Atherosclerosis and Ischemic Heart Disese Flashcards
list 6 contributing factors to athero patho
chronic endothelial injury, high LDL, oxidation of LDL, leukocyte recruitment (mono/mac and lymphs), release of growth factors, proliferation and migration of SMCs and fibroblasts
what kind of things characterize endothelial dysfn
inreased permeability, leukocyte/platelet adhesion (expressing adhesion molecules), lipid depostition and modification, shift from vasodilation to constriction, procoagulant
diff b/w fatty streak and fibrofatty plaque
fatty streaks have foam cells but they are in the intima and they are flat w/ no fibrous cap
fibrofatty plaques have developed fibrous cap overlying a necrotic lipid core, are now raised and disturb blood flow
most likely arteries to get athero
abdominal aorta, coronary arteries, popliteal, descending thoracic, internal carotids
reason ischemia causes angina
release of metabolic molecules like lactate, serotonin, adenosine that activate pain fibers
how does decreasing HR affect coronary blood supply
as HR decreases, more time is spent in diastole (diastole decreases w/ high HR) and this is when coronary vessels are perfused
how to calculate coronary perfusion presure
aortic diastolic pressure-LVEDP
blood is flowing from proximal aorta to capillaries in the myocardium, high pressure within that myocardium would oppose perfusion
high LVEDP and low aortic pressure (HF) would compromise this
2 ways athero reduces coronary flow
fixed decrease in radius (stenosis) and decrease in dynamic vasodilation (endothelial dysfn- less NO, etc)
point of stress tests
provoke supply demand mismatch w/ exercise or agent (dobutamine, adenosine) and use EKG, nuclear imaging, or ECHO for detection of stenosis
when is stress test positive
angina is reproduced, ECG abnormalities (ST depressions)
gold standard to dx of CAD
coronary angiography- more invasive but better diagnostic, use for ppl not responding to drug therapy, unstable, or abnormal other tests
difference in tx of stable angina vs ACS
stable angina tx are targeted at reducing demand, ACS tx are targeted at restoring supply
major circulating regulator of demand
catecholamines- raise HR, contractility and thus CO
catecholamine effect on vascular tone
depends on state of endothelium!
if healthy coronary arteries, endothelium responds w/ vasodilator paracrine factors (NO and prostacyclin)
if atherosclerotic, more pronounced vasoconstriction and less blood supply
net effect of catecholamines w/ atherosclerosis
increase CO and demand, increase resistance and thus decrease supply
