Coronary Circulation

Question 1

Coronary Arteries

Answer 1

-Right Coronary artery-major branch acute marginal
-Left Main Coronary travels 1-1.5 cm before branches into
1- Left Anterior Descending (LAD) follows the anterior interventricular groove; major branches: diagonal branches distributing over the free wall of the left ventricle, and septal branches pentrating into the anterior portion of the ventricular septum

2- Circumflex artery (LCX)- follows the left atrioventricular groove posteriorly; major branche: obtuse marginals

3- Ramus Intermedians: it is not unusual for there to be a third branch from the LMT between the LAD and LCX

Question 2

Cardiac veins

Answer 2

• venous drainage of the myocardium is predominately to the right atrium via the coronary sinus
• the orifice of the coronary sinus has a diameter of 0.5-1 cm and opens into the RA near the inferior vena cava and ticuspid valve
• the 1.5-6.5 cm long coronary sinus rests in the posterior atrioventricular groove and receives venous blood from the left ventricle through the middle cardiac vein, posterior interventricular vein, greater cardiac vein and anterior interventricular vein
• the coronary sinus also receives blood from right ventricle through the small cardiac vein
• venous blood from the right ventricle returns to the RA through the anterior cardiac veins which empty directly and individually into the RA

Question 3

Thebesian Vessels

Answer 3

• there are vessels connecting cardiac chambers to arterioles, capillaries and venules
• the coronary flow may return to the heart chambers through the typical route (artery- arteriole- capillary- venule- vein- right atrium) and it may drain directly from Arterioles, capillaries and venules into the cardiac chambers
• the right atrium receives the majority of the thesbesian drainage but the left and right ventricles do receive some thebesian drainage

Question 4

Interconnections

Answer 4

• there is a minor amount of interconnectivity between coronary vessels including: arterial to venous shunts, arterial to arterial connections, venous to venous connections
• the circulation is a loop which force perfusion into territories whose primary route of delivery has been compromised
• sometimes during surgery requiring elective cardiac arrest, cardiologic solution is sometimes administered into the coronary arteries and the coronary sinus simulataneously without any apparent harm to the heart

Question 5

Normal anatomical variant

Answer 5

• coronary dominants, LCX left circumflex artery, connected to RCA
• all three major arteries have the same ostia in the aortic root
• each major coronary artery has its own ostia in the aortic root

Question 6

Distribution of blood flow

Answer 6

• coronary perfusion territories- coronary dominance
• redundancy of blood distribution to papillary muscle
• interdigitated borders

Question 7

Coronary Dominance

Answer 7

• the posterior descending artery (PDA) travels in the posterior interventricular groove to the apex of the heart
• 70% PDA supplied by the RCA (right dominance)
• 20% PDA supplied by both the RCA and the left circumflex artery (co-dominant)
• 10% PDA supplied by the left circumflex artery (left dominant)

Question 8

Papillary muscle blood flow

Answer 8

• the leaflets of the mitral valve are tethered to the anterior and posterior papilary muscles in the left ventricle
• failure of the papilary muscles results in acute mitral regurgitation and pulmonary edema
• the coronary circulation protects against papilary muscle failure resulting from ischemic heart disease by supply each papilary muscle from two different coronary arteries
• the posterior papillary muscle is supplied from the RCA and LCX arteries
• the anterior papillary muscle is supplied from the LAD and the LCX arteries

Question 9

Borders of perfusion territories

Answer 9

-at all points of filling the territory has irregularly shaped borders with peninsulas of perfused tissue penetrating deeply into areas of unperfused tissue

Question 10

Coronary perfusion occurs during diastole

Answer 10

• during diastole, aortic diastolic pressure is transmitted without resistance to the coronary ostia
• aortic arch and coronary sinuses act as minature reservoir, facilitating maintenance of uniform coronary inflow through diastole
• the epicardiac coronary arteries act as conductance or conduit vessels: 0.3- 5 mm diameter, no appreciable resistance to blood flow with no detectable pressure drop along the length of epicardial arteries
• the arterioles are 10-200 microns diameter- act as resistance vessels, large pressure drop
• in the right coronary arterty the flow is even in diastole and systole
• maximum flow occurs in LCA during diastole

Question 11

Coronary flow during cardiac cycle

Answer 11

• flow occurs in the arteries supplying the subendocardial portion of the left ventricle only during diastole as pressure inside the LV is slightly higher than aorta during systole
• flow in the right ventricle and atria is not appreciably reduced during systole, because aortic pressure is much higher
• because diastole is shorter when the heart rate is high, left ventricular coronary flow is reduced during tachycardia
• because no blood flow in systole in the subendocardial portion of left ventricle, the region is prone to ischemic damage and is common site of MI

