26 Questions
What is the primary purpose of beta blockers in the treatment of acute coronary syndrome?
To decrease heart rate and prolong diastole
What is the main difference between unstable angina and acute myocardial infarction?
Degree of thrombosis
What is the primary mechanism of myocardial ischemia in acute coronary syndrome?
Decreased coronary blood flow due to thrombosis
What is the significance of Troponin elevation in acute myocardial infarction?
Confirms diagnosis of acute myocardial infarction
What is the most common early complication of acute myocardial infarction?
Arrhythmias
What is the outcome of the healing process in acute myocardial infarction?
Formation of scar tissue
What is the significance of ST elevation on ECG in acute myocardial infarction?
Indicates transmural infarction
What is the primary goal of revascularization in acute coronary syndrome?
Reduce future myocardial infarction
What is the characteristic of chest pain in Stable Ischemic Heart Disease?
Predictable pattern of pain
What is the main reason for ischemia in Stable Ischemic Heart Disease?
Increased oxygen demand
Which area of the heart is more prone to ischemia?
Subendocardial area
What is the result of troponin release in the blood?
Myocardial damage
What is the characteristic of cardiac enzymes in Stable Ischemic Heart Disease?
Non-elevated
What is the primary reason for the predictable pattern of chest pain in Stable Ischemic Heart Disease?
Narrowing of coronary artery by stable plaque
What is the significance of ST depression during stress test in Stable Ischemic Heart Disease?
Evidence of ischemia
What is the primary mechanism of ischemia in Stable Ischemic Heart Disease?
Decreased blood flow due to narrowed coronary artery
What is the characteristic of cardiac enzymes in Stable Ischemic Heart Disease?
Non-elevated troponin levels
Why is the subendocardial area more prone to ischemia in Stable Ischemic Heart Disease?
Due to its location
What is the primary mechanism by which aspirin reduces the risk of acute coronary syndrome?
Inhibition of platelet aggregation
What is the typical duration of necrotic cell recognition by macrophages in acute myocardial infarction?
Within 3-7 days
What is the primary reason for cardiac remodeling in acute myocardial infarction?
Infarcted segments replaced by fibers leading to misshapen cardiac wall
What is the primary difference between non-ST elevation MI and ST elevation MI?
Type of coronary artery occlusion
What is the primary consequence of anaerobic metabolism in acute myocardial infarction?
Accumulation of lactate leading to calcium influx
What is the primary goal of anticoagulant therapy in acute coronary syndrome?
Prevention of further thrombus formation
What is the characteristic of cardiac enzymes in acute myocardial infarction?
Elevated troponin levels
What is the primary mechanism by which revascularization reduces the risk of future myocardial infarction?
Improved myocardial oxygen supply
Study Notes
Ischemic Heart Disease Syndromes
- Stable Ischemic Heart Disease: chest pain, pressure, or tightness with activity, relieved with rest, due to narrowing of coronary artery by stable slow-growing atherosclerotic plaque
- Demand ischemia: occurs when demand increases, reversible when demand decreases (rest)
- Diagnosis:
- Normal ECG during rest
- ST depression during stress test
- Cardiac enzymes (troponin): negative (non-elevated)
- Treatments:
- Beta blockers (decrease HR, prolong diastole)
- Aspirin (reduce platelets aggregation)
Acute Coronary Syndrome
- Unstable Angina:
- Acute onset of chest pain/pressure at rest or unrelieved by rest
- Due to rupture of atherosclerotic plaque with thrombosis
- Supply ischemia: not related to demand
- Reversible ischemia if thrombus is broken down
- Infarction if thrombus keeps growing
- Subendocardial area is more prone to ischemia
- Diagnosis:
- Resting ECG (no need for stress test): ST depression
- Cardiac enzymes (troponin): negative
- Treatment:
- Anticoagulant
- Revascularization: reduces future MI
Acute Myocardial Infarction
- Acute onset of chest pain/pressure at rest or unrelieved by rest
- Due to rupture of atherosclerotic plaque with 100% thrombosis
- Main artery occlusion > transmural infarct
- Distal branch occlusion > subendocardial infarct
- Arterial thrombosis produces MI (necrosis, irreversible damage), not related to demand
