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Cardio Week 2 > Lecture 16: Regulation and Pathophysiology of the Coronary Circulation > Flashcards

Lecture 16: Regulation and Pathophysiology of the Coronary Circulation Flashcards

1
Q

What is coronary heart disease?

A

CHD represents the clinical manifestation of alterations in the delivery of blood supply to the myocardium

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2
Q

What is the leading cause of death for all males and females?

A

Cardiovascular disease

Coronary heart disease is responsible for 1 in every 6 deaths

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3
Q

What happens to coronary blood flow upon physical exercise?

A

Increased demand = increased coronary flow
Coronary blood flow increases with oxygen consumption over a broad range
Heart = 10% basal metabolic rate

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4
Q

What are the determinants of myocardial oxygen demand?

A
  1. myocardial wall tension
  2. myocardial contractility
  3. heart rate
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5
Q

What are the key characteristics of the epicardial arteries?

A

Large “conductance” vessels providing blood flow to the myocardium, with relatively little role in vascular regulation
Arise from ascending aorta
Composed of a thin intimal layer, a smooth muscle media and a supportive adventitia
Site of obstruction in coronary disease
Are the site of angioplasty or bypass when revascularization is required
Composed of
i. Left coronary
ii. Right coronary artery

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6
Q

What are the key characteristics of the left coronary artery?

A

Originates as the left main and branches into the
i. Left anterior descending (LAD)
ii. left circumflex (Cx)
Provides blood flow to ANTERIOR and LATERAL portions of heart muscle

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7
Q

What are the key characteristics of the right coronary artery?

A

Divides into the posterior descending artery and posterolateral branches
Blood flow to INFERIOR portions of the heart
Supplies SA node and AV node

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8
Q

Where does the SA nodal artery arise from? Significance?

A

60% from proximal RCA

40% from circumflex

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9
Q

Where does the AV nodal artery arise from?

A

90% from distal RCA

10% from circumflex

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10
Q

What are the characteristics of the small penetrating arteries?

A

Often invisible on angiograms

Can become sources of collateral blood supply in setting of obstructive coronary disease

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11
Q

What are the characteristics of intramyocardial coronary arterioles?

A

Responsible for majority of coronary vascular resistance

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12
Q

What are the characteristics of the coronary capillaries?

A

Final step in delivery sequence

Higher density in subendocardial region than in sub-epicardial region

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13
Q

Where is coronary blood flow regulated?

A

Level of microcirculation
NOT at epicardial level
Coronary arterioles = 95% of coronary vascular resistance
Important in setting basal tone and response to increased O2 demand

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14
Q

What are the different ways coronary blood flow is regulated?

A
  1. PRESSURE and RESISITANCE determine coronary flow
  2. Many related factors influence coronary vascular resistance and flow, including
    i. myogenic regulation (response to pressure)
    ii. endothelial regulation (release of substances)
    iii. metabolic effects (accumulation of adenosine)
    iv. Neurohumoral effects (release of neurotransmitter)
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15
Q

For the heart, what is coronary blood flow determined by?

A

Determined by driving pressure into the coronary arteries and the vascular resistance of the coronary arterial system

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16
Q

How do you measure the pressure of the coronary blood flow?

A

Measuring pressure gradient between beginning and end of coronary circulation
Beginning: central aortic pressure (origin of the coronary arteries)
End: most coronary flow occurs during DIASTOLE and the downstream pressure is taken as the LV pressure at the end of diastole (LVEDP)

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17
Q

When is blood flow greatest?

A

During diastole

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18
Q

Why is coronary blood flow phasic?

A

Because of myocardial compressive forces

Systolic compressive forces limit flow in the first 1/3 of the cycle

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19
Q

What is extravascular resistance? Significance?

A

The compressive force applied to the coronary arteries during systolic muscular contraction of the heart, limiting most flow to the diastolic period

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20
Q

What is the limitation of heart rate to coronary flow?

A

With increasing HR, there is not only more oxygen demand, but less diastolic time for delivery

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21
Q

What is the effect of the extravascular compressive forces on the transmural distribution of coronary flow?

