The document discusses coronary hemodynamics, emphasizing the measurement of coronary function through various methods such as FFR, CFR, and IVUS. It highlights the complexities of coronary resistance, the role of auto-regulation in maintaining myocardial perfusion, and the significant impact of stenosis on myocardial blood flow. Additionally, it explores the relationship between hemodynamic assessments and interventions in the context of coronary artery disease.

1. Coronary Hemodynamics

2. Sketch coronary

3. Coronary feeds in diastole

4. Measurement of coronary function
Non invasive measurement
Invasive measure
MR
CT
PET
CAG
IVUS
OCT
FFR
CFR
FFR IS GOLD STANDARD

5. The bottle neck of CAG
Poor correlation of physiologic ischemia
The reason : minimal luminal dimensions and area, stenosis length,
exit and entrance angles, reference vessel diameter, and diffuse
coronary narrowing

6. intravascular ultrasound (IVUS)
Some improvement upon the decision of removing stenosis but not
satisfactory

7. Auto regulation limit
Maintain myocardial perfusion in systolic BP=60-180 mmHg

8. Auto regulation failure alarm
 Angina or equivalent
 Myocardial hibernation
 Myocardial stunning
 Myocardial infarction

9. Unique metabolism in cardiac muscle
• Myocardial blood flow α the balance of myocardial oxygen (MVO2)
demand and supply
• Heart assimilates from instantaneous oxidation of FFA, glucose, lactate,
pyruvate, and amino acids
• ATP is produced and consumed and no storage
• No oxygen debt as seen in skeletal muscle
• Any compromise in substrate=blood flow switch on alarm of energy
conservation of energy for the maintenance of cellular function
• Mechanical work is impaired =RWMA
• Myocardial sleeps in “hibernation” or death(MI)

10. ATP sharing areas
• Basal cellular metabolism: 20%
• myocardial force generation: 80%

11. MVO2[/min O2 in cardiac muscle] α CBF
Sales
• cardiac myocyte shortening
• contractility
• Relaxation
• myocardial wall tension
• heart rate
1st Qtr
2nd Qtr
3rd Qtr
4th Qtr

12. Coronary collaterals imply
• Attenuate the degree of ischemia
• Degree of collaterals is variable[number,size and location]
• Chronic severe stenosis
• Less long term mortality

13. Coronary resistance
• ΣEpicardial+precapillary arteriole+ myocardial capillary resistances
• Coronary blood flow is inversely related to coronary resistance
• Epicardial vessels are direct conduits and no resistance
• R2 is seat of coronary resistance

14. Resistance in series and Ohm’s law
R1:Epicardial vessel and resistance is zero in health
R2:Precapillary arteriole =Auto regulation site=the seat of
Coronary resistance in health
R3:Intra myocardial capillary resistance is affected by systole
And diastole
Resistance determinants
1. size of individual vessels (length and diameter)
2. Organization of the vascular network (series and parallel)
3. Physical characteristics of the blood (viscosity, laminar flow
versus turbulent flow)
4. Extravascular mechanical forces acting upon the vasculature

15. The seat of coronary resistance
• Precapillary arterioles[R1] connect the epicardial arteries to the
myocardial capillaries and are the primary determinants of coronary
resistance and flow

16. Microvasculature
• The myocardial capillary bed after Precapillary arterioles forms an
extensive network connecting each myocyte, often referred to as the
microvasculature

17. Coronary flow reserve (CFR)
• Ratio of maximum hyperaemic flow to resting flow
• X2-5 is normal
• Epicardial stenosis > 60% (diameter) limits maximal CBF in rest &work
• Stenosis >80% impairs resting blood flow

19. TIMI FLOW GRADE
• Raw and qualitative

20. Angiographic Flow Estimation
Grade
TFG
MBG/TPG
0
No antegrade flow beyond the
lesion.
Minimal or no or opacification (“blush”) of the
myocardium in distribution of culprit artery
1
Contrast passes beyond lesion but
fails to opacify entire coronary
bed.
Myocardial blush in distribution of culprit lesion
that fails to clear from microvasculature (contrast
staining present on next injection (~30 seconds).
2
Contrast passes beyond lesion
opacifies distal coronary bed but
rate of entry and/or rate of
clearance slower than comparable
areas not perfused by the culprit
vessel.
There is myocardial blush in the distribution of
the culprit lesion that is strongly persistent at the
end of the washout phase (after 3 cardiac cycles
of the washout phase and either does not or only
minimally diminishes in intensity during
washout).
3
Antegrade flow into the bed distal
to lesion occurs as promptly as
into the bed proximal to the
obstruction and clearance of
contrast material from the
involved bed is as rapid as from an
uninvolved vascular bed.
Myocardial blush in distribution of culprit lesion
clears normally and is either gone or only
mildly/moderately persistent at end of washout
phase (after 3 cardiac cycles of the washout phase
and noticeably diminishes in intensity during the
washout phase) similar to that in an uninvolved
artery. Blush that is of only mild intensity
throughout the washout phase but fades
minimally is also classified as grade 3.

