scholarly journals Apolipoprotein A-II Is a Negative Risk Indicator for Cardiovascular and Total Mortality: Findings from the Ludwigshafen Risk and Cardiovascular Health Study

2008 ◽  
Vol 54 (8) ◽  
pp. 1405-1406 ◽  
Author(s):  
Karl Winkler ◽  
Michael M Hoffmann ◽  
Ursula Seelhorst ◽  
Britta Wellnitz ◽  
Bernhard O Boehm ◽  
...  
Keyword(s):  
Cardiovascular Health ◽  
Total Mortality ◽  
Health Study ◽  
Cardiovascular Health Study ◽  
Risk Indicator ◽  
Apolipoprotein A

scholarly journals Iron Metabolism, Hepcidin, and Mortality (the Ludwigshafen Risk and Cardiovascular Health Study)

2019 ◽  
Vol 65 (7) ◽  
pp. 849-861 ◽  
Author(s):  
Tanja B Grammer ◽  
Hubert Scharnagl ◽  
Alexander Dressel ◽  
Marcus E Kleber ◽  
Günther Silbernagel ◽  
...  
Keyword(s):  
Iron Metabolism ◽  
Cardiovascular Health ◽  
Iron Status ◽  
Transferrin Saturation ◽  
Total Mortality ◽  
Cardiovascular Death ◽  
Health Study ◽  
Cardiovascular Health Study ◽  
Artery Disease ◽  
Stable Cad

Abstract BACKGROUND Anemia has been shown to be a risk factor for coronary artery disease (CAD) and mortality, whereas the role of iron metabolism remains controversial. METHODS We analyzed iron metabolism and its associations with cardiovascular death and total mortality in patients undergoing coronary angiography with a median follow-up of 9.9 years. Hemoglobin and iron status were determined in 1480 patients with stable CAD and in 682 individuals in whom significant CAD had been excluded by angiography. RESULTS Multivariate-adjusted hazard ratios (HRs) for total mortality in the lowest quartiles of iron, transferrin saturation, ferritin, soluble transferrin receptor (sTfR), and hemoglobin were 1.22 (95% CI, 0.96–1.60), 1.23 (95% CI, 0.97–1.56), 1.27 (95% CI, 1.02–1.58), 1.26 (95% CI, 0.97–1.65), and 0.99 (95% CI, 0.79–1.24), respectively, compared to the second or third quartile, which served as reference (1.00) because of a J-shaped association. The corresponding HRs for total mortality in the highest quartiles were 1.44 (95% CI, 1.10–1.87), 1.37 (95% CI, 1.05–1.77), 1.17 (95% CI, 0.92–1.50), 1.76 (95% CI, 1.39–2.22), and 0.83 (95% CI, 0.63–1.09). HRs for cardiovascular death were similar. For hepcidin, the adjusted HRs for total mortality and cardiovascular deaths were 0.62 (95% CI, 0.49–0.78) and 0.70 (95% CI, 0.52–0.90) in the highest quartile compared to the lowest one. CONCLUSIONS In stable patients undergoing angiography, serum iron, transferrin saturation, sTfR, and ferritin had J-shaped associations and hemoglobin only a marginal association with cardiovascular and total mortality. Hepcidin was continuously and inversely related to mortality.

Copper, ceruloplasmin, and long-term cardiovascular and total mortality (The Ludwigshafen Risk and Cardiovascular Health Study)

2014 ◽  
Vol 48 (6) ◽  
pp. 706-715 ◽  
Author(s):  
T. B. Grammer ◽  
M. E. Kleber ◽  
G. Silbernagel ◽  
S. Pilz ◽  
H. Scharnagl ◽  
...  
Keyword(s):  
Cardiovascular Health ◽  
Total Mortality ◽  
Health Study ◽  
Cardiovascular Health Study

scholarly journals n-3 Fatty acids and risk for fatal coronary disease

2019 ◽  
Vol 78 (4) ◽  
pp. 526-531 ◽  
Author(s):  
William S. Harris ◽  
Francis B. Zotor
Keyword(s):  
Fatty Acids ◽  
Cardiovascular Health ◽  
Controlled Trial ◽  
Total Mortality ◽  
Plasma Phospholipid ◽  
Cardiovascular Death ◽  
Health Study ◽  
Cardiovascular Health Study ◽  
Blood Levels ◽  
Omega 3