Question 12

Coronary vascular resistance

Answer 12

• epicardial conduit artery resistance: insignificant is normal, in presence of >50% stenosis, this starts contributing to total coronary resistance and may reduce resting flow with >90% stenosis
• arterioles and resistance arteries: dynamic resistance from metabolic and autoregulatory adjustments to flow, changes in response to physical forces and metabolic needs of tissue
• compressive resistance- varies with time through cardiac cycle, related to cardiac contraction and systolic pressure, higher in subendocardial than subepicardial layers

Question 13

Normal blood flow

Answer 13

• because no blood flow occurs during systole in the subendocardial portion of the left ventricle, this region is prone to ischemic damage and is most common site of myocardial infarction
• blood flow to the left ventricle is decreased in patients with stenotic aortic valves because the pressure in the left ventricle must be much higher than that in the aorta to eject the blood-vessels are severely compressed during systole
• coronary flow is also decreased when the aortic diastolic pressure is low-the rise in venous pressure in conditions such as congestive heart failure reduces coronary flow because it decreases effective coronary perfusion pressure

Question 14

Myocardial oxygen consumption

Answer 14

• the myocardium extracts nearly all of the oxygen delivered to it from coronary blood flow
• normal venous oxygen saturation of coronary sinus is 30%
• any increase in oxygen consumption requires an increase in blood flow
• the driving pressure through the coronary vessel
• extravascular compression of the coronary arteries by heart contraction and
• the resistance of the coronary vessels

Question 15

Autoregulation of coronary flow

Answer 15

• the intrinsic ability of the heart to maintain a constant blood flow over a wide range of coronary perfusion pressures
• basal blood flow remains fairly constant despite fluctuations in coronary artery pressure
• given that the myocardium extracts 70% of the oxygen supplied to it at rest, increases in MVO2 increases necessitate an increase in blood flow

Question 16

Coronary flow reserve

Answer 16

• is the maximal increase in coronary blood flow (CBF) above its resting level for a given perfusion pressure when coronary vasculature is maximally dilated
• normally, hyperaemic CBF reaches values at least 2- to 3- fold greater than resting CBF
• reduction of CFR is mainly due to epicardial coronary artery stenosis or to coronary microvascular dysfunction
• autoregulation is impaired in the presence of critical fall in aortic pressure, chronic hypertension and LV hypertrophy

Question 17

Mechanism of autoregulation

Answer 17

• both metabolic and myogenic mechanisms
• different sites in the microvasculature may have different dominant mechanisms of control
• metabolic control: result of local metabolism, may be due to NO mediated dilation, endothelium senses changes in pressure through pressure-sensitive ion channels
• myogenic control: arteriolar VSM contracts with increased intraluminal pressure

Question 18

Endothelial control of coronary vascular tone

Answer 18

• endothelium produces- powerful vasodilators: EDRF endothelium derived relaxing factor, NO, prostacyclin, EDHF endothelium derived hyperpolarizing factor
• powerful vasoconstrictors- Endothelin-1
• endothelium can be damaged by atherosclerosis and cardiac risk factors- its dysfunction leads to imbalance of coronary flow, pathogenesis of myocardial ischemia and is a central factor in evolution of atherosclerosis and thombosis
• risk factors: dyslipedimia, hypertension, diabetes, smoking, menopause, aging etc

Question 19

Preload

Answer 19

• filling pressure
• amount of stretch on muscle just before contraction
• MV stenosis
• MV regurgitation
• aortic insufficiency

Question 20

Afterload

Answer 20

• the pressure/ resistance the heart is working against while it is squeezing
• HTC
• aortic stenosis

Question 21

Myocardial O2 Consumption MVO

Answer 21

• MVO2 is the major determinant of coronary blood flow
• MVO2 may increase 4-5 times over resting states with exercise
• in a steady state, MVO2 provides an adequate measure of heart’s total metabolism- MVO2 of a beating canine heart is 8-15 ml/min/100gm
• MVO2 of noncontracting heart is 1.5 ml/min/100gm
• wall stress 25%
• contractility 45%
• pressure work 50%
• heart rate 50%
• volume work 4%

Question 22

Pathologies influencing myocardial perfusion and MVO2

Answer 22

• CAD
• ventricular hypertrophy
• ventricular dilation
• coronary fistula

Question 23

Ischemia

Answer 23

• supply ischemia or low flow ischemia-reduction in blood flow
• increased coronary vascular tone
• intracoronary platelet aggregation
• thombus formation
• demand ischemia or high flow ischemia- increase in coronary blood flow that is insuficient to meet the increase myocardial O2 demand- usually in the presence of coronary obstruction, brought upon the exercise, emotional stress or tachycardia
• hypoxia- reduced O2 supply- asphyxiation, carbon monoxide poisoning, cyanotic congenital heart disease or cor pulmonale

