Ischemic Heart Disease and ACS

Question 1

Differentiate between type 1 and type 2 MI and give 3-5 causes of type 2 MI

Answer 1

• type 1: typical MI caused by atherosclerotic plaque rupture (or erosion) and thrombosis
• type 2: oxygen supply/demand mismatch MI
  
  • Coronary embolism
  • Severe coronary artery spasm (spontaneous or cocaine-induced)
  • SCAD
  • Vasculitic syndromes
  • Severely increased mVO2 or reduced global DO2

Question 2

Which of the following is not a functional alteration of myocardium following MI

1. arrythmogenesis
2. stunned myocardium
3. ischemic preconditioning
4. ventricular remodelling
5. impaired contractility/compliance

Answer 2

a. arrythmogenesis

Question 3

Compare and contrast PCI vs CABG for ischemic heart diseas

Answer 3

PCI

• Less invasive with shorter convalescence
• Superior to medical therapy for uncontrolled angina
• No benefit to survival / MI risk in stable angina

CABG

• More invasive, with greater risk and longer convalescence.
• Better revascularization of critical occlusions
• Confers a survival advantage in pts. with severe CAD
• Pts. with Hx of multiple CABG are highly suspected for re-occlusion.

Question 4

Decribe how papillary muscle rupture in MI may be rapidly fatal

Question 5

Patients who sustain an MI in the context of recent angina are likely to experience more/less morbidity and mortality vs. non-anginal patients

Answer 5

LESS!

due to ischemic pre-conditioning.

Question 6

List and briefly describe the three non-infarction ischemic syndromes

Answer 6

• Stable Angina
  
  • transient angina associated with exertion that relieves with rest
• Unstable Angina
  
  • increase in tempo and duration of angina, with reduced exertion or at rest
• Variant (prinzmetal) angina
  
  • Caused by transient, intense coronary casospasm. Usually occurs at rest due to endothelial dysfunction

Question 7

List 3-5 factors which influence the size of myocardial infarction resulting from coronary occlusion

Answer 7

1. the mass of myocardium supplied by the occluded vessel
2. the magnitude and duration of flow impairment
3. the oxygen demand of the affected region
4. the adequacy of collateral circulation
5. the degree of tissue response to the ischemic process (less in severely atherosclerotic tissue due to endothelial dysfunction)

Question 9

What is the duration of total coronary occlusion required to cause irreversible myoacardial occlusion?

1. 30-60s
2. 2-4min
3. 6-10min
4. 20-24min

Answer 9

d. 20-24 minutes

Question 10

What are the two major causes of myocardial ischemia in CAD?

Answer 10

1. Fixed vessel narrowing
   * due to atherosclerotic plaques or thrombi
2. Endothelial cell dysfunction
   • Inappropriate vasoconstriction
   • Loss of normal antithrombotic properties

Question 11

The three key components to diagnosis of ACS are:

Answer 11

1. Pt Hx
2. ECG findings
3. Cardiac biomarkers (troponin I/T and CK-MB)

Question 12

Which of the following would not normally be part of a conservative (medical) approach for acute UA/NSTEMI?

1. clopidogrel
2. tenecteplase
3. metoprolol
4. enoxaparin

Answer 12

b. tenecteplase
* tenecteplase is a recombinant tPA. Fibrinolysis is not part of routine management of UA/NSTEMI

Question 13

First- and second-line therapies for STEMI are:

Answer 13

First: Primary PCI

Second: Fibrinolysis (tPA)

Question 14

List 5 differentials for recurrent chest pain (CVS, GI, or MSK)

Answer 14

• Myocardial ischemia (angina)
• Pericarditis
• GERD
• Peptic ulcers
• Esophageal spasm
• Biliary colic
• Costochondritis
• Cervical radiculitis

Question 15

One outcome of ischemic myocardial injury is necrosis (i.e. infarction). List and describe two other direct outcomes of myocardial ischemia (not reperfusion injury)

Answer 15

• Stunned myocardium
  
  • A region of myocardium that suffers acute ischemia but no necrosis, that exhibits a period of systolic dysfunction followed by spontaneous recovery
• Hibernating myocardium
  
  • A region of myocardium that suffers chronic ischemia and persistent systolic dysfunction, but may fully recover with restoration of appropriate blood flow

Question 16

What are two factors that determine coronary vascular resistance?