- Pathological changes:
- Myocardium oxygen deprivation > switches to anaerobic metabolism > accumulation of lactate leading to calcium getting inside the cells > damage to the cell membrane > cellular death (necrosis)
- Necrosis starts within 30 minutes and completes within 6-12 hours
- At 12 hours, necrotic cells are recognized by macrophages that infiltrate dead tissues
- Macrophages then phagocyte necrotic cells within 3-7 days
- Fibrosis results by 6 weeks, replacing necrotic cells, function of the heart will diminish
- Diagnosis:
- Resting ECG (avoid stress test)
- ST depression: non-ST elevation MI (subendocardial infarction)
- ST elevation: ST elevation MI (transmural infarction)
- Troponin is elevated
- Early complications:
- Arrhythmias: most common, dead tissue is electrically unstable, most common cause of death
- Cardiogenic shock: dead tissue does not contract
- Acute rupture of cardiac structures: dead tissues are prone to tears
- Rupture of ventricular wall, septum, and papillary muscles
- Late complications:
- Pericarditis (Dressler syndrome): myocardial inflammation (infiltration of macrophages) spreads to adjacent pericardium
- Heart failure: infarcted segments (myocytes replaced by fibers) > cardiac wall is misshapen, leading to remodeling/changing ventricular shape > inefficient contractions
Ischemic Heart Disease Syndromes
- Stable Ischemic Heart Disease: chest pain, pressure, or tightness with activity, relieved with rest, due to narrowing of coronary artery by stable slow-growing atherosclerotic plaque
- Demand ischemia: occurs when demand increases, reversible when demand decreases (rest)
- Diagnosis:
- Normal ECG during rest
- ST depression during stress test
- Cardiac enzymes (troponin): negative (non-elevated)
- Treatments:
- Beta blockers (decrease HR, prolong diastole)
- Aspirin (reduce platelets aggregation)
Acute Coronary Syndrome
- Unstable Angina:
- Acute onset of chest pain/pressure at rest or unrelieved by rest
- Due to rupture of atherosclerotic plaque with thrombosis
- Supply ischemia: not related to demand
- Reversible ischemia if thrombus is broken down
- Infarction if thrombus keeps growing
- Subendocardial area is more prone to ischemia
- Diagnosis:
- Resting ECG (no need for stress test): ST depression
- Cardiac enzymes (troponin): negative
- Treatment:
- Anticoagulant
- Revascularization: reduces future MI
Acute Myocardial Infarction
- Acute onset of chest pain/pressure at rest or unrelieved by rest
- Due to rupture of atherosclerotic plaque with 100% thrombosis
- Main artery occlusion > transmural infarct
- Distal branch occlusion > subendocardial infarct
- Arterial thrombosis produces MI (necrosis, irreversible damage), not related to demand
- Pathological changes:
- Myocardium oxygen deprivation > switches to anaerobic metabolism > accumulation of lactate leading to calcium getting inside the cells > damage to the cell membrane > cellular death (necrosis)
- Necrosis starts within 30 minutes and completes within 6-12 hours
- At 12 hours, necrotic cells are recognized by macrophages that infiltrate dead tissues
- Macrophages then phagocyte necrotic cells within 3-7 days
- Fibrosis results by 6 weeks, replacing necrotic cells, function of the heart will diminish
- Diagnosis:
- Resting ECG (avoid stress test)
- ST depression: non-ST elevation MI (subendocardial infarction)
- ST elevation: ST elevation MI (transmural infarction)
- Troponin is elevated
- Early complications:
- Arrhythmias: most common, dead tissue is electrically unstable, most common cause of death
- Cardiogenic shock: dead tissue does not contract
- Acute rupture of cardiac structures: dead tissues are prone to tears
- Rupture of ventricular wall, septum, and papillary muscles
- Late complications:
- Pericarditis (Dressler syndrome): myocardial inflammation (infiltration of macrophages) spreads to adjacent pericardium
- Heart failure: infarcted segments (myocytes replaced by fibers) > cardiac wall is misshapen, leading to remodeling/changing ventricular shape > inefficient contractions
This quiz covers different types of Ischemic Heart Disease syndromes, including Stable Ischemic Heart Disease, Acute Coronary Syndrome, Unstable Angina, and Acute Myocardial Infarction. It also explains the causes and symptoms of each syndrome.
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