SCAI CHAP 12 Coronary Physiology Flashcards
1- BSR (Basal Stenosis Resistance Index):
2- HSR (Hyperemic Stenosis Resistance Index):
3- Pd/Pa (Distal Coronary/Aortic Pressure Ratio):
4- FFR (Fractional Flow Reserve):
5- NHPRs (Nonhyperemic Pressure Ratios):
6- CFR (Coronary Flow Reserve):
7- HM (Hyperemic Myocardial Resistance):
8- IMR (Index of Microcirculatory Resistance):
9- APV (Average Peak Flow Velocity):
10- Paorta (Aortic Pressure):
11-Pdistal (Distal Coronary Pressure):
12- Tmn (Mean Transit Time):
1- Definition: Calculated as (Paorta − Pdistal)/APV or average peak flow velocity under basal conditions. It measures the resistance caused by a stenosis when the heart is at rest.
2- Definition: Calculated as (Paorta − Pdistal)/APV during hyperemia. It measures the resistance caused by a stenosis when the heart is under stress or increased demand.
3- Definition: The ratio of mean distal coronary pressure (Pdistal) to mean aortic pressure (Paorta) under basal conditions. It provides a measure of coronary pressure relative to aortic pressure at rest.
4- Definition: The ratio of mean distal coronary pressure (Pdistal) to mean aortic pressure (Paorta) during hyperemia. It assesses the severity of coronary artery stenosis under increased demand.
5- Definition: Includes indices such as iFR, dPR, dFR, RFR, and Pd/Pa, calculated as the mean Pdistal/mean Paorta during diastole. These ratios assess coronary pressure without inducing hyperemia.
6- Definition: Calculated as APVhyperemia/APVbasal. It measures the capacity of coronary circulation to increase blood flow above its basal level in response to increased demand.
7- Definition: Calculated as Pd/APVhyperemia. It measures the resistance of the myocardium during hyperemia.
8- Definition: Calculated as Pd × Tmn. It quantifies the resistance of the coronary microcirculation.
9-Definition: The average peak velocity of blood flow in the coronary arteries.
10-Definition: The pressure within the aorta.
11-Definition: The pressure within the distal coronary artery.
12- Definition: The average time it takes for blood to travel through the coronary circulation.
Q1: Coronary arterial resistance (R, pressure/flow) is the summed resistances of the epicardial coronary conductance (R1 use FFR ), precapillary arteriolar (R2 use CFR ), and ______ capillary (R3 use IMR ) resistance circuits.
Q2: Microvascular and macrovascular functions in coronary artery disease (CAD) are depicted in ______.
Q3: Normal epicardial coronary arteries in humans typically ______ gradually from the base of the heart to the apex.
Q4: The epicardial vessels are >400 µm (R1) and do not offer significant resistance to blood flow in their normal ______ state.
Q5: Epicardial vessel resistance (R1) is trivial until ______ obstructions develop.
Q6: Coronary epicardial resistance would manifest as a pressure ______ along the length of the epicardial arteries.
A1: intramyocardial
A2: Fig. 12.3
A3: taper
A4: nondiseased
A5: atherosclerotic
A6: drop
Q1: What role do precapillary arterioles (R2) play in coronary blood flow?
Q2: How do precapillary arterioles autoregulate perfusion pressure?
Q3: What is the size range of precapillary arterioles, and what do they connect?
Q4: What constitutes the microcirculatory resistance (R3), and how does it function in relation to myocytes?
Q5: How can conditions like LV hypertrophy and diabetes affect microcirculatory resistance (R3)?
Q6: What happens to coronary flow reserve (CFR) when there is increased R3 resistance?
Q7: What invasive physiologic metrics are used to measure macrocirculatory responses?
Q8: Which metrics are used to assess both macrocirculation and microcirculation?
Q9: How does increased microcirculatory resistance (R3) affect resting blood flow?
A1: Precapillary arterioles (R2) are the main controllers of coronary blood flow, connecting epicardial arteries to myocardial capillaries.
A2: Precapillary arterioles autoregulate perfusion pressure at their origin within a finite pressure range.
A3: Precapillary arterioles are 100-400 µm in size and connect epicardial arteries to myocardial capillaries.
A4: The microcirculatory resistance (R3) consists of a dense network of capillaries (<100 µm) perfusing each myocyte adjacent to a capillary.
A5: Conditions such as LV hypertrophy, myocardial ischemia, or diabetes can impair microcirculatory resistance (R3), blunting normal increases in coronary flow.
A6: Increased R3 resistance may increase resting blood flow, resulting in reduced coronary flow reserve (CFR).
A7: Fractional flow reserve (FFR) and nonhyperemic pressure ratio (NHPR) are used to measure macrocirculatory responses.
A8: The index of microvascular resistance (IMR) and CFR (coronary vasodilator reserve [CVR]) are used to assess both macrocirculation and microcirculation.
A9: Increased microcirculatory resistance (R3) may increase resting blood flow, reducing coronary flow reserve (CFR).
Q1: What causes energy loss and a pressure gradient (ΔP) across a stenosis in a diseased arterial segment?
Q2: How is pressure loss across a stenosis estimated using fluid dynamics?
Q3: What does the variable Q represent in the simplified Bernoulli formula for pressure loss across a stenosis?
Q4: How does the pressure drop (ΔP) change with reduced lumen cross-sectional area and lesion length?
Q5: What are some additional factors that contribute to stenosis resistance?
Q6: What does the first term (f) in the pressure loss formula account for?
Q7: How is the second term (s) in the pressure loss formula related to flow, and what does it reflect?
Q8: Why are the increases in the pressure-flow relationship curvilinear?
Q9: How does the shape of the entrance and exit orifices affect stenosis resistance?
Q10: What does the family of pressure-flow relationships reflect in the context of a given stenosis?
