Ischemic Heart Disease Pathology Flashcards
Ischemic heart disease (IHD) broad term
Caused by myocardial ischemia (imbalance between supply and demand for oxygen)
90% of causes are due to obstructive atherosclerotic vascular diseases that takes decades to form
- because of this IHD is commonly known as CAD as well.
Angina pectoris
Intermittent Chest pain that is induced by reversible and transient ischemia
- this ischemia however, is insufficient to cause myocytes death
The pain is a consequence of ischemia induced build up of adenosine and BK that stimulates autonomic nociceptive nerves
Can be classified in two ways
- stable angina: caused by vessel spasms due to certain levels of exertion. (Monitor and take action but usually no ER unless indicated)
- unstable angina: caused regardless of activity and is present at rest. (ER immediately)
Myocardial infarction (MI)
Cardiomyocyte death due to ischemia
- the ischemia is high enough to cause cell death
Underlying cause is almost always atherosclerosis and/or acute thrombosis within the coronary arteries
Can occur at any age
Race plays no factor but Men are at higher risk if all comorbidities (external factors) are equal
Sudden cardiac death
Caused by a lethal arrthmia that prevents systemic blood flow
Why has IHD/CAD rates gone down?
Interventions that diminish the following cardiac risk factors
- HTN treatments
- smoking prevention
- diabetes treatments
- high cholesterol treatments
3 coranary arteries that are most often effected by atherosclerosis
Left anterior descending (LADs)
Left circumflex (LCXs)
Right coronary artery (RCAs)
more often is a combo rather than just one
What is the cut off for atherosclerotic occlusion before symptoms arise?
70%
- after 70% vessel occlusion, often starts to cause symptoms such as stable angina w/ exertion
90% is considered unstable angina since the pain is always prominent
Acute coronary syndromes
Include all the heart syndromes such as unstable angina, MI, SCD, etc.
- however, these are caused due to an eroded or ruptured plaque somewhere within the heart
This form is lethal because it is asymptomatic before the event occurs (hence impossible to predict)
Typical or stable angina
Predictable episodic chest pain that is associated with a level of exertion and often w/ tachycardia present
- pain is often described as a crushing or squeezing of the sub sternal sensation that radiates down the left arm or to the jaw
- the pain is caused by transient and reversible ischemia
Treatment is rest w/ potential nitroglycerin drug use if needed
Prinzmetal (variant) angina
Similar to stable but is caused by a coronary artery spasm rather than ischemic demands
Treatment is nitroglycerin or CBBs
Unstable (crescendo) angina
Increased pain with little to no exertion (often at rest)
Usually associated with plaque disruption and is the harbinger of MI
Treatment: ER and requires nitroglycerin and direct thrombolytic agents
Typical MI step-by-step pathogenesis
1) atheromatous plaque is eroded exposing subendothelial collagen
2) platelets adhere to this collagen and activate thromboxane A2, ADP and serotonin to jack up rates of platelet aggregation and induce vasospasm
3) activation of coagulation by exposure of tissue factors and other mechanisms adds to the growing thrombus
4) thrombus evolves to occlude the whole coronary artery lumen (can occur within minutes)
5) aerobic metabolism ceases leads to drop in ATP supply and decreases in pH. Overall decrease in contractility
What is the time frame for irreversible MI damage
Prolonged ischemia = 20-40 minutes
Because of time sensitivity, direct thrombolysis and angioplasty are used (both are invasive procedures)
- irreversible injury first occurs in the sub endocardial zone (area of most internal cardiac tissue), especially in the apex of the heart*
- this is because it is the LAST area to receive blood (during ischemia, the last areas to receive blood die first).
What is the time frame for an infarct to achieve its full extent (essentially kills the whole heart)
3-6 hrs
- usually at this point, with no intervention, a transmural infarct will occur (the infarct encompasses the entire wall thickness).
What is the most common area for MI?
