Chapter 36

Question 1

What happens during systolic contraction in the heart?
A. redistributes perfusion from the subendocardial to the subepicardial layers
B. coronary arterial inflow increases
C. increase in tissue pressure
D. A and C

Answer 1

D
Increases tissue pressure, redistributes perfusion from the subendocardial to the subepicardial layers, and impedes coronary arterial inflow.

Coronary arterial inflow increases with a transmural gradient favoring perfusion to the subendocardial vessels in diastole.

Question 2

What is the approximate myocardial oxygen extraction percentage at rest?

Answer 2

70% to 80% of arterial oxygen content.

Question 3

What are the major determinants of myocardial oxygen consumption?

Answer 3

• Heart rate
• Systolic pressure (myocardial wall stress)
• Left ventricular (LV) contractility

Question 4

What is the coronary flow reserve?

Answer 4

Ability to increase flow above resting values in response to pharmacologic vasodilation.

Question 5

What happens to subendocardial flow when coronary pressure falls below 40 mm Hg?

Answer 5

Subendocardial flow begins to decrease.

Question 6

What are the three major components of resistance to coronary blood flow?

Answer 6

• Conduit resistance (R1) of epicardial arteries
• Coronary resistance (R2) from microcirculatory resistance arteries
• Extravascular compressive resistance (R3)

Question 7

What is the role of nitric oxide in coronary blood flow?

Answer 7

Produced in endothelial cells, it causes relaxation of vascular smooth muscle through a reduction in intracellular calcium.

Question 8

True or False: Endothelial dysfunction can lead to coronary vasospasm.

Answer 8

True.

Question 9

Which factor is a potent vasoconstrictor released during platelet aggregation?

Answer 9

Thromboxane A2.

Question 10

What does the term ‘coronary vasospasm’ refer to?

Answer 10

Transient functional occlusion of a coronary artery that is reversible with nitrate vasodilation.

Question 11

What is the effect of nitroglycerin on coronary blood flow?

Answer 11

Dilates epicardial conduit arteries and small coronary resistance arteries.

Question 12

What is the relationship between stenosis severity and maximum myocardial perfusion?

Answer 12

Epicardial artery stenoses increase coronary resistance and reduce maximal myocardial perfusion.

Question 13

Fill in the blank: The critical stenosis occurs when stenosis severity exceeds _______.

Answer 13

90%.

Question 14

What is Absolute Flow Reserve?

Answer 14

Ratio of maximally vasodilated flow to corresponding resting flow in a specific region of the heart.

Question 15

What does Relative Flow Reserve assess?

Answer 15

Relative differences in regional perfusion during maximal pharmacologic vasodilation.

Question 16

What is Fractional Flow Reserve used for?

Answer 16

To assess the physiologic significance of an intermediate stenosis.

Question 17

What happens to coronary flow reserve during exercise?

Answer 17

Reductions in coronary flow below the lower limit of autoregulation can occur.

Question 18

What is the effect of elevated preload on coronary driving pressure?

Answer 18

Elevated preload reduces coronary driving pressure and diminishes subendocardial perfusion.

Question 19

What are the effects of tachycardia on diastolic perfusion?

Answer 19

Decreases diastolic time available for subendocardial perfusion.

Question 20

How does coronary resistance change in heart failure?

Answer 20

Compressive effects from elevated ventricular diastolic pressure impede perfusion.

Question 21

What is the minimum value of zero flow pressure (Pf=0) in the maximally vasodilated heart?

Answer 21

Approximately 10 mm Hg.

Question 22

What is the role of adenosine in coronary blood flow?

Answer 22

Dilates coronary arteries through activation of A2 receptors on vascular smooth muscle.

Question 23

What is the impact of hypercholesterolemia on coronary flow reserve?

Answer 23

Can lead to microcirculatory impairment in flow or attenuated vasodilator responsiveness.

Question 24

What is the relationship between measured pressure during vasodilation and maximum vasodilated perfusion?

Answer 24

Directly proportional

This indicates that as the pressure increases during vasodilation, the perfusion also increases.

Question 25

What does the FFR index represent?

Answer 25

Mean distal coronary pressure/mean aortic pressure (Pd/Pao) ## Footnote This index is used to assess the physiological significance of coronary lesions.

Question 26

True or False: FFR values greater than 0.75 are associated with poor outcomes in patients with stable ischemic heart disease.

