Pathophysiology of Coronary Heart Disease

Endothelial layer of normal coronary arteries will be damaged by the presence of risk factors, among others: hemodynamic factors such as hypertension, vasoconstrictor agents, mediators (cytokines) from the blood cells, cigarette smoke, atherogenic diet, increased blood sugar levels and oxidation of LDL-C. 

This damage causes the endothelial cells produce a cell adhesion molecule such as silicon (interleukin -1, (IL -1)); tumor necrosis factor alpha (TNF-alpha)), chemokines (monocyte chemoattractant factor 1, (MCP-1; IL-8 ), and growth factor (bFGF). Cells Inflammation as Monocytes and T-lymphocyte entry into the endothelial surface of the endothelium and migration into the sub-endothelial. Monocytes then differentiate into macrophages and take LDL and then the macrophages become foam cells .

Oxidized LDL causes endothelial cell death and result in inflammatory responses. In addition, there was the response of angiotensin II, which cause vasodilation and trigger protombik effects involving platelets and coagulation factors.

As a result of endothelial damage occurred and formed a protective response fibrofatty and fibrous lesions, plaques atherosklerosik triggered by inflammation. Plaques that occur can be unstable (vulnerable) and ruptures that could lead to acute coronary syndrome.

Risk Factors for Coronary Heart

Risk Factors That Can’t Be Changed	Risk Factors Can Be Modified
Age	Smoking
Gender	Hipertension
Family History	Dyslipidemia
Ethnic	Diabetes Mellitus
	Obesity and Metabolic Syndrome
	Stress
	The High-Fat Diet Calories
	In Physical Activity
New Risk Factors
Inflammation
Fibrinogen
Homocysteine
Oxidative stress