A

Extravascular compressive forces are greatest on subendocardial regions (more so than subepicardial regions)
Net driving force for subendocardial blood flow is lower than for eicardium
This makes subendocardial region most vulnerable to ischemia where coronary blood flow may be reduced

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22
Q

What is the significance of transmural regulation of flow?

A

This process is regulated to make sure subendocardial area receives maximal flow
This is regulated by
i. greater capillary concentration to subendocardium
ii. increasing/decreasing arteriolar resistance

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23
Q

What is vascular resistance generated by?

A

Mainly by smaller intramyocardial arteries and arterioles

As perfusion pressure falls, resistance will fall to keep flow constant (known as autoregulation)

24
Q

What is autoregulation?

A

When the resistance decreases with the pressure gradient decrease in order to maintain a certain perfusion pressure (60-150 mmHg)
Resistance changes which keep flow constant in the face of altered pressure

25
Q

What is vasodilator reserve?

A

The amount by which resistance can be decreased, therefore preserving flow in the setting of an epicardial stenosis

26
Q

What happens when coronary arteries narrow with disease?

A

Flow and maximal flow can be maintained despite substantial epicardial stenosis
Maintained up to a point, and after this point, the difference between maximal and resting flow drops exponentially

27
Q

What is vasodilator reserve?

A

The amount by which resistance can be decreased, therefore preserving flow in the setting of an epicardial stenosis

28
Q

What is the difference between autoregulation and vasodilator reserve?

A

Both mechanisms decrease resistance when there is smaller pressure gradient to preserve flow
The former does so in a normal person
The latter does so in a diseased state

29
Q

What can the vasodilator reserve viewed as?

A

Viewed as a 2-resistor model

Ohms law here is Q = P/(R1+R2)

30
Q

What are the two parts of resistance? Significance?

A
  1. R1 = resistance of the epicardial vessels, normally low
  2. R2 = resistance of small arteries, normally high, but able to decrease to maintain constant flow
    Underlies the vasodilator reserve
    If R1 increases due to an epicardial coronary artery stenosis, R2 will decrease to maintain constant flow
31
Q

What are the characteristics of myogenic regulation of vascular resistance?

A

Constriction of vascular SMCs in response to perfusion pressure
Dilation in response to decrease in perfusion pressure
MoA of contraction = stretch-induced depol of VSMCs
MoA of vasodilation = potassium ion efflux through ATP-sensitive potassium channels

32
Q

What are the endothelial mechanisms of regulation of resistance?

A
  1. Endothelium-dependent vasodilation

2. Endothelium-independent vasodilation

33
Q

What are the characteristics of endothelium-dependent vasodilation?

A

Requires an intact functioning endothelium

Involves release of chemical mediators like nitric oxide

34
Q

What are the characteristics of endothelium-independent vasodilation?

A

Intact endothelial function isn’t required
Mediators act directly on SMCs
Examples = nitroglycerin, papavarine and calcium channel antagonists

35
Q

What are the key characteristics of NO?

A
  1. Continuously released by normally functioning endothelium
  2. Produced from L-arginine and NO-synthase
  3. Results in vasodilation via the cGMP pathway
  4. Present in small amounts under basal conditions: if NO synthase is inhibited under basal conditions, moderate vasoconstriction will occur
36
Q

How is the release of nitric oxide controlled?

A
  1. pulsatile stress
  2. acetylcholine
  3. bradykinin
  4. ATP, ADP
  5. prostacyclin
  6. histamine
37
Q

How does pulsatile stress control NO?

A

Shear stress imposed by flowing blood past endothelium and contractile function of the heart will stimulate NO release in resting state

38
Q

What neurotransmitter is an important stimulus for NO release?

A

Acetylcholine

39
Q

What is the importance of endothelin-1?

A

A vasoconstrictor released by endothelium
Release stimulated by
i. thrombin
ii. angiotensin II
iii. epinephrine
iv. cytokines
Maintains normal vascular tone with a tonic vasoconstricting effect
Mediated through endothelin A receptors in vascular SMC and activation of Phospholipase C

40
Q

What are the characteristics of metabolic regulation of vascular resistance?

