Pathology of Ischemic Heart Disease Flashcards
What branch of the right main coronary artery supplies the heart areas of right dominant hearts? Where would this come from otherwise?
Posterior descending coronary artery
- > supplies posterior 1/3 of IV septum, posterior and inferior walls of left ventricle
- > otherwise this would come from left circumflex artery
Is ischemia or hypoxemia worse? How are they related?
Related - both are causes of tissue hypoxia
Ischemia = poor blood flow Hypoxemia = low blood oxygen (pulmonary function, anemia, etc)
Ischemia is worse because you cannot properly carry in nutrients and remove waste
Why does tachycardia exacerbate ischemic heart disease?
- Increases myocardial oxygen demand
2. Reduces diastolic filling time
Is unstable angina considered reversible? How does it occur?
Yes -> due to acute atheromatous plaque disruption via hemorrhage, erosion, or rupture leading to PARTIALLY occluded vessel.
Often destabilized by mechanical stress + plaque inflammation w/metalloprotease activation via macrophages.
What is the clinical progression of unstable angina?
Progressively worsening episodes of anginal pain with increasing frequency, duration, and severity. Eventually will even occur at rest.
This is why it is called “crescendo” angina
What is the mechanistic difference between what usually causes a subendocardial and transmural infarct?
Both are totally occlusive super imposed thromboses on atherosclerotic plaques causing irreversible myocardial ischemia.
Difference: Subendocardial myocardial infarct has coronary artery thrombolysis before myocardial necrosis can evolve into a full thickness infarct
Other than a superimposed thrombosis, what are some less common pathophysiologic mechanisms for an acute MI?
- Coronary artery vasospasm w/o atherosclerosis -> cocaine abuse
- Coronary artery thromboembolism (from left sided mural thrombus) or paradoxical embolus from DVT
- Intramyocardial coronary artery pathology, i.e. vasculitis
What is one protective factor against MI in chronic stable angina?
Often, collateral circulation develops over long periods of time
When myocardial ischemia occurs, how quick is function lost, and when does irreversible injury occur? When is infarct size determined?
Functional loss: within 1-2 minuntes after myocardium has to switch to anaerobic glycolysis and lactic acid accumulates
-> organelle and cytosolic swelling occurs with loss of function and irritability
Irreversible injury: Begins at 30 minutes, infarct size is determined by around 6 hours
What is the most common coronary artery to be affected via MI? What areas of the heart will be affected grossly and microscopically early on?
Left anterior descending (LAD)
-> anterior IV septum, anterior wall of LV, and LV apex
Microscopically, subendocardium will be affected first because it is farthest from epicardial arteries
In order for the right ventricle to be affected via an RCA thrombus, where must the stenosis occur?
Very proximal -> more distally it will wrap around to supply the posterior portion of the LV in most people
How will an MI appear grossly in 1-3 days, 3-10 days, 2 months?
1-3 days: Pale infarct -> end-organ lack of perfusion
3-10 days: Soft, yellow-tan area with a red, hyperemic border (due to formation of granulation tissue and capillary growth)
2 months: After scar has formed from periphery inward, will appear a contracted, white rubbery scar
Why can some of the cells which appear to have undergone coagulative necrosis appear “wavy” in an MI?
If they are close to neighboring myocardial cells which are contracting, they may be pulled into wave-like formations
What cells are we trying to save with reperfusion?
The cells which have undergone myocytolysis change -> equivalent of reversible hydropic change in ischemia, which will die if oxygen is not restored
What is myocardial stunning?
The observation that even when reperfused, myocardial cells will take some time to regain their contractility (appear stunned)
What is contraction band necrosis? What causes it?
Finding of intracytoplasmic, deeply eosinophilic transverse bands
Occurs in some cells with coagulative necrosis due to exposure to very high intracellular Ca+2 levels prior to death -> increased myofibril contraction
What are some reperfusion-induced injuries?
- Additional cell death
- Microvascular injury w/ endothelial swelling
- Cardiac arrhythmias
How does reperfusion look in infarcted areas?
Infarcted areas will have hemorrhage due to buildup of RBCs between coagulative necrosis
What patient populations are most likely to have silent MIs?
Diabetics and women
What troponins are useful for cardiac infarction monitoring and why?
TnI and TnT, but not TnC
-> form of TnC is not specific to cardiac muscle
Why is CK-MB useful?
This MB isozyme of creatine kinase is fairly specific for cardiac muscle, and will return to normal 3 days after infarct -> about 1 week faster than troponins, to show that a new infarction has occurred if patient has new onset chest pain.
How can an MI cause worsening of an MI?
Poor coronary artery perfusion from a drop in cardiac output due to decreased contractility or arrhythmias can lead to extension of the area of necrosis
Thrombus can also expand or embolize downstream.
What is a likely complication 2-3 days after a transmural infarct? Why is it specific to this type of infarct?
Fibrinous percarditis, due to inflammatory response entering the pericardial sac
Subendocardial infarcts will not allow access of inflammatory cells to the pericardial sac
When is myocardial rupture most likely to happen and why?
4-5 days post infarct -> wall is soupy and necrosed as macrophages are eating it up.
Very weak wall with massive tissue disintegration
