The n-3 fatty acids found in fish are strongly associated with a reduced risk of sudden death among men without evidence of prior cardiovascular disease.
Background
Whether omega-3 fatty acid supplementation reduces risk of cardiovascular disease or cancer remains unclear.
Methods
The VITamin D and OmegA-3Trial (VITAL) was a randomized, placebo-controlled, 2X2 factorial trial of vitamin D3 (2000IU/day) and marine omega-3 fatty acids (1 g/day) in the primary prevention of cardiovascular disease and cancer among 25,871 U.S. men aged ≥50 and women aged >55, including 5,106 African Americans. Primary endpoints were major cardiovascular events (myocardial infarction, stroke, and cardiovascular mortality) and total invasive cancer. Secondary outcomes included individual components of the cardiovascular composite, the composite plus coronary revascularization, site-specific cancers, and cancer mortality. This paper reports the results of omega-3 and placebo.
Results
During a median 5.3 years, rates of the primary outcomes did not differ between the omega-3 and placebo groups -- 805 participants had a major cardiovascular event, hazard ratio [HR]= 0.92; 95% confidence interval [CI], 0.80–1.06, p= 0.24. Invasive cancer was diagnosed in 1,617 participants, HR 1.03 (0.93-1.13, p=0.56). In the analysis of key secondary endpoints, hazard ratios and 95% CIs comparing omega-3 to placebo were: expanded cardiovascular events, HR 0.93 (0.82-1.04); total myocardial infarction HR 0.72 (0.59-0.90); total stroke, HR 1.04 (0.83-1.31); cardiovascular mortality HR 0.96 (0.76-1.21); and cancer deaths (n=341, HR 0.97 (0.79-1.20). For all-cause mortality (n=978), the HR was 1.02 (0.90-1.15). No excess risks of bleeding or other serious adverse events were observed.
Conclusions
Omega-3 fatty acid supplementation did not reduce major cardiovascular events or cancer incidence.
These prospective data from a study of U.S. male physicians suggest that habitual vigorous exercise diminishes the risk of sudden death during vigorous exertion.
Our findings suggest that diets lower in carbohydrate and higher in protein and fat are not associated with increased risk of coronary heart disease in women. When vegetable sources of fat and protein are chosen, these diets may moderately reduce the risk of coronary heart disease.
Sudden cardiac death (SCD) from cardiac arrest is a major international public health problem accounting for an estimated 15–20% of all deaths. Although resuscitation rates are generally improving throughout the world, the majority of individuals who suffer a sudden cardiac arrest will not survive. SCD most often develops in older adults with acquired structural heart disease, but it also rarely occurs in the young, where it is more commonly due to inherited disorders. Coronary heart disease (CHD) is known to be the most common pathology underlying SCD, followed by cardiomyopathies, inherited arrhythmia syndromes, and valvular heart disease. Over the past three decades, declines in SCD rates have not been as steep as for other causes of CHD deaths, and there is a growing fraction of SCDs not due to CHD and/or ventricular arrhythmias, particularly among certain subsets of the population. The growing heterogeneity of the pathologies and mechanisms underlying SCD present major challenges for SCD prevention, which are magnified further by a frequent lack of recognition of the underlying cardiac condition prior to death. Multifaceted preventative approaches, which address risk factors in seemingly low risk and known high-risk populations will be required to decrease the burden of SCD. In this Compendium, we review the wide-ranging spectrum of epidemiology underlying SCD within both the general population and in high-risk subsets with established cardiac disease placing an emphasis on recent global trends, remaining uncertainties, and potential targeted preventive strategies.
OMOCYSTEINE LEVELS HAVEbeen directly associated with cardiovascular risk in observational studies 1 ; and daily supplementation with folic acid, vitamin B 6 , vitamin B 12 , or a combination have been shown to reduce homocysteine levels to varying degrees in intervention studies. 2 Based on these data, several randomized trials were designed to test the hypothesis that supplementation with folic acid or B vitamins or both would prevent cardiovascular disease (CVD). However, published trials on patients with preexisting vascular disease have not demonstrated a benefit of folic acid or B vitamins on CVD risk. 3 Participants in observational studies were followed up for longer durations then participants in randomized trials 1 ; therefore, it is plausible that homocysteine lowering may have had a greater effect if participants were treated and observed for longer periods of time. Metaanalyses of randomized trials sug-For editorial comment see p 2086.
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