Answer 26

False ## Footnote FFR values greater than 0.75 are linked to excellent outcomes with deferred intervention.

Question 27

What is the critical cutoff for the iFR index?

Answer 27

0.89 ## Footnote This cutoff reflects the ratio of diastolic coronary to aortic pressure.

Question 28

What is the principle behind the iFR index?

Answer 28

Resting pressure gradient does not develop until stenosis severity significantly affects maximal perfusion during vasodilation ## Footnote This principle allows for assessment without pharmacologic vasodilation.

Question 29

What does the term 'arteriogenesis' refer to?

Answer 29

Proliferation of coronary collaterals in response to repetitive stress-induced ischemia ## Footnote This process helps maintain perfusion during occlusion.

Question 30

What is the timeframe for irreversible injury and myocyte death after coronary occlusion without significant collaterals?

Answer 30

Begins after 20 minutes ## Footnote Injury starts in the subendocardium and progresses outward.

Question 31

Fill in the blank: The magnitude of residual coronary flow through collaterals is the most important determinant of the actual time course of _______.

Answer 31

irreversible injury ## Footnote This is particularly relevant in patients with chronic CAD.

Question 32

What is 'myocardial stunning'?

Answer 32

Regional myocardial function remains depressed for up to 6 hours after resolution of ischemia ## Footnote This occurs after a 15-minute occlusion in the absence of tissue necrosis.

Question 33

What happens to myocardial function after brief occlusions or prolonged moderate ischemia?

Answer 33

Complete functional recovery occurs rapidly (within 1 week after reperfusion) ## Footnote This is referred to as postischemic stunning.

Question 34

What is the consequence of elevated distal coronary pressure during transient total balloon occlusion (FFR >0.25)?

Answer 34

Lower cardiovascular event rate and improved survival ## Footnote This indicates the protective role of collateral circulation during interventions. Ischemia does not develop during PCI balloon occlusion when FFR is greater than 0.25

Question 35

What characterizes chronic hibernating myocardium?

Answer 35

Viable dysfunctional myocardium that improves after coronary revascularization ## Footnote This condition occurs when relative resting flow is reduced without symptoms of ischemia.

Question 36

True or False: Stunned myocardium can develop after demand-induced ischemia.

Answer 36

True ## Footnote This phenomenon is also responsible for postoperative pump dysfunction.

Question 37

What is the effect of increased myocardial oxygen consumption on irreversible injury?

Answer 37

Accelerates the progression of irreversible injury ## Footnote This can occur due to conditions such as tachycardia or anemia.

Question 38

What is the relationship between infarct size and collateral flow during total occlusion?

Answer 38

Inversely related ## Footnote Greater collateral flow is associated with smaller infarct size.

Question 39

What does iFR not require for its measurement?

Answer 39

Pharmacologic vasodilation ## Footnote This allows for a rapid assessment of physiological significance.

Question 40

Which of the following statement is correct? A. Irreversible injury begins after 20 minutes of coronary occlusion in the absence of significant collaterals B. Myocardial stunning is a depressed myocardial function even with normal resting myocardial perfusion C. The entire subendocardium is irreversibly injured within 1 hour of occlusion D. Transmural progression of infarction is completed within 4 to 6 hours after coronary occlusion E. all of the above

Answer 40

E

Question 41

What is myocardial stunning? A. Normal myocardial function in the setting of ischemia B. Myocardial function remains depressed despite normal resting myocardial perfusion after ischemia C. A and B D. Either A and B

Answer 41

B ## Footnote Myocardial stunning occurs after episodes of ischemia lasting longer than 2 minutes, leading to temporary dysfunction.

Question 42

Which of the following is true? A. There is rapid normalization of myocardial function after a single episode of ischemia of less than 2 minutes B. Myocardial function remains depressed up to 6 hours after a 15-minute occlusion in the absence of tissue necrosis. C. Stunning from prolonged sublethal ischemia takes 1 week to resolve D. All of the above

Answer 42

D ## Footnote Function normalizes quickly after brief ischemic episodes.

Question 43

What happens to regional myocardial function after a 15-minute occlusion in the absence of tissue necrosis?

Answer 43

It remains depressed for up to 6 hours after ischemia resolution ## Footnote This is a key characteristic of myocardial stunning.

Question 44

What is a defining feature of isolated myocardial stunning?