Answer 16

• forces that externally compress the arteries (i.e. myocardial contraction during systole)
• Intrinsic coronary arterial tone
  
  • Includes metabolic, endothelial, and neural factors

Question 17

Briefly describe Laplace’s law as it relates to myocardial wall tension and mVO2

Answer 17

σ = (P x r) / 2h

• σ is wall stress, P is intraventricular pressure, r is radius of the ventricle, h is ventricular wall thickness
• wall stress increases with increasing pressure and ventricular radius (dilated cardiomyopathy) and decreases with increasing wall thickness (myocardial hypertrophy)
• Increasing wall stress is one of 3 factors in mVO2 (the other two are contractility and HR)

Question 18

Which region of the myocardium is most susceptible to ischemia and why?

Answer 18

the subendocardium, because it is more subjected to ventricular systolic pressures (compression of coronary arteries) and blood supply to the subendocardium must pass through several layers of conttracting myocardium.

Question 19

Describe the two common management strategies for UA/NSTEMI

Answer 19

1. Invasive therapy
   
   • PCI for revascularization, usually attempted when TIMI ≥3
2. Conservative therapy
   
   • anti-ischemic treatments (beta-blockers, nitrates, CCBs)
   • antiplatelets (clopidogrel, ticagrelor)
   • anticoagulants (heparins)

fibrinolysis is not standard care for UA/NSTEMI

Question 20

What are the three classes of medication most commonly prescribed for recurrent ischemic episodes (angina)

Answer 20

• Beta-blockers
  
  • First-line treatment. Reduces myocardial oxygen demand (negative chronotropy and inotropy) and may improve supply (increased diastolic filling time)
• Organic Nitrates
  
  • primarily act through reduced preload and wall stress. MAY improve coronary supply (controversial)
• Calcium Channel blockers
  
  • Reduced preload and improved supply (coronary dilatation). Third-line treatment if angina not controlled by first two

Question 21

What is the “levine sign”?

Answer 21

placing a clenched fist over the chest during periods of ischemic chest pain

Question 22

Which of the following is not part of the spectrum of ACS?

1. STEMI
2. NSTEMI
3. unstable angina
4. stable angina

Answer 22

d. stable angina
* considered a chronic, transient ischemic condition, not an acute coronary syndrome

Question 23

Roughly, what are normal ranges for troponin T and I values

Answer 23

• TnT: <3 is good, 3-14 concerning, >14 diagnostic of MI
• TnI: <0.8 is good, >0.10 is diagnostic of MI
• Multiple biomarkers needed to definitely rule out NSTEMI
• Troponins have best diagnostic value >6 hrs. after onset of symptoms

Question 24

Describe potential outcomes of coronary thrombosis and relate them to the spectrum of ACS

Answer 24

• Partial occlusion with rapid inclusion into plaque or fibrinolysis. No necrosis. Unstable angina
• Substantial partial occlusion with prolonged or severe downstream ischemia leading to necrosis = NSTEMI
• Total occlusion with rapid lysis or extensive collateral circulation and necrosis limited to subendocardium = NSTEMI
• Total occlusion with transmural downstream necrosis = STEMI

Question 25

The most common cause of sudden cardiac death during acute MI is: 1. Ventricular wall rupture 2. Acute heart failure 3. Bradycardic PEA 4. Ventricular fibrillation

Answer 25

d. Ventricular fibrillation

Question 26

What is the purpose of exercise stress testing?

Answer 26

* non-invasive detection of significant coronary artery disease * Exercise is performed to a target HR with continuous ECG monitoring. Ischemic ECG changes, paradoxical BP reduction, ventricular arrythmogenesis, or inability to complete the test are indicative of advanced CAD

Question 27

List two factors which influence myocardial oxygen supply and three factors which influence myocardial oxygen demand

Answer 27

* Supply * Coronary artery blood oxygen content * Coronary blood flow * Combination of coronary perfusion pressure and coronary vaascular resistance * Demand * Wall stress (P x r /2h) * Heart rate * Contractility

Question 28

Which of the following is not a component of myocardial oxygen demand? 1. Endothelial cell dysfunction 2. Radius of the ventricle 3. Heart rate 4. Contractility

Answer 28

a. Endothelial cell dysfunction * This is a cotributor to decreased myocardial oxygen supply, not demand * Contributors to mVO2 are: * HR * Contractility * Wall stress, determined by: * Intraventricular pressure * Ventricular radius * Wall thickness

Question 29

What is the most sensitive and specific biomarker for MI?

