Lecture 13- Heart Disease Flashcards
describe atherosclerosis
o Monocytes adhere to endothelial surface proteins (adhesion molecules)–>monocytes migrate into intima, accumulate cholesterol, form foam cells –> release growth factors–>triggers proliferation of SMC–>lipid accumulates
o Plaque develops over decades, acute complications occur suddenly i.e. rupture of plaque (don’t know what triggers this to happen)
long term management of atherosclerosis and effects
lowering of LDL-C by statins (HMG CoA reductase inhibitors)
- reduces lipid content in plaque, inflammation and thrombosis
- relative risk reduction about 24%
lowering BP, quit smoking, control diabetes
Compare CHD event rates in secondary and primary prevention trials
secondary
- stronger the statin, the lower the mortality rate drops compared to the placebo
- event rate is so high- statin saves lives
primary
- event rate is less compared to secondary
- when event rate is already really low, then taking statin to reduce risk is not really worth it
- only worth it with other risk factors combined with elevated LDL
examples of acute coronary syndromes
- heart attack
- MI- death of myocardium
- unstable angina- presence of chest pain without myocardial damage
- sudden onset of chest pain
- myocardial damage (troponin, CK in blood)
definition difference between secondary and primary prevention trials
secondary- had an attack then put the patient on statins
primary- high LDL cholesterol but not yet had heart attack
what is a culprit lesion?
often mild plaque–>little calcification
may expand outwards in days/weeks
pathology of acute MI with reference to occlusive coronary thrombi
thrombus forms on ruptured atheromatous plaque- suddenly occludes or severely narrows artery
why do plaques rupture?
controversial
- macrophages may be responsible for decreased collagen synthesis, increased collagen breakdown by MMPs, production of procoagulants so induce thrombosis when plaque ruptures
- remember- one localised plaque ruptures, not multiple
ways to manage acute coronary syndromes
recognition- patient, ambulance, medical urgent reperfusion - thrombolysis- IV - stent (percutaneous coronary intervention) into artery to open it wide then give drugs to reduce thrombolysis - anticoagulants, antiplatelet agents -lipid lowering
most heart valve disease is ?
degenerative
valvular heart disease used be a consequence of ?
rheumatic fever
what is rheumatic fever?
immune response to strep pyogenes, antibody cross-reactivity-
Type II hypersensitivity
age group common for rheumatic fever?
children 6-15 yrs
clinical features of rheumatic fever?
heart murmur–>valvular damage especially to mitral valve
- fever, arthritis, rash, skin nodules
methods for RhF prevention
penicillin and public health
RhF is a disease of?
poverty and poor housing- lower socioeconomic communities
what is rheumatic heart disease? what happens in it?
repeated attacks of RhF that worsen heart disease
- valve thickening, narrowing
- progression to heart failure
- over long time course 5-10years
3 forms of cardiomyopathy
hypertrophic
restrictive
dilated
what occurs in hypertrophic cardiomyopathy?
increased left ventricular wall thickness- especially of septum and outflow obstruction
-cellular hypertrophy–>stiff ventricle–>ventricular arrhythmias–>sudden death
genetic basis for hypertrophic cardiomyopathy
- AD
- mutation in genes for sarcomere protein (e.g. beta cardiac myosin heavy chain)
- 2000 mutations in 11 genes
- heterogenous phenotype (partially correlated to mutation, same mutation may cause different phenotypes)
causes of dilated cardiomyopathy
multiple causes
mostly idiopathic
some genetic (sarcomere proteins, desmosomes, cytoskeleton, connections between cells)
what is bradycardia?
an arrhythmia
- sinus node dysfunction, atrio-ventricular node block
what is tachycardia?
an arrhythmia
- automatic focus, re-entry, channelopathies
other arrhythmias
atrial flutter, atrial fibrillation, AV nodal re-entry tachycardia, ventricular tachycardia
