In this review, the authors examine the evidence linking social support to physiological processes and characterize the potential mechanisms responsible for these covariations. A review of 81 studies revealed that social support was reliably related to beneficial effects on aspects of the cardiovascular, endocrine, and immune systems. An analysis of potential mechanisms underlying these associations revealed that (a) potential health-related behaviors do not appear to be responsible for these associations; (b) stress-buffering effects operate in some studies; (c) familial sources of support may be important; and (d) emotional support appears to be at least 1 important dimension of social support. Recommendations and directions for future research include the importance of conceptualizing social support as a multidimensional construct, examination of potential mechanisms across levels of analyses, and attention to the physiological process of interest.

The relationship between social support and physiological processes: a review with emphasis on underlying mechanisms and implications for health.

Jeffrey L. Anderson, MD, FACC, FAHA, Chair 

Jonathan L. Halperin, MD, FACC, FAHA, Chair-Elect 

Alice K. Jacobs, MD, FACC, FAHA, Immediate Past Chair 2009–2011 [§§][1]

Sidney C. Smith, Jr, MD, FACC, FAHA, Past Chair 2006–2008 [§§][1]

Cynthia D. Adams, MSN, APRN-BC, FAHA[§§][1]

Nancy M

2012 ACCF/AHA/ACP/AATS/PCNA/SCAI/STS guideline for the diagnosis and management of patients with stable ischemic heart disease: executive summary: a report of the American College of Cardiology Foundation/American Heart Association task force on practice guidelines, and the American College of Physicians, American Association for Thoracic Surgery, Preventive Cardiovascular Nurses Association, Society for Cardiovascular Angiography and Interventions, and Society of Thoracic Surgeons.

Jeffrey L. Anderson, MD, FACC, FAHA, Chair , Jonathan L. Halperin, MD, FACC, FAHA, Chair-Elect , Nancy M. Albert, PhD, CCNS, CCRN, FAHA, Biykem Bozkurt, MD, PhD, FACC, FAHA, Ralph G. Brindis, MD, MPH, MACC, Mark A. Creager, MD, FACC, FAHA[§§][1], Lesley H. Curtis, PhD, FAHA, David DeMets, PhD,

/pdf/2014-aha-acc-guideline-for-the-management-of-patients-with-17ab5yki53.pdf

2014 AHA/ACC Guideline for the Management of Patients With Valvular Heart Disease: Executive Summary A Report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines

Copy number variants (CNVs) account for a major proportion of human genetic polymorphism and have been predicted to have an important role in genetic susceptibility to common disease. To address this we undertook a large, direct genome-wide study of association between CNVs and eight common human diseases. Using a purpose-designed array we typed approximately 19,000 individuals into distinct copy-number classes at 3,432 polymorphic CNVs, including an estimated approximately 50% of all common CNVs larger than 500 base pairs. We identified several biological artefacts that lead to false-positive associations, including systematic CNV differences between DNAs derived from blood and cell lines. Association testing and follow-up replication analyses confirmed three loci where CNVs were associated with disease-IRGM for Crohn's disease, HLA for Crohn's disease, rheumatoid arthritis and type 1 diabetes, and TSPAN8 for type 2 diabetes-although in each case the locus had previously been identified in single nucleotide polymorphism (SNP)-based studies, reflecting our observation that most common CNVs that are well-typed on our array are well tagged by SNPs and so have been indirectly explored through SNP studies. We conclude that common CNVs that can be typed on existing platforms are unlikely to contribute greatly to the genetic basis of common human diseases.

/pdf/genome-wide-association-study-of-cnvs-in-16-000-cases-of-3slzq6gg52.pdf

Genome-wide association study of CNVs in 16,000 cases of eight common diseases and 3,000 shared controls

https://www.rpcardio.com/jour/article/download/115/124

Effect of Long-Term Exposure to Lower Low-Density Lipoprotein Cholesterol Beginning Early in Life on the Risk of Coronary Heart Disease: A Mendelian Randomization Analysis

Sebening F

Papers

Coronary artery disease