, Witold, De Lucca, Paul, Kyungah, Im, Bohula, Erin A., Reist, Craig, Wiviott, Stephen D., Tershakovec, Andrew M., Musliner, Thomas A., Braunwald, Eugene, and Califf, Robert M.
- Subjects
Male ,Simvastatin ,acute coronary syndrome ,aged ,anticholesteremic agents ,azetidines ,cardiovascular diseases ,cholesterol, ldl ,double-blind method ,drug therapy, combination ,ezetimibe ,female ,humans ,hydroxymethylglutaryl-coa reductase inhibitors ,kaplan-meier estimate ,male ,middle aged ,simvastatin ,triglycerides ,medicine (all ,[SDV]Life Sciences [q-bio] ,Kaplan-Meier Estimate ,030204 cardiovascular system & hematology ,Bococizumab ,Triglyceride ,chemistry.chemical_compound ,0302 clinical medicine ,Azetidine ,Cardiovascular Disease ,Anticholesteremic Agent ,Acute Coronary Syndrome ,Aged ,Anticholesteremic Agents ,Azetidines ,Cardiovascular Diseases ,Cholesterol, LDL ,Double-Blind Method ,Drug Therapy, Combination ,Female ,Humans ,Hydroxymethylglutaryl-CoA Reductase Inhibitors ,Middle Aged ,Triglycerides ,030212 general & internal medicine ,Medicine (all) ,Research Support, Non-U.S. Gov't ,Hazard ratio ,General Medicine ,Acute Coronary Syndrome, Aged ,Anticholesteremic Agents, Azetidines, Cardiovascular Diseases ,Ezetimibe, Female, Humans ,Male, Middle Aged ,3. Good health ,Multicenter Study ,Editorial ,Cholesterol ,Randomized Controlled Trial ,Combination ,Ezetimibe ,lipids (amino acids, peptides, and proteins) ,Human ,medicine.drug ,medicine.medical_specialty ,Acute Coronary Syndroms ,Urology ,Acute Coronary Syndrome/drug therapy ,Anticholesteremic Agents/adverse effects ,Anticholesteremic Agents/therapeutic use ,Azetidines/adverse effects ,Azetidines/therapeutic use ,Cardiovascular Diseases/epidemiology ,Cardiovascular Diseases/mortality ,Cardiovascular Diseases/prevention & control ,Cholesterol, LDL/blood ,Hydroxymethylglutaryl-CoA Reductase Inhibitors/adverse effects ,Hydroxymethylglutaryl-CoA Reductase Inhibitors/therapeutic use ,Simvastatin/therapeutic use ,Triglycerides/blood ,NO ,LDL ,03 medical and health sciences ,[SDV.MHEP.CSC]Life Sciences [q-bio]/Human health and pathology/Cardiology and cardiovascular system ,Drug Therapy ,Internal medicine ,Journal Article ,medicine ,Comparative Study ,Alirocumab ,business.industry ,PCSK9 ,ta3121 ,Lomitapide ,DOENÇAS CARDIOVASCULARES ,Endocrinology ,chemistry ,Statin Therapy ,Hydroxymethylglutaryl-CoA Reductase Inhibitor ,business ,[SDV.MHEP]Life Sciences [q-bio]/Human health and pathology - Abstract
BACKGROUND: Statin therapy reduces low-density lipoprotein (LDL) cholesterol levels and the risk of cardiovascular events, but whether the addition of ezetimibe, a nonstatin drug that reduces intestinal cholesterol absorption, can reduce the rate of cardiovascular events further is not known.METHODS: We conducted a double-blind, randomized trial involving 18,144 patients who had been hospitalized for an acute coronary syndrome within the preceding 10 days and had LDL cholesterol levels of 50 to 100 mg per deciliter (1.3 to 2.6 mmol per liter) if they were receiving lipid-lowering therapy or 50 to 125 mg per deciliter (1.3 to 3.2 mmol per liter) if they were not receiving lipid-lowering therapy. The combination of simvastatin (40 mg) and ezetimibe (10 mg) (simvastatin-ezetimibe) was compared with simvastatin (40 mg) and placebo (simvastatin monotherapy). The primary end point was a composite of cardiovascular death, nonfatal myocardial infarction, unstable angina requiring rehospitalization, coronary revascularization (≥30 days after randomization), or nonfatal stroke. The median follow-up was 6 years.RESULTS: The median time-weighted average LDL cholesterol level during the study was 53.7 mg per deciliter (1.4 mmol per liter) in the simvastatin-ezetimibe group, as compared with 69.5 mg per deciliter (1.8 mmol per liter) in the simvastatin-monotherapy group (PCONCLUSIONS: When added to statin therapy, ezetimibe resulted in incremental lowering of LDL cholesterol levels and improved cardiovascular outcomes. Moreover, lowering LDL cholesterol to levels below previous targets provided additional benefit. (Funded by Merck; IMPROVE-IT ClinicalTrials.gov number, NCT00202878.).
- Published
- 2015
48. Serum 25-hydroxyvitamin D is associated with major cardiovascular risk factors and cardiac structure and function in patients with coronary artery disease.
- Author
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Pekkanen, M.P., Ukkola, O., Hedberg, P., Piira, O.P., Lepojärvi, S., Lumme, J., Tulppo, M.P., and Huikuri, H.V.