21. TIMI Frame Count: Epicardial coronary
 Number of cine frames required for radiographic contrast to reach a
standardized distal coronary landmark in the culprit vessel in a single
scene
 CTFC is normalized to the TFC to the LAD
 Better than TIMI flow grades
 Normal CTFC is less than 20
 CTFC of up to 40 is seen in TIMI 3 flow implies vessel is diseased
 High CTFC despite an open epicardial artery in the setting of AMI is
thought to represent microvascular obstruction or dysfunction

22. TIMI myocardial perfusion grade (TMPG)
 TMPG is a semi quantitative
 Zwolle Myocardial Infarction Study Group in the Netherlands
 Blood flow in capillary
 Best angiographic projection to visualizes subtends myocardium of
interest
 Images are obtained with adequate injection allowing reflux of contrast
into the aortic root
 Injection is stopped after opacification of the coronary sinus
 Cineangiography is continued until three cardiac cycles after myocardial
blush begins to
 Poor TMPG is poor outcome despite TIMI III epicardial flow

23. Andreas Gruentzig in 1978
First to directly measure Pd
Degree stenosis
 First coronary balloon catheters with side holes
This old gold tech was the forerunner of FFR

24. Sensing using a Intra coronary wire
 Senses pressure/ Doppler/temperature
 0.014” sensory angioplasty guide wire
 Intravenous heparin (40-60 IU/Kg)
 Intracoronary NTG
 Measure pressure and flow
 Quantify stenosis, assess the microvascular circulation, and gauge the
physiologic response to mechanical or pharmacologic interventions

25. FFR
Couples hemodynamic and anatomy
Direct Coronary Pressure Measurement
Detects pressure loss distal to obstruction
Ratio of the maximal flow to the myocardium in the presence of a
coronary stenosis normalized to the theoretical maximal flow in the
same artery without a Stenosis
 Normal FFR is 1.0
<0.75 is intervention
0.75-0.80 is grey zone

26. Types of FFR
FFR myocardium
FFR coronary
FFR collateral:CFI
RELATION
(Pd –Pv) / (Pa – Pv)
(Pd – Pw) / (Pa – Pw)
(Pocc – CVP)/Pa – CVP)
FFRcor + FFRcollateral
Pd, Pa, Pv, Pw and Pocc are the mean distal, aortic, venous,wedge pressures and coronary pressure distal to occlusion

27. Coronary Flow Reserve
 Known as coronary vasodilatory reserve (CVR)
 Ratio of maximal to basal coronary flow in same artery
 No longer routinely used because of several limitations
 Doppler or thermodilution methods
 CFR=epicardial+ microvascular resistance
 Normal CFR > 3.0
 CFR of <2.0 =ischemia

28. FFR vs. CFR
FFR
CFR
 Wide clinical application
 Measure for microvascular resistance
 Limitations
 Limitations: affected by in BP,HR and other factor
1.Assumes microvascular resistance is nil but it is
affecting microvascular function
never so
2.Assumes pressure α flow but really it is relation
is curvilinear

29. Microvascular Resistance Measurements
• Newer concept
• Called index of microvascular resistance (IMR)
• Method: combination pressure and thermo dilution
• Principle: Ohm’s law like FFR
• Epicardial vessel is almost normal/opened spontaneously or by PCI
• Reproducible
• Less hemodynamic dependence

30. Applied
• Intermediated stenois
• Bifurcation
• LMCA
• Multivessel disease
• Serial stenosis
• Microvascular disease
• Heart Failure

31. Intermediated stenosis
• Defer PCI if trans-stenotic gradient (<25 mmHg) or Doppler-derived
CFR >1.7 after IV adenosine
• DEFER trial: Defer PCI if FFR>0.75
• COURAGE(using SPECT) and FAME-2(FFR) agree upon deferring PCI if
FFR>0.8

32. LMCA:R1 disease
A FFR cut off >0.8 do equally well on medical management or CABG

33. Multivessel disease and FFR
 Reduces number of stents[FAME ]
 No survival benefit revascularising FFR<0.75 of single stenosis
 MACE are more with intervention
 Revascularisation approach PCI vs. CABG is modified
 Functional SYNTAX score improves the management style

34. Bifurcation Stenting
 Provisional stenting ruled in/out
 Intervening on the “jailed” side branch only if FFR < 0.75: kissing
balloon/stenting

35. Serial stenosis or diffuse disease
 2 lesions in series impair maximal flow
 Pd/Pa of each one interdependence
 Pullback and first Rx largest step-up if both have FFR <0.8
 Equal step up,Rx distal first
 Check FFR of residual before conclusion

36. Heart failure:R3 is affected
 Extent of functional myocardium and related vessel
 Heterogeneous microvascular bed
 Few capillary beds to dilate
 FFR=1 regardless of the severity of the lesion
 If artery supplies a large Δ of myocardium outside of the normal
distribution via collateral circulation, FFR may reach ischemic
thresholds
 ↑ LVEDP may lead to underestimation of true FFR