9 research outputs found

    Coronary Heart Disease Mortality Declines in the United States From 1979 Through 2011: Evidence for Stagnation in Young Adults, Especially Women

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    Background— Coronary heart disease (CHD) mortality rates have fallen dramatically over the past 4 decades in the Western world. However, recent data from the United States and elsewhere suggest a plateauing of CHD incidence and mortality among young women. We therefore examined recent trends in CHD mortality rates in the United States according to age and sex. Methods and Results— We analyzed mortality data between 1979 and 2011 for US adults ≥25 years of age. We calculated age-specific CHD mortality rates and compared estimated annual percentage changes during 3 approximate decades of data (1979–1989, 1990–1999, and 2000–2011). We then used Joinpoint regression modeling to assess changes in trends over time on the basis of inflection points of the mortality rates. Adults ≥65 years of age showed consistent mortality declines, which became even steeper after 2000 (women, −5.0%; men, −4.4%). In contrast, young men and women (<55 years of age) initially showed a clear decline in CHD mortality from 1979 until 1989 (estimated annual percentage change, −5.5% in men and −4.6% in women). However, the 2 subsequent decades saw stagnation with minimal improvement. Notably, young women demonstrated no improvements between 1990 and 1999 (estimated annual percentage change, 0.1%) and only −1% estimated annual percentage change since 2000. Joinpoint analyses provided consistent results. Conclusions— The dramatic decline in CHD mortality since 1979 conceals major heterogeneities. CHD death rates in older groups are now falling steeply. However, young adults have experienced frustratingly small decreases in CHD mortality rates since 1990. The drivers of these major differences in CHD mortality trends by age and sex merit urgent study

    AN AGGREGATE OF PATHWAY-RELATED BIOMARKERS PREDICT RISK OF ACUTE MYOCARDIAL INFARCTION AND DEATH

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    Activation of diverse pathophysiologic processes that include thrombotic, inflammatory, and immune pathways contribute to plaque rupture and adverse outcomes in CAD. We hypothesized that an aggregate biomarker risk score comprised of C-reactive protein (CRP), fibrin degradation products (FDP)

    Telomere Shortening, Regenerative Capacity, and Cardiovascular Outcomes

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    RATIONALE: Leucocyte telomere length (LTL) is a biological marker of aging, and shorter LTL is associated with adverse cardiovascular outcomes. Reduced regenerative capacity has been proposed as a mechanism. Bone marrow-derived circulating progenitor cells (PCs) are involved in tissue repair and regeneration. OBJECTIVE: To examine the relationship between LTL and PCs, and their impact on adverse cardiovascular outcomes. METHODS AND RESULTS: We measured LTL by quantitative PCR in 566 outpatients (age 63±9 years, 76% male) with coronary artery disease (CAD). Circulating PCs were enumerated by flow cytometry. After adjustment for age, gender, race, BMI, smoking and previous myocardial infarction, a shorter LTL was associated with a lower CD34(+) cell count: for each 10% shorter LTL, CD34(+) levels were 5.2% lower (p<0.001). After adjustment for the aforementioned factors, both short LTL (<Q1) and low CD34+ levels (<Q1) predicted adverse cardiovascular outcomes (death, myocardial infarction, coronary revascularization or cerebrovascular events) independently of each other, with a hazards ratio (HR) of 1.8, 95% confidence interval (CI), 1.1–2.0, and a HR of 2.1, 95% CI, 1.3–3.0, respectively, comparing Q1 to Q2–4. Patients who had both short LTL (<Q1) and low CD34+ cell count (<Q1), had the greatest risk of adverse outcomes (HR=3.5, 95% CI, 1.7–7.1). CONCLUSION: Although shorter LTL is associated with decreased regenerative capacity, both LTL and circulating PC levels are independent and additive predictors of adverse cardiovascular outcomes in CAD patients. Our results suggest that both biological aging and reduced regenerative capacity contribute to cardiovascular events, independent of conventional risk factors
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