Обзор американских кардиологических журналов за неделю (ссылки)

[Chevychelov]

Title: Association of Marine Omega-3 Fatty Acid Levels With Telomeric Aging in Patients With Coronary Heart Disease
Topic: Prevention/Vascular
Date Posted: 1/29/2010
Author(s): Farzaneh-Far R, Lin J, Epel ES, Harris WS, Blackburn EH, Whooley MA.
Citation: JAMA 2010;303:250-257.
Clinical Trial: No
Study Question: Is there a correlation between blood levels of omega-3 fatty acids and telomere length, a potential marker of biological age?
Methods: This was a prospective cohort study of 608 ambulatory outpatients with stable coronary artery disease recruited from the Heart and Soul Study between September 2000 and December 2002 and followed up to January 2009 (median, 6.0 years; range, 5.0-8.1 years). Leukocyte telomere length was measured at baseline and again after 5 years of follow-up. Multivariable linear and logistic regression models were used to investigate the association of baseline levels of omega-3 fatty acids (docosahexaenoic acid [DHA] and eicosapentaenoic acid [EPA]) with subsequent change in telomere length.
Results: Individuals in the lowest quartile of DHA+EPA experienced the fastest rate of telomere shortening (0.13 telomere-to-single-copy gene ratio [T/S] units over 5 years; 95% confidence interval [CI], 0.09-0.17), whereas those in the highest quartile experienced the slowest rate of telomere shortening (0.05 T/S units over 5 years; 95% CI, 0.02-0.08; p < 0.001 for linear trend across quartiles). Levels of DHA+EPA were associated with less telomere shortening before (unadjusted β coefficient x 10−3 = 0.06; 95% CI, 0.02-0.10) and after (adjusted β coefficient x 10−3 = 0.05; 95% CI, 0.01-0.08) sequential adjustment for established risk factors and potential confounders. Each 1-standard deviation increase in DHA+EPA levels was associated with a 32% reduction in the odds of telomere shortening (adjusted odds ratio, 0.68; 95% CI, 0.47-0.98).
Conclusions: Among a cohort of patients with coronary artery disease, there was an inverse relationship between baseline blood levels of marine omega-3 fatty acids and the rate of telomere shortening over 5 years.
Perspective: High dietary intake of marine omega-3 fatty acids has previously been associated with reduced risk of death and cardiovascular disease. Many mechanisms for these beneficial effects have been proposed including antiplatelet, anti-arrhythmic, anti-inflammatory, and triglyceride-lowering effects. The current study raises a new potential mechanism of benefit from omega-3 fatty acids, reduced telomere shortening. During cell division, there is progressive loss of tandem repeat DNA sequences (telomeres) that form protective caps at the end of chromosomes. Eventually, this process leads to cell death. Genetic and environmental factors may influence telomere shortening, and short telomeres have been associated with cardiovascular disease and death. Factors that prevent telomere loss could lead to reduced disease burden and increased longevity. Additional studies are necessary to establish a causal relationship between omega-3 fatty acids and prevention of telomere shortening, as well as to uncover mechanisms by which this may occur. Daniel T. Eitzman, M.D., F.A.C.C.

Title: Smoking Status and Long-Term Survival After First Acute Myocardial Infarction: A Population-Based Cohort Study
Topic: Prevention/Vascular
Date Posted: 1/29/2010
Author(s): Gerber Y, Rosen LJ, Goldbourt U, Benyamini Y, Drory Y, on behalf of the Israel Study Group on First Acute Myocardial Infarction.
Citation: J Am Coll Cardiol 2009;54:2382-2387.
Clinical Trial: No
Study Question: Is cigarette smoking reduction among persistent smokers associated with lower mortality?
Methods: Consecutive patients ≤65 years of age, discharged from eight hospitals in central Israel after first acute myocardial infarction (AMI) in 1992 to 1993, were followed through 2005. Extensive data, including self-reported smoking habits, were obtained at baseline and four times during follow-up. Cox proportional hazards regressions were used to assess the hazard ratios (HRs) for death associated with smoking categories modeled as time-dependent variables.
Results: At baseline, smokers were younger, more likely to be male, and had a lower prevalence of hypertension and diabetes than nonsmokers. Over a median follow-up of 13.2 years, 427 deaths occurred in 1,521 patients. The multivariable-adjusted hazard ratios for mortality were 0.57 (95% confidence interval [CI], 0.43-0.76) for never-smokers, 0.50 (95% CI, 0.36-0.68) for pre-AMI quitters, and 0.63 (95% CI, 0.48-0.82) for post-AMI quitters, compared with persistent smokers. Among persistent smokers, upon multivariable adjustment including pre-AMI intensity, each reduction of five cigarettes smoked daily after AMI was associated with an 18% decline in mortality risk (p < 0.001).
Conclusions: Smoking cessation either before or after AMI is associated with improved survival. Among persistent smokers, reducing intensity after AMI appears to be beneficial.
Perspective: The mechanisms leading to an increase in coronary events in smokers include that it promotes lipid oxidation, low high-density lipoprotein cholesterol, inflammation, thrombosis, oxidative stress, endothelial dysfunction, and coronary vasospasm. The type of coronary plaque and plaque rupture differ between smokers and nonsmokers. Despite the well known association of cigarette smoking and coronary events, the degree to which smoking cessation reduces very long-term mortality and the contribution of the degree of continuing abstinence or reduction over 10 years had not been studied. Further, the relationship between the value of total cessation and decreasing consumption was not known. The results provide very good evidence to enhance patient education in both primary and secondary prevention. Melvyn Rubenfire, M.D., F.A.C.C.