Coronary physiology

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Information about Coronary physiology
Health & Medicine

Published on March 2, 2014

Author: ramachandrabarik



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

Coronary Hemodynamics

Sketch coronary

Coronary feeds in diastole

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

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

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

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

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

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)

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

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

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

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

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

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

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

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

TIMI FLOW GRADE • Raw and qualitative

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.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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