Abstract:The relation between nonfasting serum triglycerides and death from coronary heart disease was studied in 37,546 men aged 35-49 years who were examined during 1972-1977 in four counties in Norway. During an average follow-up period of nine years, 369 deaths from coronary heart disease occurred. In univariate analysis, log(triglycerides) were a weak, but statistically significant predictor of coronary death in the age groups 40-44 and 45-49 years. Within-area analysis showed that a high triglyceride area represe… Show more
“…Several large observational studies have assessed the association between blood lipid concentrations and cardiovascular risk. It was reported that both higher TG and TC levels were significant independent predictors of coronary death only in participants in the upper age range (Tverdal et al, 1989). After simultaneous adjustment for a variety of coronary risk factors, TG concentrations manifested significant correlation with MI, ischemic heart disease and survival after 26 years of follow-up in a large-scale prospective cohort study (Nordestgaard et al, 2007).…”
ABSTRACT. Hyperlipidemia is a well-established risk factor for the development of coronary atherosclerosis, while intermedin (IMD) has been identified as a novel calcitonin/calcitonin gene-related peptide family member involved in cardiovascular protection. However, whether IMD protects against hyperlipidemia-associated myocardial ischemia/reperfusion (MI/R) injury is unknown. We established a hyperlipidemia model using Sprague-Dawley rats, and created a MI/R condition by ligating the cardiac left circumflex artery. The possible pathophysiological role of IMD and its physiological function in MI/R was further studied. The level of IMD significantly decreased in hyperlipidemia rats (P < 0.05). After MI/R, the IMD level was increased both in the plasma and myocardial tissue of hyperlipidemia rats compared to the sham-operated rats (P < 0.001). As evaluated by the activity of LDH, CK-MB, MDA and SOD, additional IMD was revealed to alleviate MI/R heart injury in hyperlipidemia rats (P < 0.05). By regulating the process of cardiomyocyte apoptosis and inflammatory reaction, IMD could perform an important role in cardio-protection, especially against hyperlipidemia-associated MI/R injury. Additional IMD could protect cardiac myocytes against MI/R injury via reduction of apoptosis and inflammation in the hyperlipidemia rat model, and thus, it may play a potential role as a novel therapeutic target for cardiac ischemic injury in hyperlipidemic patients.
“…Several large observational studies have assessed the association between blood lipid concentrations and cardiovascular risk. It was reported that both higher TG and TC levels were significant independent predictors of coronary death only in participants in the upper age range (Tverdal et al, 1989). After simultaneous adjustment for a variety of coronary risk factors, TG concentrations manifested significant correlation with MI, ischemic heart disease and survival after 26 years of follow-up in a large-scale prospective cohort study (Nordestgaard et al, 2007).…”
ABSTRACT. Hyperlipidemia is a well-established risk factor for the development of coronary atherosclerosis, while intermedin (IMD) has been identified as a novel calcitonin/calcitonin gene-related peptide family member involved in cardiovascular protection. However, whether IMD protects against hyperlipidemia-associated myocardial ischemia/reperfusion (MI/R) injury is unknown. We established a hyperlipidemia model using Sprague-Dawley rats, and created a MI/R condition by ligating the cardiac left circumflex artery. The possible pathophysiological role of IMD and its physiological function in MI/R was further studied. The level of IMD significantly decreased in hyperlipidemia rats (P < 0.05). After MI/R, the IMD level was increased both in the plasma and myocardial tissue of hyperlipidemia rats compared to the sham-operated rats (P < 0.001). As evaluated by the activity of LDH, CK-MB, MDA and SOD, additional IMD was revealed to alleviate MI/R heart injury in hyperlipidemia rats (P < 0.05). By regulating the process of cardiomyocyte apoptosis and inflammatory reaction, IMD could perform an important role in cardio-protection, especially against hyperlipidemia-associated MI/R injury. Additional IMD could protect cardiac myocytes against MI/R injury via reduction of apoptosis and inflammation in the hyperlipidemia rat model, and thus, it may play a potential role as a novel therapeutic target for cardiac ischemic injury in hyperlipidemic patients.
“…The previous study on men also included the Oslo study and the Troms0 study (1974), in which only men were studied. 6 A detailed description of the study procedures has been given by Bjartveit et al7 All people participating answered a questionnaire at home about history of cardiovascular disease, diabetes, treatment for hypertension, symptoms of angina pectoris, physical activity during leisure, smoking habits, and stress factors in social life. In this study the healthy group consists of those who gave negative answers to questions about myocardial infarction, angina pectoris, other heart disease, atherosclerosis of legs, cerebral stroke, diabetes, treatment for hypertension, use of nitroglycerine, and symptoms suggesting angina pectoris or atherosclerosis obliterans, or both.…”
Section: Methodsmentioning
confidence: 99%
“…From these studies we have previously reported non-fasting triglyceride concentration to be a weak predictor of death from coronary heart disease in men; the strength of association depending heavily on whether total cholesterol concentration was accounted for. 6 The period of follow up is now sufficient (12 to 16 years) to give fairly precise estimates of the relation between triglyceride concentration and mortality from coronary disease in women.…”
“…We collapsed current and former smokers to ever-smokers. We further categorized ever-smokers according to the following factors: age at smoking initiation (16,(17)(18)(19)(20)(21)(22)(23)(24), 25 years), numbers of cigarettes smoked per day (1-9, [10][11][12][13][14][15][16][17][18][19]20), smoking duration in years (1-19, 20-29, 30-39, 40), and number of pack-years (i.e., number of cigarettes smoked per day, divided by 20, multiplied by the duration of smoking in years; 0-9, 10-19, 20). All subjects not being current or former smokers were classified as never smokers.…”
Background: Smoking is a recently established risk factor for colon cancer. We wanted to explore the hypothesis that women may be more susceptible to smoking-attributed colon cancer than men as one of the possible explanations for the high colon cancer risk of Norwegian women.Methods: We followed 602,242 participants aged 19 to 67 years at enrollment in 1972-2003, by linkage to national registries through December 2007. We used Cox proportional hazard models to estimate HRs and 95% confidence intervals (CI).Results: During a mean follow-up of 14 years, altogether 3,998 (46% women) subjects developed colon cancer. Female ever-smokers had a 19% (HR ¼ 1.19, 95% CI ¼ 1.09-1.32) and male ever-smokers an 8% (HR ¼ 1.08, CI ¼ 0.97-1.19) increased risk of colon cancer compared with never smokers. For all the four dose-response variables examined, female ever-smokers in the most exposed category of smoking initiation, (HR ¼ 1.48, 95% CI ¼ 1.21-1.81), of daily cigarette consumption (HR ¼ 1.28, 95% CI ¼ 1.06-1.55), of smoking duration (HR ¼ 1.47, 95% CI ¼ 1.11-1.95), and of pack-years of smoking (HR ¼ 1.33, 95% CI ¼ 1.11-1.57) had a significantly increased risk of more than 20% for colon cancer overall and of more than 40% for proximal colon cancer, compared with never smokers. A test for heterogeneity by gender was statistically significant only for ever smoking and risk of proximal colon cancer (Wald c
scite is a Brooklyn-based organization that helps researchers better discover and understand research articles through Smart Citations–citations that display the context of the citation and describe whether the article provides supporting or contrasting evidence. scite is used by students and researchers from around the world and is funded in part by the National Science Foundation and the National Institute on Drug Abuse of the National Institutes of Health.