Various coronary physiological measurements can be made in the cardiac catheterization laboratory using sensor-tipped guidewires; they include the measurement of poststenotic absolute coronary flow reserve, the relative coronary flow reserve, and the pressure-derived fractional flow reserve of the myocardium. Ambiguity regarding abnormal microcirculation has been reduced or eliminated with measurements of relative coronary flow reserve and fractional flow reserve. The role of microvascular flow impairment can be separately determined with coronary flow velocity reserve measurements. In addition to lesion assessment before and after intervention, emerging applications of coronary physiology include the determination of physiological responses to new pharmacological agents, such as glycoprotein IIb/IIIa blockers, in patients with acute myocardial infarction. Measurements of coronary physiology in the catheterization laboratory provide objective data that complement angiography for clinical decision-making
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%
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
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
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
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