A1: Energy loss and a pressure gradient (ΔP) across a stenosis are caused by turbulence, friction, and separation of laminar flow as blood traverses a diseased arterial segment.
A2: Pressure loss across a stenosis is estimated using a simplified Bernoulli formula for fluid dynamics, expressed as ΔP = fQ + sQ², where ΔP is the pressure drop, and Q is the flow across the stenosis.
A3: In the simplified Bernoulli formula, the variable Q represents the flow across the stenosis (mL/s).
A4: The pressure drop (ΔP) rises exponentially with reduced lumen cross-sectional area and linearly with lesion length.
A5: Additional factors contributing to stenosis resistance include the stenotic segment cross-sectional area (As), blood density (p), blood viscosity (µ), stenosis length (L), and normal artery cross-sectional area (An).
A6: The first term (f) in the pressure loss formula is linearly related to flow and accounts for energy losses due to viscous friction of laminar flow ‼️through the stenosis.
A7: The second term (s) in the pressure loss formula is related to flow in a quadratic manner (squared) and reflects energy loss when accelerated high-velocity flow exits the stenosis, creating turbulent ‼️poststenotic distal flow.
A8: The increases in the pressure-flow relationship are curvilinear due to the quadratic relationship of the second term (s) in the pressure loss formula.
A9: The shape of the entrance and exit orifices affects stenosis resistance by influencing how blood flow enters and exits the stenotic segment, impacting energy loss.
A10: The family of pressure-flow relationships reflects the ischemic potential of the stenosis, considering variables such as area and size of the reference normal vessel.
same stenosis but different reference vessel size and area !
1- What is the main limitation of Coronary Flow Reserve (CFR) in defining angiographic stenosis?
2- Who are the researchers credited with developing the pressure-only method for estimating normal coronary blood flow through a stenotic artery?
3- What does FFR stand for, and how is it defined?
4- Into which three components can FFR be subdivided?
5- What is the formula for calculating FFR of the coronary artery (FFRcor)?
6- What are the key variables used in the FFR calculations, and what do they represent?
7-How is FFRcor different from FFRmyo and FFRcoll?
8-Why is the simplified ratio Pd/Pa used in daily clinical practice for calculating FFR?
9-What is considered the normal value for FFR, and what does it indicate?
10-At what FFR value is provocable myocardial ischemia strongly related in patients with stable angina?
11-Why is FFR considered more epicardial lesion-specific compared to CFR?
12-What conditions are excluded from the FFR computation since it is calculated only at peak hyperemia?
13-How does FFR relate to provocable myocardial ischemia in patients with stable angina?
14-What is the nonischemic threshold value for FFR used in recent clinical outcome studies for deferring PCI?
15-How does a normal FFR value affect the decision to perform stenting in patients with an abnormal microcirculation?
A1. The main limitation of Coronary Flow Reserve (CFR) in defining angiographic stenosis is its inability to account for the presence of microvascular disease in patients with epicardial narrowings. CFR fails to define a stenosis.
A2. The researchers credited with developing the pressure-only method for estimating normal coronary blood flow through a stenotic artery are Pijls et al. and de Bruyne et al.
A3. FFR stands for Fractional Flow Reserve, defined as the ratio of the poststenotic pressure to aortic pressure during minimal and fixed resistance (maximal hyperemia).
A4. FFR can be subdivided into three components: FFR of the coronary artery (FFRcor), the myocardium (FFRmyo), and the collateral supply (FFRcoll).
A5. The formula for calculating FFR of the coronary artery (FFRcor) is: FFRcor = FFR myo - FFR coll.
A6. The key variables used in FFR calculations are:
( Pa ): mean aortic pressure
( Pd ): mean distal coronary pressure
( \Delta P ): mean translesional pressure gradient
( Pv ): mean right atrial pressure
( Pw ): mean coronary wedge pressure or distal coronary pressure during balloon occlusion
A7. FFRcor is different from FFRmyo and FFRcoll in that it specifically measures the flow contribution by the coronary artery, while FFRmyo measures the myocardial contribution, and FFRcoll measures the collateral supply.
A8. The simplified ratio ( Pd/Pa ) is used in daily clinical practice for calculating FFR because it assumes ( Pv ) is negligible relative to ( Pa ), simplifying the calculation.
A9. The normal value for FFR is unequivocally 1, indicating normal coronary blood flow through the artery for each patient, coronary artery, myocardial distribution, and microcirculatory status.
A10. An FFR value of <0.75 in patients with stable angina is strongly related to provocable myocardial ischemia using multiple stress testing methods.
A11. FFR is considered more epicardial lesion-specific compared to CFR or resting pressure gradients, because it is independent of hemodynamic and loading conditions and reflects both antegrade and collateral perfusion.
A12. Since FFR is calculated only at peak hyperemia, it excludes the microcirculatory resistance from the computation.
A13. FFR is strongly related to provocable myocardial ischemia in patients with stable angina, as it serves as a comparative standard using different clinical stress testing modalities.
A14. The nonischemic threshold value for FFR used in recent clinical outcome studies for deferring PCI is >0.80.
A15. A normal FFR value indicates that the epicardial conduit resistance (stenosis) is not a major contributing factor to perfusion impairment, suggesting that stenting would not restore normal perfusion even in patients with an abnormal microcirculation.
1-True or False: Nonhyperemic pressure ratios (NHPRs) require the use of adenosine for measurement.
2-True or False: NHPRs have been proven to be clinically inferior to Fractional Flow Reserve (FFR) in large multicenter trials.
3-True or False: The instantaneous wave-free ratio (iFR) was the first NHPR developed.
4-True or False: iFR is measured during a specific systolic interval of the cardiac cycle.
5-True or False: During the wave-free period used for iFR, microvascular resistance is constant but not minimal.
6-True or False: All NHPRs use the ratio of distal coronary pressure to aortic pressure.
7-True or False: NHPRs differ in the portion of the systolic period of the cardiac cycle that is measured.
