Cardiovascular Disease

Question 1

Cardiovascular disease

Answer 1

“Disease and dysfunction to the myocardium and blood vessels, includes numerous problems, many of which are related to a process called atherosclerosis.”

Defined by the presence of stenosis which impairs blood flow

Question 2

Major causes of CVD

Answer 2

• atherosclerosis
• thrombo-embolism
• vasculitis

Question 3

Non modifiable risk factors for CVD

Answer 3

• Gender (Male>Female)
• Age
• Male >40
• Female >50 (post menopause)
• Race (African American or Asian)
• Family History

Question 4

Modifiable risk factors for CVD

Answer 4

• Hypertension
• Tobacco use
• Elevated blood glucose (IFG/diabetes)
• Physical inactivity - 150min/week Moderate (3-6METs) - 75min/week Vigorous (<6METs)
• Overweight and obesity - Overweight BMI 25-29.9 - Obsese BMI >30
• Cholesterol/lipids - Total<180 mg/dLis considered optimal. - HDL 40-60mg/dL - LDL 100-129mg/DL

Question 5

atherosclerosis

Answer 5

• hardening of the arteries
  •Recent evidence demonstrates that atherosclerosis is a dynamic chronic inflammatory condition.
  •Pathogenesis involves lipids, thrombosis, elements of the vascular wall, and immune cells.

Question 6

Atherosclerosis characteristics

Answer 6

• Slow, progressive disease
• Starts in 2nd& 3rd decade of life
• Very long incubation period
• Often undetectable
• Even with moderate to high grade
• Initially Plaques are sparsely distributed
• Increase in number and size over time
• Can affect any artery

Question 7

Role of Endothelial Cells

Answer 7

• EC normally produce antithrombotic molecules that prevent blood clots.
• EC modulate the immune response by resisting leukocyte adhesion and therefore inhibiting inflammation.
• Branch points are subjected to turbulent flow and tend to lack these effects.
• When subjected to various stressors, EC can also produce prothrombotic molecules. - In response to injury or infection, - EC secrete chemokines and produce cell surface adhesion molecules.

Question 8

Laminar shear stress favors what?

Answer 8

• NO production
• Kruppel Like Factor 2 (KLF-2); mediates the immune response, prevents deposition
• ++ Superoxide Disumutase(SOD) protects against reactive oxygen species (ROS).

Question 9

Endothelial dysfunction

Answer 9

• Increases Adhesiveness of the endothelium (Increases expression of vascular cell adhesion molecules-for leukocytes, T cells, platelets and increases permeability to oxidized LDL).
• Macrophages engulf oxidized LDL and become foam cells
• Endothelium becomes procoagulant vs. anticoagulant and local adhesion of the above molecules is associated with secretion of cytokines and growth factors
• Transmigration of molecules (e.g., leukocytes) into the wall

Question 10

Evolution of atherosclerotic plaque: fatty streaks

Answer 10

• Characterized by lipid-filling smooth muscle cells

* Potentially reversible

Question 11

Evolution of atherosclerotic plaque: fibrous plaque

Answer 11

• Lipoproteins transport/deposits LDLs into the arterial intima
• Fatty streak is covered by collagen and calcium deposits forming a fibrous plaque that appears grayish or whitish
• Result = Narrowing of the vessel lumen

Question 12

Evolution of atherosclerotic plaque: complicated lesion/ unstable plaques

Answer 12

• Continued inflammation can result in plaque instability, ulceration, and rupture.
• Lipid core is exposed to the blood stream, platelets accumulate, and thrombus forms.
• Result = Narrowing of lumen or thrombo-embolotic event

Question 13

Pathophysiology of therosclerosis

Answer 13

• Endothelial dysfunction
• Inflammatory process involving many cellular markers within the lesion
• Deposits of fatty streaks initiating event
• Lesions occur in large and medium sized vessels
• Maybe present throughout a person’s life-time

Question 14

Complications of atherosclerosis

Answer 14

• Calcification of atherosclerotic plaque
• Rupture or ulceration
• Hemorrhage into the plaque leads to further narrowing
• Embolization
• Weakening of the vessel wall leads to aneurysm