Question 24

Coronary blood flow

Answer 24

• maximum myocardial perfusion is ultimately determined by the coronary pressure distal to the stenosis
• autoregulation maintains constant flow with increasing stenosis severity. Resting perfusion is inadequate to distinguish between hemodynamically significant stenosis. In contrast, the maximally vasodilated pressure-flow relationship is much more sensitive to detect stenosis
• normal coronary flow reserve is up to 5 x the rest flow- no significant pressure drop up to 50% severity, worsening stenosis severity causes increasing pressure drop, at critical levels of >90%, resting flow is reduced

Question 25

Coronary flow reserve

Answer 25

- the healthy heart has the ability to increase the blood flow to the myocardium in response to local metabolic demand by reducing coronary artery resistance (dilating the coronary arteries) - typically the surface arteries offer very little resistance to blood flow - the development of coronary artery disease however can produce blockages in the arteries that become the dominant point of resistance to coronary blood flow

Question 26

Ventricular Hypertrophy

Answer 26

- stenosis of the aortic valve will force the LV to work harder to pump blood across a small orifice - as a result, the left ventricular tissue will hypertrophy and the increased muscle mass will require greater oxygen supply - additionally, the coronary flow reserve is reduced due to a change in the ration of blood supply to mass of tissue - with LVH, myocardial mass increases without an increase in microcirculatory resistance arteries - because max absolute flow per min during vasodilation remains unchanged, the max flow per gram of tissue falls inversely with the change in LV mass - the increase in LV mass also requires a higher resting flow - the net effect is decreased coronary flow reserve at any pressure - even a milder stenosis can be ischemic

Question 27

Clinical evaluation

Answer 27

- coronary angiogram - MRA magnetic resonance angiogram - CTA computed tomography angiogram - echo doppler - cardiac MRI - cardiac PET scan - FFR in the cath lab - ischemia testing- exercise stress tests: echo or nuclear - pharmacological stress tests- Dobutamine, vasodilators- dipyridamole, adenosine, lexiscan

Question 28

Methods of improving coronary blood flow

Answer 28

- Pharmacologic: Nitroglycerine, Adenosine - Invasive: Angioplasy (with stent) and CABG - Other: IABP, Controlled arrest- cardioplegia, transplant

Question 29

Coronary Angiogram

Answer 29

- Coronary anatomy- vessel dominance, vascular territories, anomalous vessels, collaterals - coronary lumen obstruction - coronary blood flow - limitations- invasive, potential underestimation of lesion severity, no info on hemodynamic significance, no info on vessel wall - injection of iodinated contrast selectively into coronary ostia by catheter - contrast fills the vessel lumen - X ray radiation releases photons from the iodine, which is taken up in the camera

Question 30

Nitroglycerine

Answer 30

- Administration: Sublingual, transdermal, intravenous - vasodilator - dilates epicardial conduit arteries and small coronary resistance vessels - improves subendocardial perfusion by reducing LV end diastolic pressure by venodilation - dilates coronary collateral vessels

Question 31

Other pharmacological vasodilatiors

Answer 31

- Dipyridamole- inhibits the myocyte reuptake of adenosine released locally, mechanism of action similar to adenosine, reversed by adenosine receptor antagonists- aminophylline - Papaverine- causes endothelium independent relaxation of VSM by inhibitng phosphdiesterase and increasing cAMP

Question 32

Adenosine

Answer 32

- very powerful coronary vasodilator - by relaxing VSM cells - released from cardiac myocytes- when the rate of ATP hydrolysis exceeds its synthesis during ischemia or increased myocardial metabolic demand - extremely short half life <10 secs - binds to A2 receptors on VSM, increases cAMP and opens intermediate Ca activated K channels - endothelium independent - primarily dilates vessels less than 100 um - no direct effect on larger arteries - increased production with imbalance of O2 supply demand- rise in interstitial adenosine levels parallels coronary flow

Question 33

Nitric Oxide

Answer 33

- NO is produced from the amino acid L-arginine by the enzymatic action of nitric oxide synthase (NOS) in the vascular endothelium - under normal, basal conditions in blood vessels, NO is continually - increased blood flow stimulates NO formation (flow dependent NO formation) because shear force on the vascular endotheloum causes a release of calcium and cNOS activation - inhibition of NO can cause vasoconstriction - NO increases blood flow during metabolic stimuli - inhibition of NO reduces the magnitude of metabolic dilation - NO production is increased in response to hypoxia - NO is a principal mediator of flow-mediated dilation - NO production is associated with hypertension, obesity, diabetes, heart failure

Question 34

Intra Aortic Balloon Pump (IABP)

Answer 34

- afterload reduction: deflation of the balloon will acutely reduce the patients ABP immediately prior to systole and therefore allow the heart to pump against a lower pressure, reducing the work of the heart - diastolic augmentation- balloon inflation just after aortic valve closure will increase the diastolic pressure in the aorta and improve coronary blood flow during diastole, increasing oxygen supply to the heart