8-True or False: Examples of NHPRs include dPR, DFR, relative CFR, and Pd/Pa.
9-True or False: NHPRs have similar threshold values and are considered as a group with class action.
10-True or False: The use of NHPRs eliminates the need for inducing hyperemia in patients.
A1. False: Nonhyperemic pressure ratios (NHPRs) do not require the use of adenosine for measurement.
A2. False: NHPRs have been shown to be clinically noninferior to Fractional Flow Reserve (FFR) in large multicenter trials.
A3. True: The instantaneous wave-free ratio (iFR) was the first NHPR developed.
A4. False: iFR is measured during a specific diastolic interval of the cardiac cycle.
A5. True: During the wave-free period used for iFR, microvascular resistance is constant but not minimal.
A6. True: All NHPRs use the ratio of distal coronary pressure to aortic pressure.
A7. False: NHPRs differ in the portion of the diastolic period of the cardiac cycle that is measured.
A8. True: Examples of NHPRs include dPR, DFR, relative CFR, and Pd/Pa.
A9. True: NHPRs have similar threshold values and are considered as a group with class action.
A10. True: The use of NHPRs eliminates the need for inducing hyperemia in patients.
Q1. Defined as average Pd/Pa during the wave-free period.
Q2. Begins 25% into diastole and ends 5 ms before the end of diastole.
Q3. Average Pd/Pa measured during the entire diastole.
Q4. Associated with Boston Scientific.
Q5. Defined as average Pd/Pa during diastole when Pa is less than mean Pa with a negative slope.
Q6. Lowest filtered mean Pd/Pa during the entire cardiac cycle.
A1. Instantaneous wave-free ratio (iFR)
A2. wave free period
A3. Diastolic pressure ratio or DPR
A4. Resting full-cycle ratio (RFR)
A5. diastolic hyperemia-free ratio or DFR
A6. Resting full cycle ratio or RFR
Questions:
Q1. What study assessed 157 stenoses with iFR and FFR?
Q2. Which study compared the diagnostic accuracy of iFR and Pd/Pa with FFR?
Q3. How many patients were involved in the RESOLVE study?
Q4. What was the optimal iFR value to predict an FFR <0.8?
Q5. What was the cut point for the resting Pd/Pa ratio in terms of accuracy?
Q6. What percentage accuracy did both iFR and Pd/Pa have in predicting positive FFR?
Q7. What is the overall accuracy with FFR for resting indices of lesion severity?
Q8. What factor does the reproducibility of NHPRs depend on?
Q9. What can artifactually lower NHPR measurements?
Q10. What are some factors that affect both NHPR and FFR measurements?
Answers:
A1. The Adenosine Vasodilator Independent Stenosis Evaluation (ADVISE) study.
A2. The RESOLVE study.
A3. 1768 patients.
A4. 0.92.
A5. 0.92 with an overall accuracy of 92%.
A6. 90% accuracy ( Both measures have 90% accuracy to predict positive or negative FFR in 65% and 48% of lesions, respectively)
A7. About 80%, which can be improved to 90% in a subset of lesions.
A8. Stable resting coronary blood flow.
A9. Saline flushing, contrast, or nitroglycerin (NTG) administration.
A10. Drift, guide catheter dampening, and artifacts.
FFR and NTG
NTG (100-200 µg) is given to vasodilate and block vasoconstriction of the artery. NTG has no effect on hemodynamic measurements unless the stenosis is vasoconstricted.
CFR dogs vs humans
FFR and MAX HYPEREMIA
Lesion assessment by FFR requires measurements during maximal hyperemia. At maximal hyperemia, autoregulation is abolished, and microvascular resistance is fixed and minimal. Under these conditions, coronary blood flow is directly related to coronary pressure.
FFR and Adenosine
Adenosine, a potent short-acting hyperemic stimulus, is the most widely used hyperemic agent. Adenosine is benign in the appropriate dosages (50-100 µg in the right coronary artery (RCA) and 100-200 µg in the left coronary artery or infused intravenously at 140 µg/kg/min).
Intravenous (IV) and IC adenosine produce equivalent hyperemia.
Table 12.4 lists the characteristics of pharmacologic hyperemia-inducing agents that can be used in coronary flow studies.
IC nitroprusside (50 and 100-µg bolus) produces nearly identical results to IV and IC adenosine.
Q1. CVR, also known as CFR, measures the ratio of maximal hyperemic to resting coronary flow or flow velocity.
Q2. CFR describes the coronary vascular bed’s ability to increase flow in response to increased myocardial oxygen demand from only mechanical stimuli.
Q3. Gould et al. showed that increasing coronary stenosis severity was associated with a predictable decline in CFR.
Q4. CFR begins to decline with a 60% diameter narrowing in dog experiments.
Q5. It was initially thought that stenoses of physiologic importance could be identified by angiographic stenoses of >50%.
Q6. The observation about CFR decline with stenosis severity extends consistently to human coronary angiography.
A1. True. CVR, also known as CFR, measures the ratio of maximal hyperemic to resting coronary flow or flow velocity.
A2. False. CFR describes the ability of the coronary vascular bed to increase flow in response to increased myocardial oxygen demand from both mechanical ( exercise) and pharmacologic stimuli ( adenosine )
A3. True. Gould et al. showed that increasing coronary stenosis severity was associated with a predictable decline in CFR.
A4. True. CFR begins to decline with a 60% diameter narrowing in dog experiments.
A5. True. It was initially thought that stenoses of physiologic importance could be identified by angiographic stenoses of >50%.
A6. False. The observation about CFR decline with stenosis severity does not extend consistently to human coronary angiography ( because in patients who have microvascular disease, CFR does not correlate with stenosis )
Questions:
Q1. Normal coronary flow at baseline and during hyperemia ranges from 2× to 5× resting flow in humans.
Q2. At diameter stenoses greater than 80% to 90%, all available coronary reserves have been exhausted, and resting flow begins to decline.
