Ischemic Heart Disease Flashcards
What is ischemia?
Decreased blood supply ot a heart musle
an imbalance between supply and demand for oxygenated blood
What type of tissue is shown in the provided image?
Identify the indicated features
Cardiac Myocytes
Why is it important that cardiac myocytes receive blood flow?
What is the reslt of ischemia?
Need: oxygen, glucose
Rely on oxidative phosphorylation
blood supply to bring this & to carry away metabolic waste
-
Ischemia (suffocated, starved & forced to retain waste)
- hypoxia
- reducted nuteients
- reduced removal of waste products
What risk factors increase the risk for developing coronary artery disease?
- Increasing systolic pressure
- high cholesterol
- low HDL-C
- diabetes
- cigarettes
- Left ventricular hypertrophy by ECG
What is the most common cause of ischemic heart disease?
coronary artery atherosclerosis
What are the risk factors for atherosclerosis?
- diabetes
- bad diet
- hypertension
- hypercholesterolemia
- smoking
- stress
- male sex
- older age
- obesity
- family history
- lack of exercise
Describe the progession & 3 major consequences of atherosclerosis
- Development of atherosclerosis
- Normal artery
- Fatty streak (earliest sign)
- Develops fibro-fatty plaque
- portion of arterial wall that is normal & portion that is envelepoed by the plaque
- Advanced/Vulnerable plaque
- plaque will continue to grow & you may develop critical stenosis (narrowing of the lumen) or the fibrous cap can thin out & you can get a much larger lipid core that can be vulnerable to rupture
- Clinical Phase
- Aneurysm and Rupture
- mural thrombosis, embolization & wall weakening
- Occlusion by Thrombosis
- the plaque ruptures or is eroded, which can lead to hemorrahge & a thrombus
- thrombus can dissolve or remain permanant & can can break off and embolize
- Critical Stenosis
- when the plaque continues to grow & does not rupture
- lumen becomes very narrow and can have chronic ischemia
- Aneurysm and Rupture
What pathology is shown in the provided image?
Identify the indicated features?
What determines a stable plaque vs. an unstable (vulnerable) plaque?
- Stable
- lipid core is small & not underminging the edges of the fibrous cap
- fibrous cap is typically fairly thick
- scattered inflammatory cells, but not marked
- Unstable (vulnerable)
- larger lipid core & the edges seep into the edges of the fibrous plaque (sharper angle)
- Thinner fibrous cap
- Marked inflammatory cells
What is different about the two arteries depicted in the provided image?
- A: even though there is no thrombus, you can see ther is a little plaque rupture where the arrow is pointing
- B: within the thrombus, a lot of fibrin, inflammatory cells, probably some cholesteral crystals
- notice the thinned firbrous cap
What is Angina Pectoris?
What are the 3 types?
It most commonly affects what demographics?
Substernal or precordial chest pain from transient myocardial ischemis lasting <15 minutes
-
Types
- stable
- unstable
- prinzmetal
-
Demographics
- middle aged & older patients (esp males)
- post-menopausal women
- premenopausal women have a decreased risk
What is the most common variant of angina?
Stable (typical) angina
What is stable angina?
Supply of blood doesn’t meet the demand, but you have a stable plaque
- Angina with exercise, excitement, or other sudden increase in cardiac load (b/c fixed supply of blood)
- Typically associated with >70% chronic stable stenosis of a coronary artery
- Not usually associatd with plaque disruption
What is unstable angina?
- Occurs with progressively lower levels of physical activity or at rest
- Increases in frequence over time
- worsening atherosclerosis, unstable plaques
- may not develop a thrombus, or the thrombus may dissolve
- Often of prolonged duration
- Usually caused by disruption of plaque and superimposed partial thrombosis
- Infarct doesn’t occur becasue of either fragmentation or fibrinolysis of the thrombi, or subsiding of the vasospasm
What is Prinzemtal Angina?
Most common causes?
- Episodic angina at rest due to intense coronary artery vasospasm
- Attackes are unrelated to exercise, heart rate or blood pressure
- Generally responds to nitroglycerin or calcium channel blockers
- any other type of vasodilator
-
Causes
- Intrinsic hyper-reactivity of medial smooth muscle cells
- High levels vasoactive mediators
- pheochromocytomas (increased norepnephrine)
- cocaine or phenyleprine
- Thyrotoxicosis causes a smimlar effect, as it increases the sensitivity of vessels to circulating catecholamines
- autoantibodies and T-cells in scleroderma can cause vascular instability adn vasospasm
- extreme psychological stress and associated release of catecholamines can lead ot pathologic vasospasm
Identify the stage and type of acute coronary syndromes
What problmes can arise from a occlusive thrombus?
Myocardial Infarction
Arrhythmia, which can cause sudden cardiac death
Describe the sequence of events in coronary arterial occlusion
- Rupture of the plaque
- platelets immeditely form a platelet plug
- simultaneous activation of the coagulation cascade
- Formation of a clot (thrombus)
- blood, platelets, inflammatory cells
- Can have complete occlusion of the artery
What pathology is shown in the provided image?
