Coronary Artery Disease Flashcards
collection of diseases of the heart and arterial vascular system
arteriosclerotic cardiovascular disease
ASCVD diseases (6)
coronary heart/artery disease
congestive heart failure/cardiomyopathy
peripheral artery disease (Carotid/peripheral)
aortic atherosclerosis
CVA/stroke
valvular heart disease
etiologies of CVD
atherosclerosis and hypertension
diseases of coronary arteries result in:
stable angina
acute coronary syndromes (unstable angina, STEMI, NSTEMI)
Arteriosclerosis pathophysiology
begins in early life (visible disease in arteries)
- lipoproteins penetrate endothelial layer and aggregate
- Expression of adhesion molecules attract and bind monocytes
- monocytes move into intima and ingest lipoproteins = foam cells
- endothelial cell death decreases prostacyclin and NO production (vasoconstriction, pro clotting)
- Foam cell releases inflammatory cytokines
- fibrous cap formation
- calcium deposition (decreased flexibility)
- foam cell necrosis and lipid pool formation
- enzymatic break down and inflammation cause degradation of fibrous cap (rupture risk and thrombogenic particles)
- plaque ages and becomes more stable
in what regions to atheroma typically occur?
- branching and curvature of vessels
- areas where vessel is irregular shape
- where blood has sudden change in velocity
*all sites of turbulent flow
accumulation of lipoproteins in the intimidating is accelerated by
systemic HTN
hypercholesterolemia
cigarette smoking
inflammation/oxidative stress
loss of prostacyclin in due to endothelial cells causes
inability to relax and vasodilate vessels
which plaques are more vulnerable to rupture
small new ones
they are not blocking artery but they are weaker and have pro-thrombogenic abilities
which plaques are more likely to cause ACS/stroke/Cva?
young, easily ruptured plaques
which plaques are more likely to cause stable angina, claudication, unstable angina
long known, established plaques
two ways atherogenesis can end:
- plaque slowly grows to block vessels
2. plaque ruptures and causes occlusion
40-70% occlusion clinical presentation
asymptomatic
may or may not cause a change on stress test
70% occlusion clinical presentation
exertion symptoms
extertional angina and claudication
90% occlusion
symptoms at rest
unstable angina
plaque remodel the coronary artery in two ways
- positive remodeling (bulging of wall)
2. negative remodeling (narrowing
positive remodeling
most common, less likely to cause angina
arterial wall BULDGES out at plaque
negative remodeling
plaque narrows the vessel lumen as it grows
etiologies of cardiac tissue ischemia
vasospasm (prinzmetal angina)
emboli
congenital lesions
arteriosclerosis
when oxygen demand increases, supply must also increase or ischemia occurs
what causes increased myocardial oxygen demand
increased heart rate
increased wall stress/tension (LVH)
increased contractility