Answer 29

cardiac troponin (cTnI and cTnT) * troponins are also found in skeletal muscle, but the cardiac isozymes are unique * CK-MB is a creatine kinase specific to cardiac muscle cells and also used in infarction detection. * CK-MB testing is neither as sensitive nor as specfic for MI

Question 30

Compare and contrast unstable angina and NSTEMI in terms of thrombus involvment

Answer 30

* both usually involve a partially-occlusive thrombus * NSTEMI involves myocyte **necrosis** (infarction = necrosis) while unstable angina has none.

Question 31

List 4 modifiable risk factors for atherosclerosis

Answer 31

1. dyslipidemia 2. smoking 3. hypertension 4. diabetes

Question 32

Describe the clinical relevance of a TIMI score ≥ 3

Answer 32

* TIMI is a thrombolysis in MI risk stratification score * TIMI ≥ 3 is associated with high risk of morbidity/mortality and is the threshold for **early invasive revascularization**

Question 33

Which is the most common cause of thrombus formation in ACS, plaque rupture or endothelial erosion?

Answer 33

plaque rupture endothelial erosion without plaque rupture is seen as an increasingly important, but not dominant cause of ACS

Question 34

What are the 2 ways in which atherosclerosis contributes to coronary thrombus formation?

Answer 34

1. plaque rupture * exposes blood to thrombogenic substances 2. endothelial dysfunction * impairment of normal antithrombotic and vasodilatory mechanisms

Question 35

The major diagnostic distinction between UA and NSTEMI is:

Answer 35

absence/presence of cardiac serum biomarkers (troponin and CK-MB)

Question 36

Which of the following is not a standard treatment for recurrent ischemic chest pain (angina)? 1. Nitroglycerin 2. Captopril 3. Metoprolol 4. Diltiazem

Answer 36

b. captopril captopril is an ACE-inhibitor. Standard medical care for chronic angina consists of: 1. Beta-blockers (metoprolol) 2. Nitrates (nitroglycerin) 3. Calcium-channel blockers (diltiazem)

Question 37

List two cause of myocardial ischemia **not** related to CAD

Answer 37

1. Decreased perfusion (as in shock) 2. Decreased blood oxygen content (anemia or respiratory failure)

Question 38

Differentiate between ECG changes seen in stable/unstable angina vs. variant angina vs. infarction

Answer 38

Stable/unstable angina * ST-depression and T-wave flattening or inversion. Rapid reversal with resolution of symptoms Variant angina * ST-elevation may be present! Rapid reversal with resolution of symptoms Infarction * Dynamic ST-T changes leading to STE and Q-waves which may not resolve for days/weeks or may be permanent

Question 39

Differentiate between myocardial ischemia, injury, infarction, and angina

Answer 39

* Ischemia = insufficient oxygen supply to meet tissue demand (i.e. local hypoxia) * Injury = reversible tissue damage and dysfunction secondary to prolonged ischemia * Infarction = a region of non-reversible ischemic damage. i.e. necrosis * Angina = the uncomfortable sensation felt in the chest of myocardial ischemia

Question 40

Describe the role of nitric oxide in coronary vacular resistance and identify its source in normal cardiac physiology

Answer 40

* NO is released by **endothelial cells** in response to a number of aggravating factors * NO causes cGMP-mediated **vasodilation**

Question 41

List three endogenous mechanisms of antithrombosis, and relate them to medical treatments for thrombotic disease

Answer 41

* Inactivation of clotting factors * analogous to **abticoagulant therapy (blood thinners)** * includes warfarin, heparin, apixaban, dabigatran, etc. * Fibrinolysis * tPA used both endogenously and therapeutically for fibrinolysis * Platelet inhibition / vasodilation * Prostacyclin/NO endogenously * ASA and clopidogrel therapeutically

Question 42

Describe the role of adenosine in regulation of coronary vascular resistance

Answer 42

* during hypoxia, excess free adenosine is produced from breakdown of ATP * Free adenosine binds to receptors on vascular smooth muscle, inhibiting calcium influx * Net effect is **hypoxia-induced vasodilation**