X hits on this document

PDF document

Common Congenital Heart Lesions - page 29 / 126





29 / 126

29 of 126

  • Contributions to the development of atherosclerosis include:

    • o

      Creating injury to the endothelium and increasing its permeability to lipoproteins

      • o

        Increased numbers of scavenger receptors on macrophages, thus enhancing the formation of foam cells

      • o

        Increased production of proteoglycans by the SMCsÆaccumulation of modified LDL

      • o

        Promotion of inflammation via the presence of Angiotensin II, which serves as both a mediator of hypertension and as a proinflammatory cytokine.

Diabetes Mellitus

  • Diabetics have a 3 to 5-fold increased risk of suffering cardiovascular events

  • Contributions to the development of atherosclerosis include:

    • o

      Non-enzymatic glycation of lipoproteins in diabetic patientsÆenhanced cholesterol uptake by macrophages

      • o

        Prothrombotic or anti-fibrinolytic states common in diabetes

      • o

        Impaired endothelial function as evidenced by low levels of NO & increased WBC adhesion

*Recall that diabetes (particulary insulin-resistant), dyslipidemia, obesity, and hypertension are all part of the “Metabolic Syndrome,” a condition that predisposes one to atherosclerosis.

Physical Activity

  • Low levels of physical activity correlate with obesity and an increased risk for cardiovascular events

  • Contributions to lowering the risk of atherosclerosis include:

    • o

      Improvements in the lipid profile

      • o

        Improvements in blood pressure

      • o

        Enhancement of insulin sensitivity

      • o

        Increased production of NO by endothelial cells

Major, nonmodifiable risk factors include the following:

  • Advanced age

  • Male gender

  • History of coronary disease among family members of a young age

(specifically, males >55 years and/or females >65 years)

  • Estrogen status

Document info
Document views141
Page views141
Page last viewedFri Oct 21 17:35:41 UTC 2016