A

Adenosine is released from ATP breakdown
Adenosine increases when myocardial oxygen demand > supply
Ultimately increases vasodilation
Targets SMC in arterioles, pathway = cAMP

41
Q

What is the significance of adenosine?

A

Adenosine concentration increases when myocardial oxygen demand exceeds oxygen supply
-results in a feedback loop to increase vasodilation and therefore increase coronary flow
Increases cAMP in arterioles

42
Q

What are the characteristics of neurohormonal regulation of vascular resistance?

A

Alpha-adrenergic = vasoconstriction
Beta 1 = vasodilation via increased metabolic demand
Beta 2 = direct vasodilatory effects
Cholinergic effects has TWO opposing (pseudoparadoxical) effects
i. Intact endothelium = vasodilation with ACh
ii. damaged endothelium = vasoconstriction with ACh because ACh travels to smooth muscle

43
Q

What can impair endothelial function?

A

Hyperlipidemia
Atherosclerosis
HTN
Treatment of these conditions can return endothelial function back towards normal

44
Q

How does one test endothelial function?

A

Through acetylcholine administration
Healthy endothelium = vasodilation (because of NO release)
Damaged endothelium = vasoconstriction (because acetylcholine binds SMC)

45
Q

How does the coronary diameters compare between a CAD patient taking statins and a patient not taking statins?

A

The patient taking statins will have a greater diameter because the endothelium is more intact

46
Q

What is the effect of exercise on endothelial function?

A

It has a positive response
Decreases endothelial damage
Thus if you give exercise group acetylcholine, you see larger diameter and greater blood flow

47
Q

How can acetylcholine be predictive of future coronary events?

A

Patients with greater epicardial vasodilation response have shown less subsequent coronary events

48
Q

What is a hallmark of early and late CAD?

A

Endothelial dysfunction is a hallmark of early and late CAD, and may be identified even before critically important coronary narrowing is seen

49
Q

How can endothelial dysfunction be modified?

A

Endothelial dysfunction may be modified through standard treatments for CAD, including lipid lowering and exercise

50
Q

What are the syndromes of CAD?

A
  1. Angina pectoris
  2. acute MI
  3. coronary artery spasm
  4. small vessel disease
51
Q

What is angina pectoris?

A

Occurs because of narrowing of one or more coronary arteries
Symptoms often do not occur until a stenosis is >70% because of the compensatory vasodilation of small arterioles to maintain flow
Treatment with nitrates, anti-platelet agents, beta-blockers and eventually stents/CABG

52
Q

Why use beta-blockers to treat angina pectoris?

A

While it may vasodilate, it is outweighed by the effect to slow heart rate and reduce demand for oxygen in myocardium

53
Q

What causes pain in angina?

A

Buildup of toxic metabolites (because not enough blood to carry that shit away)

54
Q

What are stents?

A

Stainless steel devices placed to open stenotic vessels during a coronary angioplasty procedure
Some current devices have a drug-eluting polymer to reduce re-narrowing of blood vessel (Drug eluting stents)
Requires hospitalization and stent or CABG
A type of acute coronary syndrome
What are the characteristics of coronary bypass grafts?
Harvests a vein graft that is attached from aorta to aorta
OR
Artery is re-directed from chest wall (internal mammary artery) to affected coronary artery

55
Q

What is acute myocardial infarction?

A

When plaque rupture and secondary thrombus and platelet accumulation result in complete or nearly complete occlusion of a coronary vessel
Treated urgently with stent or with thrombolytic medications to restore blood flow
Can result in significant loss of myocardial muscle function

56
Q

What is coronary artery spasm?

A

Severe, focal, reversible narrowings in epicardial arteries, sometimes in the presence of a pre-existing atherosclerotic plaque
Often reversible with nitrates or calcium-channel blockers to prevent spasm
Prinzmetal’s type II (will see later in angina)

57
Q

What is small vessel disease?

A

Poorly defined syndrome characterized by angina, with no obvious narrowings in the epicardial arteries, but with decreased vasodilator reserve

Cardio Week 2 (11 decks)

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