Ischemic Heart Disease

Question 1

• 4 steps in atherosclerosis process?
• Treatable risk factors that decrease risk? (3) Treatable but unclear risk? (5) Not treatable? (3)
• How does smoking affect endothelium? (3)
• Hypertension? (3)
• Diabetes?
• Lipids? HDL?
• Inflammation?
• Coronary O2 extraction at rest? Implications?
• When is LV perfused?

Answer 1

• Fatty streak (endo injury, lipid deposition, mac and T cell recruitment), fibrous plaque (activated mac foam cells, fibrous plaque with lipid core), occlusive plaque, plaque rupture
• Smoking, htx, dyslipidemia; diabetes, obesity, PA, inflamm, stress; Male, age, genetics
• plt. activation, NO dysfunction, adverse lipoproteins
• Shear tress, AT2/aldo hormones, LVH
• Inflamm
• Oxidized LDL pro inflammatory; reverse chol. transport
• CRP and IL6 increase inflamm
• Max extraction; BFR is only way to increase perfusion
• Diastole only

Question 2

• What effects coronary circulation supply? Treat?
• Demand? Treat?
• Acute MI leads to what type of failure?
• Problem with angiography?
• Treatment? (4)
• Immediate MI treatment? (3)
• Vessels with CABG?
• Supply equation?
• Vessel does what next to stenosis?

Answer 2

• CBF (perfusion pressure (auto-regulation), time (1/HR), vascular resistance (LaPlace); Oxygen content; Treat hypo, diastolic with BB, resistance with VD’s
• HR, wall tension, inotropic state; anti hypertensives, BB, nitrates, Ca channel blocker
• systolic
• Only see’s lumen and not wall of vessels
• statins, anti plt., anti anginal (BB, Ca, nitrates), LV dys (ACE, ARB)
• Internal mammary, saphenous, prosthetic
• BF = content * CBF rate
• Dilation when there is arteriolar resistance

Question 3

• Plaque pathogenesis? (5)
• LDL content? Low risk goal? High risk?
• HDL content?
• VLDL content?
• Chylomycrons? Arethrogenic?
• Cholesterol equations? (3)
• Chylomicrons: Made where? Increase with? In fasting plasma when?
• VLDL: Made where? Normal levels? Increase with?
• HDL: Main protein? Can mediate what? How? If HDL is too high? Function vs. amount?

Answer 3

• LDL trapped in intima; LDL oxidized; Mac digestion; Cytokines released; proinflamm plaque
• Chol loaded with a little protein; 500
• Liver; Tgt clear it; fxn more impor

Question 4

• Apo-lipoproteins:
  1. ) Apo-B: On what? How many? Potentially? Helps distinguish? Correlated with?
  2. ) Lipo(a): Acts like? Levels most regulated by? Risk?
• What are lipoproteins?
• Atherosclerotic risk with lipoproteins? Leads to?

Answer 4

• VLDL, LDL; 1/molecule; aherogenic; risk of CHD; non-HDL cholesterol
• LDL; genetics; pro thrombotic
• Transport for lipids
• Increase risk with LDL, Tg (women>men), Lipo(a), decreased with HDL; increased inflamm.

Question 5

• Endothelium: Naturally what? (5)
• Intima composition? Media? Adventitia?
• Large arteries? Small? Arterioles?
• NO pathway? (4)
• Generation of inflammatory state? (5)
• What degrade fibrous cap? What distinguishes stable from vulnerable plaque?
• Stoke often caused by? (2)
• MI caused by?
• CAD often caused by?
• Venous vs. arterial clots?
• 3 things that cause endo dysfunction?

Answer 5

• Anti inflamm; anti thrombotic; vasodilatory; impermeable to big molecules; resist leukocyte adhesion
• Endo + CT layer; SM + CT; Loose CT
• Elastin; Collagen; SM
• L-arginine –> NO –> cGMP –> relaxation
• Increased selectins, CAM, cytokines, ox stress and less NO
• MMP’s; Stable = Big fibrous cap with small lipid core; calcified; less inflamm
• Atheroembo from carotid bifurcation; Thromboemboli from left atrial appendage
• in-situ thrombosis
• Claudification
• Venous = Fibrin rich; RBC; genetics; environment
  Arterial = plt rich; plaque rupture
• Thrombosis, inflamm; spasm

Question 6

• Epi of ACS? What percent die?
• Usually due to?
• Transmural usally due to? Subendo?
• ECG:ST vector with transmural? Subendo?
• Markers? (2) Rise when? Peak when? More specific?
• UA, NSTEMI, STEMI: Symptoms? Occlusion? Biomarkers? ECG?

Answer 6

• 1.7 million/ year; 38%
• Rupture of an athero plaque
• full occlusion; partial
• ST vector away; towards leads; opposite
• TnT/TnI: More sensitive/soecific: 3-4 hours; 18 hours
• CK: 3-8 hours; 24 hours
  1. ) UA: Escalating, rest or new angina; partial; No; ST depression or normal
  2. ) NSTEMI: Prolonged chest pain; partial; yes; ST depression
  3. ) STEMI: Prolonged chest pain; total; yes; ST elevation