Ischemic heart disease Flashcards
effect of LDL cholesterol
pro-inflammatory, atherogenic; taken up by macrophages; activates platelets
effect of HDL cholesterol
opposes atherothrombosis; inhibits oxidation of LDLs/tissue factor/endothelial adhesion molecules; stimulates endothelial NO production; enhances reverse cholesterol transport
risk factors for coronary atherosclerosis
treatable: smoking, hypertension, dyslipidemia; treatable/might reduce risk: diabetes/insulin resistance, obesity, inflammation, stress, sedentary lifestyle; not treatable: male gender, age, genetics
inflammation and CHD
lipid-laden macrophages are proinflammatory; extravascular inflammation; circulating markers: inflammatory cells in arterial atheroma release IL-6; hepatocytes recognize IL-6 and respond with CRP; can measure in peripheral blood
what is unique about coronary circulation
myocardium depends on aerobic metabolism; to increase supply, must increase flow rate, because maximal amount of O2 extracted at rest; LV perfused in diastole only (systole constricts intramural coronary vessels)
calculate O2 delivery
O2 delivery = CBF rate x O2 content
how stenosis affects perfusion pressure
normal - autoregulation in arterioles prevents changes in perfusion pressure; stenosis - autoregulation (dilation of resistance vessels) exhausted if deltaP too great; deltaP proportional to stenosis length and 1/diameter^4
determinants of myocardial O2 supply
coronary blood flow rate (perfusion pressure, perfusion time (1/HR) (tachycardia shortens diastole), vascular resistance); O2 content of blood
determinants of myocardial O2 demand
heart rate; wall tension (systolic BP and chamber dimension); inotropic state
pathophysiology of stable coronary heart disease
obstructive coronary lesion limits flow, causes myocardial ischemia; cardinal symptom = angina pectoris (chest pain)
treatment of stable coronary heart disease
increase O2 supply; perfusion pressure - prevent hypotension; diastolic time - rate slowing drugs (beta blockers); coronary resistance - vasodilator drugs (nitrates, Ca2+ blockers); coronary angioplasty or bypass surgery; O2 content - treat anemia and hypoxemia (incomplete saturation of hemoglobin); OR reduce O2 demand; systolic pressure - antihypertensive drugs; heart rate - rate slowing drugs (beta blockers, Ca2+ blockers); wall tension - limit LV cavity size by limiting preload (diuretics, nitrates); inotropic state - give negative inotropes
pathophysiology of unstable coronary heart disease
inflammation in arterial wall - weakening of fibromuscular cap - plaque fissure/rupture; thrombogeneic components exposed to blood; trhombosis; MI or necrosis
treatment of unstable coronary heart disease
early reperfusion; hospitalization; intravenous nitroglycerin; beta blockers; aspirin and anti-platelets; anticoagulation; early catheterization OR if unavailable give thrombolytics
diagnosis of CAD from ECG
resting ECG: ST segment changes (depression usually); T wave inversion; Q-waves; stress ECG: dynamic ST segment changes ; check with perfusion imaging
what is the problem with using angiography to look at CAD?
angiography underestimates severity of CAD
