Abstract
An essential prerequisite for the calculation of FFR from aortic and coronary pressure is to obtain the measurements under conditions of maximum hyperemia. Only in this situation it can be assumed that the resistance of the vascular bed is minimal and therefore equal to the resistance in the same vascular bed but not depending on an epicardial stenosis. This condition has been demonstrated in animals (chapter 7) and in humans (chapter 8). Only when the resistance of the vascular bed depending on an epicardial stenosis equals the resistance of the same vascular bed but without stenosis, these resistances can be cancelled in the calculation of FFR2. It has been shown in animals and in humans, in the physiological range of aortic pressure, that the relation between myocardial flow and driving pressure is linear during maximum microvascular vasodilation3–4 This implies that, during maximum hyperemia, the ratio of two myocardial flows (which corresponds to the definition of FFR) equals the ratio of their respective driving pressures. The key point with respect to FFR is not the slope but the linearity of the pressure-flow relation under conditions of maximum vasodilation. When maximum hyperemia is not achieved the relation between hyperemic flow and driving pressure is curvilinear, and thus, the ratio of these (‘non-hyperemic’) flows does not equal the ratio of their respective driving pressures.
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References
De Bruyne B, Baudhuin T, Melin JA, Pijls NHJ, SYS SU, Bol A, Paulus WJ, Heyndrickx GR, Wijns W. Coronary flow reserve calculated from pressure measurements in man. Validation with positron emission tomography. Circulation 1994; 89: 1013–1022.
Pijls NHJ, Van Son JAM, Kirkeeide RL, De Bruyne B, Gould KL. Experimental basis of determining maximum coronary, myocardial, and collateral blood flow by pressure measurements for assessing function stenosis severity before and after percutaneous transluminal coronary angioplasty. Circulation 1993; 87: 1354–67.
Hoffman JIE, Spaan JAE. Pressure-flow relations in coronary circulation. Physiol Rev 1990; 70: 331–390.
Di Mario C, Krams R, Gil R, Serruys PW. Slope of the instantaneous hyperemic diastolic coronary flow velocity-pressure relation. A new index for assessment of the physiological significance of coronary stenosis in humans. Circulation 1994; 90: 1215–1224.
Lee KS, Marwick TH, Cook SA, Go RT, Fix JS, James KB, Sapp SK, Maclntyre WJ, Thomas JD. Prognosis of patients with left ventricular dysfunction, with and without viable myocardium after acute myocardial infarction. Circulation 1994; 90: 2687–2694.
Califf RM, Topol EJ, Gersh BJ. From myocardial salvage to patient salvage in acute myocardial infarction: the role of reperfusion therapy. J Am Coll Cardiol 1989; 14: 1382–1388.
Uren NG, Crake T, Lefroy DC, De Silva R, Davies GJ, Maseri A. Reduced coronary vasodilator function in infarcted and normal myocardium after myocardial infarction. N Engl J Med 1994; 331–222–227.
Maseri A, Crea F, Kaski JC, Crake T. Mechanisms of angina pectoris in syndrome X. JAm Coll Cardiol 1991; 17: 499–506.
Claeys MJ, Vrints CJ, Bosmans J, Krug B, Blockx PP, Snoeck JP. Coronary flow reserve during coronary angioplasty in patients with a recent myocardial infarction: relation to stenosis and myocardial viability. J Am Coll Cardiol 1996; 28: 1712–1719.
Pitt B. Evaluation of the postinfarct patient. Circulation 1995; 91: 1855–1860.
Kern MJ, Deligonul U, Tatineni S, Serota H, Aguirre FV, Hilton TC: Intravenous adenosine continous infusion and low dose bolus administration for determination of coronary vasodilatory reserve in patients with and without coronary artery disease. JAm Coll Cardiol 1991; 18: 718–729.
Uren NG, Camici PG, Melin JA, Bol A, De Bruyne B, Radvan J, Olivotto I, Rosen SD, Impallomeni M, Wijns W. Effect of aging on myocardial perfusion reserve. JNucl Med 1995; 36: 2032–2036.
Harris CN, Aronow WS, Parker DP, Kaplan MA. Treadmill stress in left ventricular hypertrophy. Chest 1973; 63: 353–359.