- Abstract
Background and aims Vitamin D deficiency has been associated with increased risk for cardiovascular (CV) disease, but the possible effects of Vitamin D on cardiac structure and function are not well characterized. Methods and results The correlation between 25-hydroxyvitamin D levels and metabolic and cardiac echocardiographic parameters was studied in ARTEMIS study population including 831diabetic and 659 non-diabetic patients with stable coronary artery disease (CAD). Low levels of Vitamin D were associated with high BMI (p < 0.001), high total and LDL cholesterol and triglyceride levels (p < 0.001 for all) in both diabetics and non-diabetics. Among non-diabetic patients, low Vitamin D was also associated independently with elevated systolic and diastolic blood pressure (p < 0.005). Low Vitamin D levels were independently associated with reduced left ventricular (LV) ejection fraction (p < 0.005) and increased left atrial diameter (p < 0.03) measured by cardiac ultrasound by 2-dimensional echo. In the non-diabetic group, low Vitamin D levels were associated with impaired LV filling (high E/E′) (p < 0.03) and low E/A mitral flow pattern measured by Doppler echocardiography (p < 0.05). Among diabetics, low Vitamin D levels were also related to increased LV end-systolic diameter (p < 0.05) and right ventricular diameter (p < 0.005). The association between LV diastolic filling (E/E′) and Vitamin D levels was significant (p < 0.01) after adjustment for the commonly recognized risk factors of diastolic dysfunction in linear regression analysis. Conclusions Low Vitamin D is associated with several major cardiovascular risk factors and cardiac structural changes including impaired systolic and diastolic function, which together may explain the association of low Vitamin D to worse cardiovascular outcome. [ABSTRACT FROM AUTHOR]
- Published
- 2015
- Full Text
- View/download PDF
49. Resistin is linked to inflammation, and leptin to metabolic syndrome, in women with inflammatory arthritis.
- Author
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Kontunen, P, Vuolteenaho, K, Nieminen, R, Lehtimäki, L, Kautiainen, H, Kesäniemi, YA, Ukkola, O, Kauppi, M, Hakala, M, and Moilanen, E
- Subjects
RESISTIN ,JOINT diseases ,ENDOCRINE diseases ,CELLULAR immunity ,C-reactive protein - Abstract
Objective: To investigate how inflammation and metabolic syndrome (MetS) are associated with adipokine levels in patients with inflammatory arthritis. Methods: Fifty-four female patients with arthritis were enrolled in the study. Twenty (37%%) of these patients had MetS, which was diagnosed according to the definition of the International Diabetes Federation (IDF). Interleukin (IL)-6 and four adipokines (resistin, leptin, adiponectin, and adipsin) were determined by immunoassay. Healthy women with body mass index (BMI) between 22 and 25 kg//m
2 served as controls. Results: The patients with arthritis had higher levels of resistin than the healthy controls. This difference was clear in patients without MetS (17.4 in patients vs. 10.8 ng//mL in controls, p < 0.001), and even higher resistin levels were found in the patients with MetS (20.7 ng//mL; p < 0.001 vs. healthy controls; and p == 0.095 vs. patients without MetS). In the patients with arthritis and MetS, resistin correlated positively with IL-6 (Pearson's r == 0.5, p == 0.03). Leptin levels were increased in arthritis patients with MetS as compared to healthy controls, but not in patients without MetS. The statistically significant difference between patients with MetS and controls remained when leptin was adjusted with BMI. Accordingly, adiponectin levels were lower in patients with MetS than in healthy controls (p < 0.05). Leptin, adiponectin, and adipsin did not correlate with the inflammatory cytokine IL-6 or with C-reactive protein (CRP). Conclusions: The results show that high resistin levels are associated with arthritis independently of MetS, whereas leptin is increased only in arthritis patients with MetS. [ABSTRACT FROM AUTHOR]- Published
- 2011
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- View/download PDF
50. Early atherosclerosis and IgG2 to bacteria are associated with FcγRIIa genotype in non-smokers.
- Author
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Sämpi, M., Ukkola, O., Päivänsalo, M., Kesäniemi, Y. A., and Hörkkö, S.
- Subjects
- *
ATHEROSCLEROSIS , *HIGH density lipoproteins , *IMMUNE complexes , *PHAGOCYTOSIS , *STREPTOCOCCUS pneumoniae , *POLYSACCHARIDES , *MICROBIAL mutation , *GENETIC polymorphisms - Abstract
Background Involvement of low density lipoprotein (LDL) immune complexes (ICs) in atherogenesis has been proposed. Human FcγRIIa receptor (CD32) plays a crucial role in the phagocytosis of IgG2 ICs and a functional point mutation 131His/Arg diminishes IgG2 binding to the receptor. Study design We examined FcγRIIa-131His/Arg polymorphism, IgG2 antibody titres to oxidized low-density lipoprotein (OxLDL) and Streptococcus pneumoniae cell wall polysaccharide (CWPS) and subclinical atherosclerosis in a large cohort of Finnish subjects ( n = 1041). Results Non-smoking subjects with homozygous 131His/His genotype had more premature atherosclerosis ( P = 0·004) and higher IgG2 to bacterial CWPS ( P = 0·002) compared with other genotypes. Smoking subjects had significantly higher intima-media thickness (IMT) than that of non-smokers ( P < 0·001) and genotype-dependent associations were indistinct. There was no association between FcγRIIa genotype and antibody titres to OxLDL. Conclusions Our data demonstrate that FcγRIIa 131His/Arg polymorphism is associated with subclinical atherosclerosis in non-smoking subjects. Furthermore, FcγRIIa genotype is associated with IgG2 titres to bacterial CWPS, but not to OxLDL. These data propose possible involvement of FcγRIIa receptor in atherogenesis. [ABSTRACT FROM AUTHOR]
- Published
- 2009
- Full Text
- View/download PDF
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