The purpose of this review is to consider the effects of the long-chain n-3 fatty acids found in marine foods, EPA and DHA, on risk for CVD, particularly fatal outcomes. It will examine both epidemiological and randomised controlled trial findings. The former studies usually examine associations between the dietary intake or the blood levels of EPA + DHA and CVD outcomes or, on occasion, total mortality. For example, our studies in the Framingham Heart Study and in the Women's Health Initiative Memory Study have demonstrated significant inverse relations between erythrocyte EPA + DHA levels (i.e. the Omega-3 Index) and total mortality. Recent data from the Cardiovascular Health Study reported the same relations between plasma phospholipid n-3 levels and overall healthy ageing. As regards randomised trials, studies in the 1990s and early 2000s were generally supportive of a cardiovascular benefit for fish oils (which contain EPA + DHA), but later trials were generally not able to duplicate these findings, at least for total CVD events. However, when restricted to effects on risk for fatal events, meta-analyses have shown consistent benefits for n-3 treatment. Taken together, the evidence is strong for a cardioprotective effect of EPA + DHA, especially when consumed in sufficient amounts to raise blood levels into healthy ranges. Establishing target EPA + DHA intakes to reduce risk for cardiovascular death is a high priority.

Abstract 20: Circulating Omega-6 Polyunsaturated Fatty Acids and Total and Cause-Specific Mortality: the Cardiovascular Health Study

Circulation ◽  
2014 ◽  
Vol 129 (suppl_1) ◽  
Author(s):  
Jason H Wu ◽  
Rozenn Lemaitre ◽  
Irena King ◽  
Xiaoling Song ◽  
David Siscovick ◽  
...  
Keyword(s):  
Fatty Acids ◽  
Linoleic Acid ◽  
Polyunsaturated Fatty Acids ◽  
Cardiovascular Health ◽  
Cox Regression ◽  
Total Mortality ◽  
Health Study ◽  
Cardiovascular Health Study ◽  
Specific Mortality ◽  
Omega 6

Background: While omega-6 polyunsaturated fatty acids (n-6 PUFA) have been recommended to reduce CHD, controversy remains about benefits vs. harms, including depending on types of n-6 PUFA and diseases examined. Aims: To assess associations of circulating n-6 PUFA including linoleic acid (LA, the major dietary PUFA), Γ-linoleic acid (GLA), dihomo-Γ-linoleic acid (DGLA), and arachidonic acid (AA),with incident total and cause-specific mortality in the Cardiovascular Health Study (CHS), a community-based US cohort. Methods: Among 2,692 participants age≥65y and free of CVD at baseline, plasma phospholipid n-6 PUFA were measured at baseline using standardized methods. All-cause and cause-specific mortality, and total (fatal or nonfatal) incident CHD and stroke, were assessed and adjudicated centrally. Associations of PUFA biomarkers with risk were assessed by multivariable Cox regression. Results: During 33,091 person-years of follow-up (1992-2010), 1920 deaths occurred (including 660 cardiovascular deaths), as well as 414 fatal and 410 nonfatal CHD events, and 150 fatal and 384 nonfatal strokes. In multivariable models, higher LA was associated with lower risk of total mortality, with extreme quintile HR 0.84 (95% CI 0.71-0.98, P- trend 0.002). Lower death was largely attributable to CVD rather than non-CVD causes, especially nonarhythmic CHD mortality (HR 0.50, 95% CI 0.31-0.80, P- trend 0.001). Phospholipid GLA, DGLA, and AA levels were not associated with total or cause-specific mortality; e.g., for AA and CHD death, the extreme quintile HR was 0.98 (95% CI 0.71-1.37, P- trend 0.72). Evaluated semi-parametrically, LA showed graded (monotonic) inverse associations with total mortality ( Figure 1A ). There was little evidence that associations of n-6 PUFA with total mortality varied by age, sex, race, or plasma n-3 PUFA (Bonferroni corrected P =NS, Figure 1B ). Conclusion: Higher circulating LA, but not other n-6 PUFA, is inversely associated with total and CHD mortality in older adults.

