Ischemic Heart Disease Flashcards
What are the three major blood supply of the heart?
1) Left anterior descending (LAD)
2) Left circumflex (LCX)
3) Right coronary artery
What is an ischemic heart disease?
- AKA Coronary artery disease, Coronary heart disease
- They are a group of related syndromes that result from myocardial infarction (an imbalance between the supply “perfusion” and demand of the heart for oxygen
- In more than 90% of the cases it is due to the atherosclerosis of the coronary artery
What are the different classifications of IHD based on the clinical presentation?
1) Angina pectoris
2) Myocardial Infarction (MI)
3) Sudden cardiac death
4) Chronic HD with HF
What is a myocardial infarction?
Death to part of the cardiac muscle due to ischemia (there is necrosis due to infarction)
What is meant by sudden cardiac death?
Death within 1 hour of symptoms (arrhythmias) without a previous cardiac disease
Till which percentage of stenosis can the heart compensate?
75% after that symptoms will appear
- 75%+ = symptoms while exercising
- 90%+ = symptoms at rest
What is meant by acute coronary syndrome?
- Sudden, reduced blood flow to the heart which is applied to (Unstable angina, Myocardial infarction, and Sudden cardiac death)
Describe the pathogenesis of ischemic heart diseases
- Mainly due to diminished coronary perfusion relative to the myocardial demand due to:
1) Atherosclerotic narrowing of the coronary artery
2) Intraluminal thrombosis, overlying a disrupted plaque, platelet aggregation, or vasospasm
- The prognosis of IHD depends on the extent of obstruction and severity (related to the location of the blockage) and on the dynamic changes in the coronary plaque morphology
What are the factors that contribute to the development of coronary atherosclerosis?
1) Decreased coronary perfusion
2) Erosion, Ulceration, Hemorrhage, rupture, thrombosis of the plaque
3) Inflammation
4) Coronary thrombus
5) Vasoconstriction
What are the factors that trigger changes in the plaque?
1) Intrinsic influences
- For example Composition into the plaque
2) Extrinsic
- Like Blood pressure
What are the types of plaque?
1) Stable plaque
- Strong fibrous cap and smooth muscle proliferation, with a smaller lipid core (this is why ppl with atherosclerosis might not have problems for years)
2) Vulnerable plaque
- Thin fibrous cap with a large necrotic core, which is easily ruptured
- Fissures frequently occur at the junction of the fibrous cap and the adjacent normal arterial segment
What is angina pectoris?
- Temporary, reversible ischemia due to hypoperfusion, which is not enough to produce ischemic necrosis or death
- It is a “symptom complex” of IHD characterized by paroxysmal and recurrent attacks of substernal/precordial chest discomfort (constricting, squeezing, choking, or knifelike) due to a transient (15sec - 15min) Myocardial ischemia which does not induce infarction
What are the different patterns of angina pectoris?
1) Stable/typical angina
2) Prinzmetal/variant angina
3) Unstable/crescendo angina
What is stable/Typical angina?
The most common form, is due to reduced coronary perfusion to a critical level from a stenotic coronary atherosclerosis making the heart more vulnerable to emotions, physical activity, or any other activity that increases the cardiac workload
- Usually relieved by rest or nitroglycerin (a strong vasodilator)
What is prinzmetal/variant angina?
- Vasospasm reduced perfusion
- Uncommon pattern of angina pectoris that occurs at rest, due to coronary artery spasm
- Usually, the ST segment is elevated
- The anginal attack is unrelated to the physical activity, heart rate, or blood pressure
- It responds to vasodilators like nitroglycerin and CCB
How to differentiate between prinzmetal variant angina and myocardial infarction?
By using a biomarker test (Troponin T or I)
What is unstable/crescendo angina?
- Progression of a stable angina
- Increasingly frequent pain (aggressive worsening of pain) at low cardiac demand or even at rest
- Induced by a disruption of an atherosclerotic plaque with mural thrombosis, hemorrhage, or vasospasm that might embolize or induce vasospasm
What is myocardial infarction?
- AKA Heart attack
- It is the irreversible death of the cardiac muscle due to ischemia, which heals by fibrosis
- The leading cause of death in the US, more in males, and the major risk factors are DM, HTN, Smoking, and hypercholesterolemia
Describe the pathogenesis of myocardial infarction
- Coronary vessel occlusion: Atherosclerosis with thrombus (90% of cases), Others like vasospasm (10%)
1) Sudden disruption of an atheromatous plaques
2) Exposure to subendothelial collagen and necrotic plaque content
3) Platelets will undergo adhesion, aggregation, activation, and release of potent aggregators like TXa2, serotonin, and platelet factors 3 and 4
4) Vasospasm (due to mediators)
5) Coagulation (by other mediators)
6) The thrombus will immediately evolve occluding the lumen of the coronary vessel
- After 30 minutes the changes are irreversible, and the cell dies from necrosis (coagulative)
What are the clinical features of MI?
1) Rapid weak pulse
2) Profused sweating (diaphoretic)
3) Dyspnea
4) Chest pain
How to diagnose MI?
1) Troponin (T & I) “They are the best markers, as they are sensitive and cardio-specific
2) Creatine kinase (CK-MB)
What are the different patterns of infarction?
The location, size, and morphologic features depend on the size and distribution of the involved vessel, the rate of occlusion development and duration, the metabolic demands of the myocardium, and the extent of the collateral supply.
1) Transmural infarcts
- When the coronary artery is blocked/obstructed, and thus the area supplying that region will suffer from necrosis
- Involves the full thickness of the wall in the distribution of a given coronary artery, it is usually associated with coronary atherosclerosis, acute plaque change, and superimposed by thrombosis
2) Non-transmural infarcts (subendocardial)
- When there is hypoperfusion, the area around the coronary “pericardium” will receive an acceptable amount of blood while the area further away will suffer from ischemia, shock can happen due to low perfusion
Describe the microscopic morphology of MI
1) No change in the first 12 hours
2) Coagulative necrosis + neutrophils (12h - 3days)
3) Granulation tissue in 1-2 weeks (loose collagen and abundant capillaries)
4) Fine scarring if more than 3 weeks
5) Dense scarring if more than 2 months
- The more the pink = more eosinophils = dying
How can arrhythmia cause death after MI?
The scar made of fibrosis (dense collagen) gives strength to prevent the rupture of the heart and keeps it intact, but it won’t be good in contractility and electrical conduction and thus arrhythmias could lead to death