Longitudinal section of anterior descendign artery with thrombus within the lumen
This arose in a rupture complex atherosclerotic plaque, and resulted in a fatal myocardial infarcation
Describe the sequence of events in severe myocardial ischemia
- Cut off blood supply to myocytes
- unable to product ATP (b/c they rely on oxidative phosphorylation)
- lactate levels will increase
- function & viability of the cells will decrease
- If you can reverse some of that in the first 30 minutes, you can salvage some of that myocardium
- if you can’t, the viability will continue to drop off & will be completed by 6-12 hours
What effects does 100% occlusion have on myocardial viability & function?
- If you have 100% occlusion of that arterial wall by a thrombus
- while still viable (for next 30 min or so), the function of the myocyte will drastically decreas in the first 1-2 minutes
- the myocytes will not be pumping & you will have severe ventricular dysfunction
- If you can reestablish the blood floow in the next 30 min, the myocytes can be saved, even through function is dropping off dramatically
What is the effect of reperfusionon myocardial viability & function?
- If you restore blood flow, function will not restore immediately (will take ~ 2 hrs to begin to res
- You can have some level of reperfusion injury
- free radicals
- These cells will also be more susceptible to if an additional infarct does occur
Describe the initiation & progressin of myocardial necrosis during a MI
- Progression of myocardial necrosis will start in the zone of risk & spread out - by 6-12 hours the infarct will be
- myocardial cells immediately underneath the endocardium will be able the get oxygen & nutrients from cells within the lumen of the ventricle (on the other side of the endocardium)
- myocytes that are a little inward from the endocardium will be at high risk because they are farthest from the actual arterial supply
- therefore, the infarct begins at the subendocardial zone if the thrombus is not releived you can have a full-thickness, transmural myocardial infarction.
Identify the cause of the types of infarcts depicted in the diagram
** not tested in this class, but tested in MEDI & I liked this graphic
Approximately how long ago was the MI of the provided specimen?
How do you know?
24 hours
left side of image = LV; right side of image = RV
Arrows: dark mottling you see post MI
Of the provided samples, which is a normal myocardium & which is of an infarct? How long ago did that infarct occur? How do you know?
- wavy fibers of cardiac myocytes
- more eosinophilic & denser than the normal cells
- the white area between cell is fluid, indicating edema
- will typically have a few scattered neutrophils (multiple lobes to the nuclei)
- one of the first thing that arrive w/ nerosis – don’t cause necrosis, but come in to clean up the mess
The provided image is a sample of myocardium post MI. How long ago did that infarct occur? How do you know?
- more neutrophils moving in
- nuclei of myocytes become “ghost” nuclei
- still fair amount of edema
The provided image is an exmale of a heart the experience an infarct how long ago? How do you know?
7-10 days post MI
- Will notice softening & it will become more pale
- notice piece that juts out at the top of the image
- have some dark red areas, but there are also pale areas
- The infarcts look “sunken”
- Tan-yellow w/ patches of red infarcts & fairly distint margins
The provided image is a sample of myocardium post MI. How long ago did that infarct occur? How do you know?
7-10 days post MI
- lots of macrophages
- come in once the neurtophils have broken everything down
The provided image is a sample of myocardium post MI. How long ago did that infarct occur? How do you know?
About 2 weeks after an infarct
- influx of new capillaries (granulation tissue)
- lay down a lot of collagen
- blue fibers
- fair amout of edema (wide open white spaces)
The provided image is a sample of myocardium post MI. How long ago did that infarct occur? How do you know?
Greater than 2 months post-MI
- well developed scars
- white spaces in the middle of the myocardium
- indicates old MI, not what the person died from
The provided image is a sample of myocardium post MI. How long ago did that infarct occur? How do you know?
Greater than 2 months Post-MI
- Residual myocytes
- Dense collagen at the top & between the myocytes
What are the possible complications of mycardial infarction?
Darth Vader
- D: death
- A: arrhythmia
- R: rupture
- T: tamponade
- H: heart failure
- V: valve disease
- A: aneurysm of ventricle
- D: dressler’s syndrome
- E: embolism
- R: recurrence/regurgitation
*
What MI complication is shown in the provided image?
Anerior wall rupture
What MI complication is shown in the provided image?
Rupture of Septum
What MI complication is shown in the provided image?
Rupture of nectoric papillary muscle
What MI complication is shown in the provided image?
Intramural thrombi
b/c myocytes are not pumping properly & that sets up a scenario where you get blood stasis- you can get activated coagulation factors that come in contact w/ each other and lead to a clot formation
also, notice the thin outer wall of the ventricle
What MI complication is shown in the provided image?
Pericarditis
What MI complication is shown in the provided image?
Notice how thin the outer wall of the left ventricle is
Evidence that it was not pumping blood
What pathology is depicted by the provided image?
Chronc heart disease can occur when you have chronic ischemia that falls short of developing a MI
What feature of chronc heart disease is shown in the provided image?
ventricular dilation
** rememer, Left heart failure can lead to right heart failure b/c back up of blood into the lungs
What pathology is depicted in the provided image?
Chronic Ischemic Heart Disease
- Progressive congestive heart failure due to chronic ischemic damage
- Often a result of previous infarcts
- Right: pale pink areas of interstitial fibrosis (collagen)
- H&E stain