Q3. CFR can be reduced due to angiographic epicardial stenoses as well as the presence of microvascular disease in patients.
Q4. An abnormal CFR can be solely attributed to a coronary stenosis.
Q5. CFR is used to assess the presence of microvascular disease in the absence of epicardial obstructions.
A1. True. Normal coronary flow at baseline and during hyperemia ranges from 2× to 5× resting flow in humans.
A2. True. At diameter stenoses greater than 80% to 90%, all available coronary reserves have been exhausted, and resting flow begins to decline.
A3. True. CFR can be reduced due to angiographic epicardial stenoses as well as the presence of microvascular disease in patients +++++++
A4. False. An abnormal CFR cannot be solely attributed to a coronary stenosis because it may also be influenced by microvascular disease.
A5. True. CFR is used to assess the presence of microvascular disease in the absence of epicardial obstructions.
Factors Responsible for !!Microvascular Disease!! and Reduction of Coronary Flow Reserve
Abnormal vascular reactivity
Abnormal myocardial metabolism
Abnormal sensitivity toward vasoactive substances
Coronary vasospasm
Myocardial infarction
Hypertrophy
Vasculitis syndromes
Hypertension
Diabetes
Recurrent ischemia
True or False
Q1. In adult patients with chest pain undergoing cardiac catheterization with angiographically normal vessels, the average CFR is 2.7 ± 0.64.
Q2. CFR values less than 2.0 have been associated with inducible myocardial ischemia on stress testing.
Q3. Changes in heart rate, blood pressure, and contractility do not affect CFR.
Q4. CFR is altered by changes in resting basal flow or maximal hyperemic flow or both.
A1. True. In adult patients with chest pain undergoing cardiac catheterization with angiographically normal vessels, the average CFR is 2.7 ± 0.64.
A2. True. CFR values less than 2.0 have been associated with inducible myocardial ischemia on stress testing.
A3. False. Changes in heart rate, blood pressure, and contractility do affect CFR.
A4. True. CFR is altered by changes in resting basal flow or maximal hyperemic flow or both.
Q1. FFR is measured at hyperemia only and is unaffected by changes in basal flow.
Q2. CFR is the ratio of hyperemic to basal flow, and any change in either changes the CFR value.
Q3. NHPR, such as iFR and Pd/Pa, can be easily computed at constant basal flow.
Q4. Any change in basal flow will change the NHPR measurement.
A1. True. FFR is measured at hyperemia only and is unaffected by changes in basal flow.
A2. True. CFR is the ratio of hyperemic to basal flow, and any change in either changes the CFR value.
A3. True. NHPR, such as iFR and Pd/Pa, can be easily computed at constant basal flow.
A4. True. Any change in basal flow will change the NHPR measurement.
Questions:
Q1. FFR values <0.75
Q2. FFR values >0.80
Q3. Sensitivity of FFR values <0.75
Q4. Specificity of FFR values <0.75
Q5. Positive predictive value of FFR values <0.75
Q6. Overall accuracy of FFR values <0.75
Q7. Predictive accuracy of FFR values >0.80
Q8. Initial FFR validation study
Q9. Myocardial perfusion scintigraphy
Q10. Stress echocardiography
Q11. Overlapping FFR results range ( based on multiple stress tests modailties )
Q12. FFR as a specific index
Answers:
A1. Associated with ischemic stress testing
A2. Associated with negative ischemic results
A3. high 88%
A4. 100%
A5. 100%
A6. high 93%
A7. high 95%
A8. Compared FFR to three different stress tests in the same patients before and after PCI.
A9. Difficult standard for ischemia due to relative flow comparison ( since it compares relative and not absolute myocardial flow in different coronary beds making the determination of the ischemic potential of individual lesions in patients with multivessel CAD challenging )
A10. Severe ischemia in one region may mask less severe lesions yet HD significant in other regions
A11. 0.75-0.80
A12. FFR is Vessel- and lesion-specific index of ischemia ( not like stress tests ).
IFR vs FFR
While FFR was validated against several different ischemic tests, iFR was validated against FFR and subsequently found to have a threshold value of 0.89, which correlated with FFR <0.80 and demonstrated a good diagnostic performance.
iFR and FFR have similar diagnostic efficiency for detection of ischemia-inducing stenoses when tested against a third comparator.
Ischemic thresholds ( attention whole cycle Pd/Pa means probably RFR which is the one in launwood so threshold is 0.92 not 0.89 which is for iFR)
Q1. iFR/FFR discordance occurrence rate
Q2. Condition associated with high flow
Q3. Favors FFR+/NHPR−
Q4. Favors FFR+/NHPR−
Q5. Separation coefficient (sQ2) is larger in
Q6. Favors FFR−/NHPR+ in diffuse lesions
Q7. Most iFR−/FFR+ disparity is due to
Q8. iFR+/FFR− is seen more in
Q9. Clinical significance of discordant FFR/NHPR
Q10. Highest adverse clinical event rates are in
A1. 20% of cases
A2. Left anterior descending (LAD), large myocardial mass, high CO
A3. high flow conditions
A4. focal lesions
A5. Focal lesions
A6. Lower net CFR
A7. High translesional flow with high CFR
A8. Diffuse coronary disease with lower CFR
A9. Remains under study
A10. iFR+/FFR+
Q1. Lower adverse clinical event rates for discordant values
Q2. Best outcomes for medical therapy in
Q3. Recommended approach for decision-making
A1. iFR+/FFR−, iFR−/FFR+
A2. iFR−/FFR−
A3. Step-wise fashion from NHPR to cFFR and/or adenosine FFR
Q1. Both FFR and NHPR can be used to determine the appropriateness of ______.
Q2. The DEFER study randomized ______ patients scheduled for PCI into three groups.
Q3. If FFR was >0.75, patients were randomly assigned to the deferral group or the ______ performance group.