LAD artery “widow maker” = 40-50%
- kills the anterior 2/3 of the IVS, anterior wall of the left ventricle and the heart apex first
LCX = 15-20%
- kills the lateral wall of the ventricle first
RCA =. 30-40%
- kills the right ventricle first
Gross apperance of MI
Depends on the age of injury
- usually are not apparent without a stain if they are less than 12hrs old
- if greater than 3 hrs, can use a triphenyl-tetrazolium chloride stain which stains for lactate dehydrogenase (this will be over the areas of the infarct)
- this appears yellow*
- if 12-24 hrs, the infarct section will appear red-bluish
- if 10-14 days, infarct is rimmed with granulation tissue followed by a fibrous scar
- Starts with coagulative necrosis -> acute/chronic inflammation -> fibrosis all over*
Microscopic appearance of MI
Again based on age
- within 4-12 hrs the infarct will show coagulative necrosis: no nuclei and disorganized cells.
- will also show wavy fibers at the edge of the infarct (reflect stretching and buckling of noncontractile dead myofibrils) *
- after 1-3 days, will show waves of macrophages
- after 5-10 days, will show necrotic macrophages and lymphocytes
- after 1-2 was will show granulation tissue (dispurse little blue stains)
- after 6 wks shows scaring (large blue stains)
Difference between MI and angina pain
MI: lasts longer and is NOT relieved by nitroglycerin or rest
- note: silent infarcts occur 10% of the time and often in diabetics and 70+ yr olds*
What type of MIs are STEMIs
Transmural MIs
- show elevated ST segments, large negative Q waves with sometimes no R waves
Consequences after an acute MI
75% of patients experience one of these after an MI
Contractile dysfunction
Arrhythmias
Pericarditis
Myocardial ruptures
Ventricular aneurysms
Mural thrombus
Papillary muscle dysfunction
Progressive heart failure
Contractile dysfunction
Left ventricular pump function is lowered (the degree of lowered function is proportional to amount of ventricular damage)
- manifests as pulmonary congestion/edema and/or hypotension
Can be cardiogenic shock if more than 40% of left ventricle is dysfunctional
Pericarditis
Fibrino-hemorrhagic inflammation of the cardiac tissue
- usually develops 2-3 days following a transmural infarct from the underlying inflammation of the infarct
Myocardial rupture
Rare (1-5%) and is most common in left ventricle
- pretty much always fatal
Can also result in IVS ruptures (left->right shunting) and papillary muscles (mitral valve regurgitation)
Occurs 3-7 days after infarction (which is when the ventricular wall is thin w/ no new collagen due to cleaning out of the dead tissue)
Ventricular aneurysm
Late complication of the ventricle usually resulting from a large transmural anteroseptal infarct
- can lead to thrombi or heart failure, but DOESNOT show rupture since the new collage is already laid down
What are the factors that determine overall prognosis after an infarct
Size:
- larger infarcts are associated with high chance of cardiogenic shock, arrhythmias and CHF
Transmural vs sub endocardial:
- transmural is more dangerous
Anterior vs posterior:
- anterior is more dangerous ( high chance of wall rupture, aneurysm formation and mural thrombi
- posterior is less dangerous but still dangerous (high chance of heart blocks)
Overall mortality rates after having an MI treated
30% in the 1st year
3-4% annual after the first year
Classic MI pain description and where can it radiate/be referred?
Severe, crushing sub sternal chest pain
Can radiate to the following
- neck
- jaw
- epigastrum
- left arm
Possible arrhythmias post MI
- approximately 90% experience one of these*
- most commonly experienced in the 1st hr after.
- bradycardia
- asystole
- SVTs
- PVCs
- ventricular fibrilation
Why do we use cardiac troponin levels more than CK-MB?
Troponin levels peak higher and stay peaked (elevated) much longer than CK-MB levels
- CK-MB lasts for 72 hours
- troponin levels last 7-10 days
- note they both start to elevate at roughly the same time*