Marcus ML, Mueller TM, Gascho JA, Kerber RE. Effects of cardiac hypertrophy secondary to hypertension on the coronary circulation. Am J Cardiol 1979;44:1023–1031.
Hoffmann JIB: Maximal coronary flow and the concept of coronary vascular reserve. Circulation 1984; 70: 153–159.
De Bruyne B, Pijls NHJ, Heyndrickx GR, Hodeige D, Kirkeeide R, Gould KL. Pressure-derived fractional flow reserve to assess serial epicardial stenoses: theoretical basis and animal validation. Circulation 2000 (in press).
Vanoverschelde JL, Wijns W, Depre C, Essamri B, Heyndrickx GR, Borgers M, Bol A, Melin JA. Mechanisms of chronic regional post-ischemic dysfunction in humans. New insights from the study of non-infarcted collateral-dependent myocardium. Circulation 1993; 87: 1513–1523.
Gould KL. Coronary atherosclerosis and reversing atherosclerosis. 2“d Edition, Arnold Publishers, 1999; distributed by Oxford University Press.
Hanekamp C, Koolen JJ, Pijls NHJ, Bonnier JJRM, Michels HR. Comparison of quantitative coronary angiography, intravascular ultrasound, and pressure-derived fractional flow reserve to assess optimal stent deployment. Circulation 1999; 99: 1015–1021.
De Bruyne B, Stockbroeckx J, Demoor D, Heyndrickx GR, Kern MJ. Role of side holes in guide catheters: observations on coronary pressure and flow. Cath Cardiov Diagn 1994; 33: 145–152.
Gage JE, Hess OM, Murakami T, Ritter M, Grimm J, Krayenbuehl HP. Vasoconstriction of stenotic coronary arteries during dynamic exercise in patients with classic angina pectoris: reversibility by nitroglycerin. Circulation 1986; 73: 865–876.
Gordon JB, Ganz Peter, Nabel EG, Fish RD, Zebede J, Mudge GH, Alexander GW, Selwyn AP. Atherosclerosis influences the vasomotor response of epicardial coronary arteries to exercise. JClin Invest 1989; 83: 1946–1952.
Ludmer PL, Selwyn AP, Shook THL, Wayne RR, Mudge GH, Alexander RW, Ganz P. Paradoxical vasoconstriction induced by acetylcholine in atherosclerotic coronary arteries. NEngl JMed 1986; 315: 1046–1051.
Nabel EG, Ganz P, Gordon JB, Alexander RW, Selwyn AP. Dilation of normal and constriction of atherosclerotic coronary arteries caused by the cold pressor test. Circulation 1988; 77: 43–52.
Bartunek J, Wijns W, Heyndrickx GR, De Bruyne B. Effects of dobutamine on coronary stenosis physiology and morphology. Comparison with intracoronary adenosine. Circulation 1999; 100: 243–249.
Wijffels E, Wijns W, Heyndrickx GR, De Bruyne B. Does high dose dobutamine induce a paradoxical coronary vasoconstriction of atherosclerotic arteries ? Eur Heart J 1998; 19: 334 (abstract).
Tamimi HE, Mansour M, Wargovich TJ, Hill JA, Kerensky RA, Conti R, Pepine CJ. Constrictor and dilator responses to intracoronary acetylcholine in adjacent segments of the same coronary artery in patients with coronary artery disease. Circulation 1994; 89: 45–51.
Penny WF, Rodman H, Long J, Bhargava V, Carrigan K, Ibriham A, Shabetal R, Ross J, Peterson KL. Heterogeneity of vasomotor response to acetylcholine along the human coronary artery. JAm Coll Cardiol 1995; 25: 1046–1055.
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Pijls, N.H.J., De Bruyne, B. (2000). FFR in Some Specific Conditions. In: Coronary Pressure. Developments in Cardiovascular Medicine, vol 195. Springer, Dordrecht. https://doi.org/10.1007/978-94-015-9564-3_13
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DOI: https://doi.org/10.1007/978-94-015-9564-3_13
Publisher Name: Springer, Dordrecht
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