Q4. The deferral group consisted of ______ patients.
Q5. The PCI performance group consisted of ______ patients.
Q6. If FFR was <0.75, patients were entered into the ______ group.
Q7. The event-free survival was not different between the deferred and performed group, with percentages of ______% and ______%, respectively.
Q8. The event-free survival in the reference PCI group was ______%.
Q9. The composite rate of cardiac death and acute myocardial infarction (MI) in the deferred group was ______%.
Q10. The composite rate of cardiac death and MI in the reference group was ______%
A1. angioplasty
A2. 325
A3. PCI
A4. 91
A5. 90
A6. reference
A7. 80, 73 ( both FFR > 0,75)
A8. 63 ( they did worse than A7, so the event free survival was better when FFR > 0.75 ).
A9. 3.3
A10. 15.7 ( PCI done when FFR > 0.75 did better than when PCI done when FFR <0.75)
Q1. The foundational studies for the use of FFR in multivessel disease patients are the ______ family of studies.
Q2. FAME 1 tested whether ischemia (FFR)-directed PCI was better than ______ guided stenting of all angiographic lesions.
Q3. FAME 1 found that compared to angiographically guided PCI, FFR-guided PCI demonstrated lower ______ at 1, 2, and 5 years.
Q4. van Nunen et al examined ______ patients with multivessel CAD undergoing PCI with drug-eluting stents (DES).
Q5. For the FFR-PCI group, all lesions had FFR measurements and only those with an FFR <______ were stented.
Q6. For the Angio-PCI group, all lesions identified were ______.
Q7. Clinical characteristics and angiographic findings were similar in both groups, with an average SYNTAX score of ______.
Q8. The SYNTAX score of 14.5 indicates ______ risk patients.
Q9. The FFR-PCI group consisted of ______ patients.
Q10. The Angio-PCI group consisted of ______ patients.
A1. FAME
A2. angiographically
A3. major adverse cardiac event (MACE)
A4. 1005
A5. 0.80
A6. stented
A7. 14.5
A8. low-intermediate
A9. 496
A10. 509
Still in the Van Nunen study
Q1. Compared to the Angio-PCI group, the FFR-PCI group used fewer ______ per patient.
Q2. The FFR-PCI group used ______ stents per patient on average.
Q3. The Angio-PCI group used ______ stents per patient on average.
Q4. The FFR-PCI group used less ______ compared to the Angio-PCI group.
Q5. The FFR-PCI group had a lower procedure ______ compared to the Angio-PCI group.
Q6. The FFR-PCI group had a shorter ______ stay compared to the Angio-PCI group.
Q7. The 2-year rates of mortality or MI were ______% in the Angio-PCI group.
Q8. The 2-year rates of mortality or MI were ______% in the FFR-PCI group.
Q9. Composite rates of death/nonfatal MI or revascularization were ______% in the Angio-PCI group.
Q10. For lesions deferred based on an FFR of >0.80, the rate of MI was ______% after 2 years.
A1. stents
A2. 1.9 ± 1.3
A3. 2.7 ± 1.2
A4. contrast
A5. cost
A6. hospital
A7. 13
A8. 8
A9. 22 ( 18% for FFR-PCI )
A10. 0.2
Q1. The FAME 2 trial addressed whether ______ for CAD was better than OMT with PCI in patients with multivessel CAD.
Q2. The FAME 2 trial involved a total of ______ patients with angiographic disease.
Q3. Patients with lesions having an FFR of ______ or less were randomized to either PCI or medical therapy alone.
Q4. The primary end point was a composite of all-cause mortality, nonfatal MI, or unplanned hospitalization leading to urgent ______ during a 2-year follow-up.
Q5. Patients whose lesions had FFR values of >0.80 were entered into a ______ and followed.
Q6. The registry patients had a low rate of the primary end point of death (0), MI (______%), or urgent revascularization (2.4%) over the follow-up of 12 months.
Q7. The FAME 1 and 2 trials demonstrate that ______ will not improve outcomes in patients with stenoses with nonischemic FFR.
Q8. The FAME 2 trial involved patients with angiographic disease in one, two, or ______ vessels.
Q9. The findings of the FAME 2 trial reproduced the findings of the pre-DES era ______ trial.
Q10. The primary end point included unplanned hospitalization leading to urgent ______.
A1. optimal medical therapy (OMT)
A2. 1220
A3. 0.80
A4. revascularization
A5. registry
A6. 1.8
A7. revascularization
A8. three
A9. DEFER
A10. revascularization
Q1. The FAME 3 study tested whether FFR-guided PCI would be noninferior to ______ for patients with multivessel CAD.
Q2. In the FAME 3 trial, ______ patients with three-vessel CAD were randomly assigned to undergo CABG or FFR-guided PCI.
Q3. The 1-year incidence of the composite primary endpoint (death, MI, stroke, or repeat revascularization) was ______% for those having PCI compared with CABG ( 6.9%).
Q4. The hazard ratio (HR) for the primary endpoint was ______, with a 95% confidence interval of 1.1-2.2.
Q5. The FAME 3 trial did not meet the noninferiority boundaries for FFR-guided PCI, with pnoninferiority = ______.
Q6. The complexity of the CAD should be considered, as FFR-guided PCI was better than CABG for patients with lower ______ scores.
Q7. The SYNTAX score stands for Synergy Between Percutaneous Coronary Intervention with ______ and Cardiac Surgery.
Q8. Multiple large trials comparing FFR-guided PCI to angiographically guided PCI consistently demonstrate the superiority of an ______ (FFR)-guided approach.
Q9. The FAME 3 study was a multicenter ______ trial.
Q10. The FAME 3 study considered the complexity of CAD in evaluating the effectiveness of FFR-guided PCI versus ______.