Abstract P265: Plasma Phospholipid Trans Fatty Acids, Cardiovascular Diseases, and Total Mortality: The Cardiovascular Health Study

Circulation ◽  
2013 ◽  
Vol 127 (suppl_12) ◽  
Author(s):  
Qianyi Wang ◽  
Fumiaki Imamura ◽  
Rozenn N Lemaitre ◽  
Eric B Rimm ◽  
Frank M Sacks ◽  
...  
Keyword(s):  
Fatty Acids ◽  
Ischemic Stroke ◽  
Trans Fatty Acids ◽  
Cardiovascular Health ◽  
Total Mortality ◽  
Plasma Phospholipid ◽  
Health Study ◽  
Cardiovascular Health Study ◽  
Cvd Risk ◽  
Cvd Mortality

Introduction: Whereas trans fatty acids (TFAs) have generally been evaluated as a group, emerging evidence suggests that trans18:2, but not trans18:1 or trans16:1, isomers are especially adverse for health. Few studies have investigated how biomarkers of different TFA isomers relate to CVD or total mortality. Objective: To examine prospective associations of circulating trans16:1n9 (16:1n9t), total trans18:1 (18:1t, the sum of 18:1n5-12), and n9cis/n6trans, n9trans/n6cis, and n9trans/n6trans 18:2 (18:2ct, 18:2tc, 18:2tt) with incident CVD events and total mortality. Methods: We prospectively evaluated 2,788 adults in the Cardiovascular Health Study, age 72±5y, free of prevalent CVD, and having plasma phospholipid TFA measures from blood stored in 1992. CVD events and mortality were centrally adjudicated through 2010, including total mortality, CVD death, CHD death, nonfatal MI (NFMI), and ischemic stroke. Risk associated with each TFA was assessed using Cox proportional hazards adjusting for sociodemographics, lifestyle, dietary habits, prevalent diseases, and the 5 TFA mutually. Results: During 31,863 person-years, 1,681 deaths occurred including 581 CVD and 373 CHD deaths; as well as 383 NFMI and 328 ischemic strokes. 18:2ct was associated with higher CVD mortality (quintile 5 vs. 1 HR 1.48, 95%CI 0.98-2.23, p trend 0.04), but not total mortality or nonfatal CVD events. 18:2tc was related to higher NFMI (HR 1.69, 95%CI 1.06-2.69, p trend<0.01), while 18:2tt was not significantly associated with mortality or CVD endpoints. Similarly, 16:1n9t was positively associated with NFMI (HR 2.96, 95%CI 1.80-4.88, p trend<0.01), and ischemic stroke (HR 2.00, 95%CI 1.19-3.36, p trend 0.02), but not mortality endpoints. 18:1t was associated with lower CVD (HR 0.52, 95%CI 0.34-0.79, p trend=0.01) and CHD (HR 0.49, 95%CI 0.29-0.84, p trend 0.02) mortality, but these findings for 18:1t were substantially (~50%+) weakened when analyses did not mutually adjust for all 5 TFA, which were intercorrelated (r -0.08 to 0.78). Conclusions: Specific 18:2 TFA isomers, 18:2ct and 18:2tc but not 18:2tt, as well as 16:1n9t are prospectively associated with higher incidence of CVD events. 18:1t is associated with lower CVD risk, perhaps owing at least partly to co-adjustment for multiple correlated TFAs. The general specificity of all findings for CVD events, rather than total mortality or non-CVD mortality, is consistent with adverse physiologic effects of TFA on CVD risk factors. These results highlight the need for further investigation of effects and determinants of specific TFA subclasses and isomers.

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