Pathophysiology - Coronary Atherosclerosis

Coronary Atherosclerosis

• Abnormal accumulation of lipid or fatty substance and fibrous tissue in the vessel wall
• Reduced blood flow to the myocardium
• Causes repetitious inflammatory response to artery wall injury
• Progressive inadequate blood flow deprives the muscle cell of oxygen

A.  Risk Factors

• Non-modifiable
• Hereditary
• Age (over 40 years old)
• Race 
• higher in African – American than whites
• more in non-Hispanic whites
• Sex 
• 3x in men than premenopausal women, 
• more in postmenopausal women
• more in early menopause than late
• more in women who take contraceptive pills
• more in smoking
• Modifiable
• 7x more prevalent in North America, Europe, New Zealand
• Urban than rural population
• In developing countries, more in the affluent; in Britain and America it’s the reverse
• Lack of estrogen in women
• Cigarette smoking = tar being carcinogenic, nicotine which causes increase release of epinephrine and norepinephrine, carbon monoxide which reduces the amount of blood
• Hypertension
• Elevated cholesterol level
• Physical inactivity
• Obesity
• Diabetes

B.  Pathophysiology

Atherosclerosis, or the narrowing of arteries due to the build-up of plaque along the inner lining, is the single most lethal condition in the United States. The plaques consist principally of fat and cholesterol deposits but also contain blood platelets, decomposing muscle cells and other tissue. Since plaques usually reduce blood flow in major arteries, their presence represents a serious health risk, leading to heart disease, stroke and the disruption of kidney and intestinal function. Poor circulation, also a result of plaque build-up, impairs movement of the limbs. Fragments of the plaques may break off and travel through the bloodstream to obstruct smaller vessels. The plaques unfortunately become larger and more numerous with age, especially in people with high levels of cholesterol in their diet and bloodstream.

Fatty streaks deposited in the intima of arterial wall

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Continued atherosclerosis (thickening and loss of elasticity)

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Inflammatory response

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T –lymphocytes and monocytes ingest the lipid and then die

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Smooth muscle cells proliferate to replace the dead fat core (atheroma)

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Forming of a fibrous cap or a seal

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Atheroma protrudes the vessel wall causing further obstruction

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Thick fibrous cap resistant to stress and blood flow

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Thin fibrous cap may rupture and bleed causing a thrombus

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Thrombus obstruct blood flows