A1. CABG
A2. 1500
A3. 10.6
A4. 1.5
A5. 0.35
A6. SYNTAX
A7. TAXUS
A8. ischemia
A9. international
A10. CABG
NHPR and intermediate lesion assessment:
Q1. The two largest randomized noninferiority trials of iFR and FFR were DEFINE-FLAIR and ______.
Q2. Participants in the trials were randomized to iFR- or FFR-guided PCI or ______ therapy.
Q3. The DEFINE-FLAIR study was a multinational trial that enrolled ______ patients from 17 countries.
Q4. IFR-SWEDEHEART enrolled ______ patients at 15 centers in Sweden, Denmark, and Iceland.
Q5. The dichotomous threshold of iFR <______ produced noninferior clinical outcomes when compared to FFR <0.80.
Q6. At 1 year, there were no significant differences between iFR and FFR for the composite primary endpoint of all-cause mortality, MI, or ______.
Q7. Both studies showed reduced chest discomfort and procedure times due to the administration of ______ IV.
Q8. The major methodologic difference between iFR and FFR was the use of ______.
Q9. NHPRs are now in common use as they streamline the workflow for coronary lesion assessment by obviating the need for ______.
Q10. IFR-SWEDEHEART was conducted in Sweden, Denmark, and ______.
A1. IFR-SWEDEHEART
A2. medical
A3. 2492
A4. 2037
A5. 0.89
A6. revascularization
A7. adenosine
A8. adenosine
A9. hyperemia
A10. Iceland
Q1. Angiographic assessment alone is often not reliable to determine the clinical importance of a ______ artery narrowing.
Q2. ______ physiology is a valuable tool for accurate decision making in left main artery narrowing.
Q3. For assessment by FFR, large studies support the use of FFR >______ to safely defer revascularization.
Q4. FFR is used to assess ______ stenosis in the left main artery.
Q5. The use of FFR >0.80 is supported by a number of ______ studies.
A1. left main (LM)
A2. Translesional
A3. 0.80
A4. intermediate
A5. large
Q1. Warisawa et al examined ______ patients with intermediate LM stenosis using iFR.
Q2. Based on an iFR threshold of ______, revascularization was deferred or instituted.
Q3. In the deferred group, MACE occurred in ______ patients (9.2%) at 30 months of follow-up.
Q4. In the revascularized group, MACE occurred in ______ patients (14.6%).
Q5. The P-value comparing MACE between the deferred and revascularized groups was ______.
Q6. The deferral of revascularization of LM stenosis based on iFR appears to be ______, with similar long-term outcomes to those who were revascularized.
A1. 314
A2. 0.89
A3. 15
A4. 22 ( no statistical difference between deferred and revasc. when we use iFR: normal ifr did not die more) .
A5. .26
A6. safe
Q1. What relationship is necessary to understand for LM assessment with downstream CAD?
Q2. Which vessels are reflected in the LM FFR?
Q3. What is required to compute LM FFR?
Q4. What constitutes the myocardial bed for the LM?
Q5. What additional involvement occurs if the RCA is occluded?
Q6. What does an LM narrowing without other disease reflect?
A1. Myocardial bed size and FFR
A2. LAD and CFX
A3. Maximal flow in the bed supplied by the target vessel
A4. Summed territories of LAD and CFX
A5. Collateral from the left coronary system ( even larger territory then only LAD and LCXIn this case, the flow through the LM would involve supply to the inferior LV as well as the anterior LV. )
A6. Physiologic significance of just the LM narrowing
Q1. What does an LM narrowing without other disease reflect?
Q2. How does an LM narrowing plus LAD stenosis affect the LM FFR?
Q3. What happens to the LM bed when there is an LAD stenosis?
Q4. Can the LM FFR alone be accurately measured when there are serial lesions?
Q5. Who demonstrated the impact of downstream disease on FFR measurement of LM?
Q6. How many patients were involved in Fearon et al’s study on LM FFR?
Q7. What conditions were created by Fearon et al to study LM FFR?
Q8. What was used to create intermediate left main coronary artery stenosis in the study?
Q9. How does the FFR across the LM and LAD affect the FFR LM measured in the CFX?
Q10. What is the threshold for the net LM/LAD FFR to alter the FFR LM measured in the CFX?
A1. The physiologic significance of just the LM narrowing.
A2. It could produce a higher LM FFR.
A3. The LM bed is decreased due to the LAD stenosis.
A4. No, the LM FFR alone cannot be accurately measured just when there are serial lesions.
A5. Fearon et al.
A6. 25 patients.
A7. Intermediate left main coronary artery stenosis, and LAD or CFX stenosis with deflated balloon catheters.
A8. Deflated balloon catheters.
A9. It alters the FFR LM measured in the CFX only when the net LM/LAD FFR is <0.60.
A10. <0.60.
Serial lesions and diffuse CAD :
Q1. What limitation does FFR have when assessing lesions in series?
Q2. Why can’t FFR identify an accurate individual lesion value in series?
Q3. What is the interaction between lesions in series called?
Q4. How can the individual FFR of each stenosis be predicted?
Q5. What variables are used in the FFR equation from Pijls et al.?
Q6. Why is the calculation for FFRpredicted impractical for routine diagnostics?
Q7. What method provides more information for determining the hemodynamic significance of multiple lesions?
Q8. Which is easier to use for assessing serial lesions, iFR or FFR?
Q9. What did Kikuta et al. present about iFR pullback measurements?
Q10. How often did iFR pullback change the revascularization plan?
Q11. What was the effect of iFR pullback on the number and length of stents?
Q12. How many vessels were used to predict post-PCI iFR measurements?
Q13. What was the mean difference between predicted and actual post-PCI iFR?
Q14. How does angiographic coregistration of NHPR (e.g., iFR) impact PCI outcomes?
Q15. What does Fig. 12.22 illustrate about iFR coregistration?
A1. FFR cannot identify an accurate individual lesion value.
A2. The first lesion blunts the hyperemia of the second and vice versa.
A3. Crosstalk.