Answer 44

Function remains depressed while resting myocardial perfusion is normal ## Footnote There is a dissociation between subendocardial flow and function.

Question 45

What can cause demand-induced ischemia leading to stunned myocardium?

Answer 45

Exercise-induced ischemia ## Footnote This can result in depressed regional function distal to a coronary stenosis.

Question 46

What is the potential impact of repetitive ischemia on myocardial stunning? A. exarcerbate myocardial dysfunction B. collateral formation C. resilience of the myocardium D. all of the above

Answer 46

A. It can lead to cumulative stunning ## Footnote Repetitive ischemia may exacerbate the dysfunction.

Question 47

True of the stunned myocardium: A. common cause of reversibly dysfunctional myocardium in acute coronary syndrome B. cause of postoperative pump dysfunction after cardiopulmonary bypass C. Acutely stunned myocardium will normalize during stimulation with inotropic agents D. all of the above

Answer 47

D ## Footnote It plays a significant role during acute reductions in blood flow.

Question 48

What occurs if repetitive episodes of reversible ischemia develop before function normalizes?

Answer 48

They can cause persistent dysfunction or chronic stunning ## Footnote This indicates the need for careful management of ischemic episodes.

Question 49

What cellular mechanisms are involved in myocardial stunning?

Answer 49

Free radical-mediated myocardial injury and reduced myofilament calcium sensitivity ## Footnote These mechanisms contribute to the dysfunction observed.

Question 50

Is necrosis present in stunned myocardium?

Answer 50

No, necrosis and pathologic evidence of infarction are absent ## Footnote However, ischemia can still lead to myocyte apoptosis.

Question 51

What is the effect of brief ischemia on troponin I levels?

Answer 51

It leads to elevations in troponin I ## Footnote This indicates myocardial injury even without necrosis.

Question 52

Matching type 1. Postischemic stunning 2. Short-term hibernation 3. Chronic stunning 4. Chronic hibernating myocardium 5. Subendocardial infarction 6.Remodeled, tethered myocardium A. recovers <24 hours with revascularization B. normal functional recovery within 7 days with revascularization C.variable contractile reserve with reduced resting flow and improved functional recovery with revascularization D. present contractile reserve, normal resting flow and takes months to improve with revascularization E. reduced resting flow and variable contractile reserve with variable response to revascularization F. normal resting flow and contractile reserved, with improved functional recovery within weeks to months with revascularization

Answer 52

1. A 2. B 3. F 4. C 5. E 6. D

Question 53

What is the process termed arteriogenesis?

Answer 53

The proliferation of coronary collaterals in response to repetitive stress-induced ischemia and development of transient interarterial pressure gradients.

Question 54

The resting distal coronary pressure consistently falls as stenosis severity exceeds _ _? A. 70% B. 50% C. 90% D. 60%

Answer 54

A

Question 55

What increases endothelial shear stress in pre-existing collaterals smaller than 200 μm in diameter?

Answer 55

The resultant interarterial pressure gradient.

Question 56

What causes the progressive enlargement of collaterals?

Answer 56

Physical forces and growth factors, particularly vascular endothelial growth factor (VEGF), mediated by NOS.

Question 57

What may limit the development of coronary collaterals in patients?

Answer 57

Impaired NO-mediated vasodilation caused by coronary risk factors.

Question 58

What is the typical diameter range of mature vessels formed from arteriogenesis?

Answer 58

1 to 2 mm.

Question 59

What does angiogenesis refer to?

Answer 59

The sprouting of smaller, capillary-like structures from preexisting blood vessels.

Question 60

What effect does capillary angiogenesis have within the ischemic region?

Answer 60

It can reduce the intercapillary distance for oxygen exchange. May provide nutritive collateral flow when they develop in the border between ischemic and nonischemic regions ## Footnote increases in capillary density in the absence of changes in arteriolar resistance will not significantly increase myocar- dial perfusion

Question 61

Why may increases in capillary density not significantly increase myocardial perfusion?

Answer 61

Because capillary resistance is already a small component of microcirculatory resistance.

Question 62

What has been the outcome of many interventions aimed at improving myocardial function?

Answer 62

They have demonstrated favorable angiogenesis of capillaries but few have increased arteriogenesis in mature collaterals. Did not result to measurable increases in maximum vasodilated myocardial perfusion or coronary flow reserve indices.(functional collateral formation) Did not significantly increase myocardial perfusion.