A4. By a different FFR equation from Pijls et al.
A5. Pa, Pm, Pd, and Pw.
A6. It requires the use of Pw during balloon inflation.
A7. Pullback pressure tracings from distal to proximal.
A8. iFR.
A9. The value of iFR pullback measurements before angioplasty.
A10. 31% of the time.
A11. It reduced the average number and length of stents implanted (iFR pullback procedure identified the relative ischemic contribution of each stenosed segment to the iFR value of the entire vessel )
A12. 134 vessels (128 patients).Pre-PCI iFR pullback was used to predict the post-PCI iFR measurement
A13. 0.011 ± 0.004.
A14. It improves the way PCI is performed and outcomes by reducing residual and unsuspected ischemia.
A15. Identifying lesions appropriate for revascularization.
Q1. What can the pressure pullback recording identify in the setting of diffuse disease?
Q2. How is an abnormal FFR in the absence of focal epicardial stenoses often treated?
Q3. How is diffuse disease characterized during a pullback recording?
Q4. What indicates the absence of focal regions during pressure pullback?
A1. The location of focal lesions.
A2. Medically or with surgical revascularization.
A3. By a continuous and gradual pressure recovery.
A4. No abrupt increase in pressure related to a focal region.
Q1. What is impacted to a variable degree remote from the infarct zone?
Q2. What may be altered in the nonculprit artery, especially when near the infarct zone?
Q3. How does an increase in sympathetic tone affect resting coronary flow?
Q4. What effect does microvascular dysfunction have on hyperemic flow in nonculprit arteries?
Q5. What does a false negative FFR imply about stenosis severity in nonculprit vessels?
Q6. How do changes in coronary flow related to acute myocardial injury affect NHPR and FFR?
Q7. Increase coronary flow at rest
Q8. microvascular dysfunction and subsequent decrease in hyperemic flow
A1. The territory remote from the infarct zone.
A2. Resting flow, hyperemic flow, and microvascular function.
A3. It may increase resting coronary flow, reducing iFR.
A4. It potentially decreases hyperemic flow, producing a false negative FFR.
A5. FFR would underestimate stenosis severity in nonculprit vessels.
A6. They affect both NHPR and FFR.
A7. Reduces iFR
A8. False negative FFR.
- If the muscle territory supplied by the artery is very large, Pd beyond the lesion is lower than usual and FFR becomes lower ( abnormal ). A mild lesion may show abnormal FFR in this case
- If the muscle territory supplied by the artery is small, Pd beyond the lesion is higher than usual and FFR is higher than usual ( normal ). A severe lesion may show normal FFR in this case.
- In STEMI, a myocardial scar shrinks down the territory supplied by the infarct related artery and an FFR of 0.5 in acute MI ( acute phase ) becomes 0.84 ( normalizes ) in recuperation phase.
- Since scars can be adjacent to territories supplied by nonculprit artery as well, similar conditions may exist for the noninfarct-related artery assessments.
- Changing FFR values may influence decision making at the time of STEMI.
Q1. The predictive ability of FFR in ACS is limited because the microvascular bed in the infarct zone may not have ______, constant, or minimal resistance.
Q2. The severity of stenosis may evolve as thrombus and ______ abate.
Q3. FFR measurements are not meaningful when normal perfusion, or maximal ______, cannot be achieved.
Q4. !!!!!!!!!! In nonculprit lesions AND target lesion assessment during the RECOVERY phase of MI, FFR retains its value for ______ decision making.
Q5. FFR is not used in the STEMI culprit artery until ______ days after the event, when myocardial function is believed to stabilize.
Q6. For the non-IRA in STEMI/NSTEMI patients, the zone of myocardial injury of the culprit vessel is ______.
Q7. In the FAME study subset, 101 patients undergoing PCI for both STEMI and NSTEMI had ______ non-IRA lesions assessed by FFR.
Q8. The non-IRA FFR was ______ ± 0.13 at baseline and IDENTICAL at follow-up remeasurement.
Q9. The follow-up remeasurement of non-IRA FFR occurred ______ ± 4 days later.
Q10. In ACS, FFR was unchanged over ______ months following the presentation, for non-IRA lesions.
A1. uniform
A2. vasoconstriction
A3. hyperemia
A4. clinical
A5. 4 to 6
A6. unknown
A7. 112
A8. 0.77
A9. 35
A10. 3
Q1. Post-PCI functional assessment predicts long-term patient outcomes and provides insights into the residual ______ potential of the treated vessel.
Q2. Suboptimal functional results should be examined and if possible, ______.
Q3. Agarwal and Uretsky demonstrated that the higher the final ______/NHPR, the fewer the adverse events.
Q4. Mechanisms for suboptimal post-PCI physiology are not always ______.
Q5. The DEFINE-PCI study showed that ______% of angiographically adequate interventions have residual hemodynamic impairment.
Q6. Residual hemodynamic impairment can be due to diffuse CAD, unsuspected new narrowing, edge stent dissection, proximal vessel narrowing, or ______.
Q7. A significant association was observed between ΔFFR and ______ relief.
Q8. The larger the improvement in FFR, the larger the symptomatic relief and the lower the ______ rate.
Q9. Measuring FFR before and after PCI provides clinically useful ______ data.
Q10. The DEFINE-PCI study highlighted residual hemodynamic impairment in interventions that appeared ______ adequate.
A1. ischemic
A2. treated
A3. FFR
A4. evident
A5. 25
A6. vasospasm
A7. symptomatic
A8. event
A9. prognostic
A10. angiographically
Q1. What are the two types of testing involved in invasive coronary circulation assessment?
Q2. What characterizes epicardial disease?
Q3. What methods can assess the microcirculation?
Q4. What techniques are used to measure CFR or IMR?
Q5. How is IC Doppler flow velocity measured?
Q6. During what procedure is IC Doppler flow velocity measured continuously?
A1. Macrovascular or epicardial testing and microvascular testing.
A2. NHPR or FFR.
A3. CFR or IMR.
A4. Doppler flow velocity or thermodilution techniques.
A5. Measured at baseline.
A6. During bolus injection of IC adenosine.
Q1. What is the most common method of measuring CFR due to limited availability of Doppler wire?
Q2. What does the shaft of the angioplasty pressure sensor guidewire act as?
Q3. What is injected to measure temperature arrival times?
Q4. What do temperature arrival times serve as surrogates for?
Q5. When are measurements taken to compute CFR?
Q6. How is thermodilution CFR (CFRthermo) defined?
A1. Coronary thermodilution technique.
A2. A proximal thermistor with temperature-dependent electrical resistance.
A3. Bolus saline.
A4. Coronary flow velocity.
A5. At rest and during adenosine hyperemia ( Hyperemic times are faster than basal times reflecting faster flow ).
A6. CFRthermo = (1/Tmn rest) / (1/Tmn hyper), where Tmn is mean transit time arrival in seconds ( CFR is measured as the ratio of the averaged basal temperature arrival time divided by the average of the hyperemic arrival times) !!!! 2 contradictory formula: i think it should be resting time /hyperemic time so that CFR is > 1 usually around 2,.. )
Q1. For what purposes are simultaneous measurements of CFR and FFR currently obtained?
Q2. What can CFR measurements provide when combined with pressure measurements?
Q3. How does CFR differ from FFR in terms of flow usage?
Q4. What factors cause CFR to vary?
Q5. How is FFR computed in relation to basal flow?
Q6. For what is CFR used alongside IMR?
A1. Both clinical and research studies on coronary and myocardial resistance.
A2. A complete description of the pressure-flow relationship and microcirculation response.
A3. CFR uses basal flow as well as hyperemic flow, while FFR uses only maximal flow.
A4. Changes in basal flow due to heart rate, blood pressure, and contractility ( Changes in the slope of maximal hyperemia will also alter the CFR ).
A5. FFR is computed only at maximal flow and is largely INDEPENDENT of basal flow (FFR is unaffected by changing hemodynamics or the status of the microcirculation ).
A6. Assessment of microvascular disease.
Q1. How is IMR ( index of microcirculatory resistance ) defined?
Q2. What unique feature does IMR have compared to epicardial CAD?
Q3. Why is IMR considered superior to CFR?
Q4. What does IMR predict better than other indices after STEMI?
Q5. What was the outcome for patients with IMR >40 in Fearon et al’s study?
Q6. How might IMR be used in selecting patients for therapy?
A1. Ratio of distal coronary pressure to the inverse of mean transit time during maximal hyperemia [ IMR = Pd/(1/t) ].
A2. It is unique to the microcirculation and independent of epicardial CAD.
A3. It is not affected by resting hemodynamics, making it more reproducible.
A4. Amount of myocardial damage and left ventricular recovery.
A5. Higher rate of death or rehospitalization at 1 year (17% vs 7%).
A6. Selecting patients who might benefit from regional delivery of regenerative cell therapies.
Q1. What did Fearon et al demonstrate about IMR after primary angioplasty?
Q2. Compared to what other measures was the prognostic value of IMR demonstrated?
Q3. What IMR value was associated with a higher rate of death or rehospitalization at 1 year?
Q4. What was the percentage of death or rehospitalization at 1 year for patients with IMR >40?
Q5. During follow-up, what was IMR >40 an independent predictor of?
Q6. How might IMR be used in patient selection?
A1. The prognostic value of IMR compared with other measures, after primary angioplasty.
A2. CFR, thrombolysis in MI perfusion grade, and clinical variables.
A3. IMR >40.
A4. 17%.
A5. Death alone.
A6. Selecting patients who might benefit from regional delivery of regenerative cell therapies.
Formula :
Doppler CFR = DPV hyperemia/DPV basal
TD IMR = Hyper Pd /Tmn
Practical approach based on contrast FFR:
TRUE OR FALSE ( see table last slide ) :
Q1. In stable ischemic heart disease, NHPR equals FFR in terms of better modality , and if borderline, check cFFR, then FFR, and use pullback pressure recording.
Q2. In acute coronary syndrome nonculprit lesions, use FFR or NHPR. There is extensive data on NHPR, and FFR is unaffected by proximity to the infarct zone.
Q3. In diffuse disease, NHPR is not as helpful as FFR, with fewer iFR+/FFR− lesions, and pullback pressure recording is not recommended.
Q4. For focal residual lesions, FFR is as helpful as NHPR and is associated with more iFR−/FFR+ results.
Q5. For focal RCA lesions, FFR is as helpful as NHPR, Consider using RFR better than IFR. iFR is more impacted by systolic flow in the RCA.
Q6. In TAVR patients, NHPR is greater than FFR due to less flow change with NHPR
Q1. True. In stable ischemic heart disease, NHPR is generally equal to FFR. When results are borderline, it is recommended to check contrast FFR (cFFR) and then FFR, using pullback pressure recording to better assess the lesion.
Q2. False. There is limited data on NHPR in acute coronary syndrome (ACS) nonculprit lesions, and FFR can be affected by the proximity to the infarct zone due to changes in microvascular function.
Q3. False. In diffuse disease, NHPR is often more helpful than FFR, with more iFR+/FFR− discordant lesions. Pullback pressure recording is recommended to better understand lesion significance in diffuse disease.
Q4. True. For focal residual lesions, FFR generally is as helpful as NHPR, but these lesions are associated with more iFR−/FFR+ discordant results.
Q5. True. For focal right coronary artery (RCA) lesions, RFR is typically greater than iFR and is less impacted by systolic flow variations in the RCA.
Q6. True. In patients undergoing transcatheter aortic valve replacement (TAVR), NHPR tends to be better than FFR due to less change in coronary flow with NHPR measurements.
Important case scenarios:
