(Circulation. 1996;94:1842-1849.)
© 1996 American Heart Association, Inc.
Articles |
Simultaneous Coronary Pressure and Flow Velocity Measurements in Humans
Feasibility, Reproducibility, and Hemodynamic Dependence of Coronary Flow Velocity Reserve, Hyperemic Flow Versus Pressure Slope Index, and Fractional Flow Reserve
the Cardiovascular Center, Aalst, Belgium, and the Department of Cardiology, Catharina Hospital, Eindhoven, The Netherlands.
Correspondence to Bernard de Bruyne, MD, PhD, Cardiovascular Center, Aalst, Moorselbaan, 164, B-9300 AALST, Belgium.
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Abstract |
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Background To assess coronary lesion severity in the catheterization laboratory, several guide wire–based methods have been proposed. The purpose of the present study was to compare the feasibility and the reproducibility of coronary flow velocity reserve (CFVR), instantaneous hyperemic diastolic velocity-pressure slope index (IHDVPS), and pressure-derived myocardial fractional flow reserve (FFRmyo).
Methods and Results From distal coronary pressure and flow velocity signals (0.014-in guide wires), CFVR, IHDVPS, and FFRmyo were computed in 15 stenoses (13 patients) under the four following pairs of conditions: (1) twice under baseline conditions; (2) during atrial pacing at 80 and 110 bpm; (3) before and during intravenous infusion of nitroprusside; and (4) before and during intravenous infusion of dobutamine. A total of 104 measurements were obtained. Both CFVR and FFRmyo could be calculated in all cases. IHDVPS could be calculated in only 79% of cases. The mean value of CFVR did not change between the two baseline measurements and during infusion of nitroprusside but decreased from 1.85±0.41 to 1.66±0.45 (P<.05) during atrial pacing and from 1.90±0.50 to 1.41±0.28 (P<.05) during dobutamine infusion. The mean values of IHDVPS and FFRmyo remained similar, whichever the changes in hemodynamic conditions. The coefficient of variation between two consecutive measurements was significantly lower for FFRmyo (4.2%) than for CFVR (17.7%) and for IHDVPS (24.7%).
Conclusions CFVR is easy to measure but sensitive to hemodynamic changes. IHDVPS can be measured only in <80% of cases and is highly variable even without changes in hemodynamic conditions. FFRmyo is easy to measure and almost independent of hemodynamic changes.
Key Words: stenosis • hemodynamics • blood flow • pressure
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Introduction |
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To gain information on the physiological significance of epicardial coronary stenoses, in the catheterization laboratory several approaches have been proposed as a complement to coronary angiography. These methods include coronary flow reserve,1 2 3 hyperemic flow versus pressure slope index,4 5 6 7 and pressure-derived fractional flow reserve.8 9 The recent development of Doppler-tipped guide wires10 and of pressure monitoring guide wires11 12 has facilitated the measurements of coronary flow velocity and distal coronary pressure in humans, thus reviving the interest in the invasive physiological assessment of coronary artery disease.
However, during catheterization, and even more during interventional procedures, fluctuations in heart rate, blood pressure, and contractile state are likely to occur. Therefore, to avoid any ambiguity in the interpretation of the results, the evaluation of the coronary circulation should rely on methodologies that are independent from these hemodynamic changes. Moreover, in the era of interventional cardiology, a method will become accepted in everyday clinical practice only if the data can be easily obtained, without excessive delay of the procedure.
Accordingly, the goal of the present study was first, to compare the feasibility of the measurements of coronary flow velocity reserve (CFVR), the slope of the instantaneous hyperemic diastolic coronary flow velocity–aortic pressure relation (IHDVPS), and myocardial fractional flow reserve (FFRmyo) in humans, and second, to evaluate the influence of changes in heart rate, blood pressure, and contractility on the measurements of these indices.
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Methods |
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Patients
The study population consisted of 13 patients scheduled for percutaneous transluminal coronary angioplasty of an isolated lesion in a major epicardial coronary artery (4 left anterior descending coronary arteries, 9 dominant right coronary arteries). The global left ventricular systolic function was normal at rest as assessed by biplane contrast angiography, and wall motion in the territory supplied by the vessel under study was normal. None of the patients had the following conditions that are known to affect resistive vessel function or baseline myocardial flow: (1) diabetes mellitus, (2) left ventricular hypertrophy or valvular heart disease as assessed by transthoracic echocardiography, (3) anemia, or (4) myocardial infarction. Informed consent was obtained from each patient.
Cardiac Catheterization
Patients were brought to the catheterization laboratory in the fasting state. Cardiac medications were not discontinued. A 7.5F introducer sheath was inserted into the right femoral artery. A 7F guiding catheter without side holes was advanced up to the coronary ostium. Through a 6F venous introducer sheath, a 6F bipolar pacemaker lead was advanced into the upper right atrium. After intravenous administration of 10 000 IU of heparin, 3 mg of isosorbide dinitrate was given through the guiding catheter. This was repeated every 30 minutes during the study protocol to ensure maximal epicardial vasodilatation. At least 2 minutes after nitrate administration, contrast angiograms of the vessel under study were taken in at least four different projections.
A 0.014-in Doppler guide wire (Cardiometrics Inc) was advanced distally to the stenosis in a smooth coronary segment and the wire was manipulated until an optimal and stable Doppler velocity signal was obtained. The characteristics of this wire and the flow velocity measurements obtained with this system have been validated in vitro and in an animal model through the use of simultaneous electromagnetic flow measurements for comparison.10 To measure distal coronary pressure, a 0.014-in, fluid-filled pressure-monitoring guide wire (Schneider Europe, n=11) or a 2.1F Venture (n=4) catheter was advanced distally to the narrowing. The side arm of the introducer sheath, the guiding catheter, and the fluid-filled pressure monitoring device were connected to three separate pressure transducers (Spectranetics, Statham P23) zeroed at mid chest level.
Femoral pressure (side arm of the sheath), aortic pressure (guiding catheter), distal coronary pressure (pressure monitoring device), and instantaneous peak flow velocity signal (Doppler guide wire) were recorded on a digital tape. All measurements were taken under resting conditions and during maximal vasodilatation induced by an intracoronary bolus of adenosine (12 µg in the right coronary artery and 18 µg in the left coronary artery).13 Care was taken not to induce an impairment of flow during maximal hyperemia by the presence of the guiding catheter in the first millimeters of the coronary artery.14 This can be detected by the occurrence of a pressure difference between the femoral artery and the guiding catheter.
To investigate the effects of hemodynamic changes on the various indices, both resting and hyperemic pressure and flow measurements were taken in the four following pairs of conditions: (1) twice under baseline conditions at 3-minute intervals without any intervention; (2) during atrial pacing at 80 and 110 bpm; (3) under basal blood pressure and during intravenous infusion of nitroprusside (0.5 to 2 µg/kg per minute) titrated to reach a decrease in systolic blood pressure of 
20 mm Hg; and (4) in basal contractile state and after a 5-minute intravenous infusion of 10 µg/kg per minute of dobutamine. After each intervention, heart rate, mean aortic pressure, coronary blood flow velocity, and distal coronary pressure were allowed to return to their baseline values after the previous intervention. Thus, to complete the protocol, both baseline and hyperemic pressure and flow recordings should have been performed 8 times in every patient. In 2 patients, the measurements were performed both before and after angioplasty so that actually 15 stenoses were investigated. However, in 5 patients the spontaneous blood pressure was too low to allow nitroprusside infusion, in 2 patients no pacemaker lead was advanced in the right atrium, and 1 patient did not receive dobutamine. Hence, two consecutive baseline pressure and flow recordings were done in 15 stenoses; the effect of tachycardia was investigated in 13 stenoses; the effect of nitroprusside was studied in 10 stenoses; and the effect of dobutamine was studied in 14 stenoses.
When pressure and/or flow velocity tracings were considered nonoptimal, resting and hyperemic assessments were repeated after verifying proper functioning of the system and repositioning of the guide wires if needed. If, after three attempts, no satisfactory tracing could be obtained, the measurements were considered nonobtainable.
Data Analysis
Figs 1 and 2
illustrate how the various indices were derived from pressure and flow velocity recordings.
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CFVR was calculated as the ratio of hyperemic to baseline mean coronary flow velocity.
IHDVPS was calculated from the simultaneously recorded aortic pressure and coronary flow velocity signals at peak hyperemia.4 7 Therefore, the aortic pressure tracing and the instantaneous peak coronary blood flow velocity were digitized with a sample frequency of 125 Hz. The instantaneous relation between coronary flow velocity and coronary pressure during one cardiac cycle was displayed as a velocity-pressure loop by a specially designed software. For each beat, the slope of the diastolic portion of the loop was calculated and expressed in cm·s-1·mm Hg-1. The diastolic interval of the velocity-pressure loop to be analyzed was selected manually from the maximal diastolic velocity to the onset of rapid decline of coronary flow velocity due to myocardial contraction. The slope values were accepted only when the correlation coefficient of the linear regression between velocity and pressure during the selected diastolic interval was >.97, thus eliminating major pressure or velocity tracing artifacts. The values reported in this study are the mean of three consecutive cardiac cycles selected during peak hyperemia.
FFRmyo was calculated as the ratio of mean distal coronary pressure and mean aortic pressure during maximal hyperemia.8 9
Quantitative Coronary Angiography
All lesions under study were analyzed during the procedure with a previously validated system operating on digital images.15 Briefly, the guiding catheter was used as a scaling device. The operator indicated the segment to be analyzed. Thereafter, a center line was generated. The edges of the vessel were automatically detected by the computer from a weighed first- and second-derivative function applied to the brightness profile of each scan line perpendicular to the center line of the vessel. Percent luminal diameter stenosis was calculated with the use of an automatic interpolated technique to measure the reference diameter.
Statistics
The results are given as mean±1 SD. Statistical analysis of hemodynamic data was performed with a two-factor ANOVA with repeated measurements on both factors. The reproducibility of the indexes of coronary stenosis severity (CFVR, IHDVPS, and FFRmyo) was assessed by the coefficient of variation (mean and 95% CI) calculated as the square root of the within-subject variance component with the use of a one-way random-effect model ANOVA based on the logarithm-transformed data values, of which the distribution did not significantly deviate from normality (Kolmogorov-Smirnov statistics with Lilliefors' significance level, P>.2). This procedure allowed estimation of the coefficient of variation in the original scale for each of the indices and to determine a 95% CI based on a 
2 distribution. Differences between the coefficients of variation were assessed by the variance ratio test (F test). Results were considered statistically nonsignificant when P>.05.
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Results |
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The angiographic degree of stenosis severity ranged from 21% to 66% diameter stenosis and from 0.91 to 3.01 mm minimal lumen diameter.
Feasibility of Measurements
A total of 104 measurements were performed. In all 104 (100%) cases, CFVR could be calculated: in 79 cases (76%) at the first attempt, in 16 cases at the second attempt (15%), and in 9 cases (10%) at the third attempt. IHDVPS could be measured in 82 of 104 cases (79%). The 26 failures were related to artifacts on the flow velocity tracing precluding the calculation of a satisfactory correlation coefficient of the diastolic velocity-pressure relation. FFRmyo could be obtained in all 104 cases (100%): in 100 cases (96%) at the first attempt and in 4 cases (4%) at the second attempt.
Intrinsic Variability of Various Indices
To study the intrinsic variability of the indices of flow reserve, two consecutive flow and pressure recordings were performed at 3-minute intervals without any intervention in 15 stenoses. The hemodynamic variables measured at rest and during hyperemia as well as the calculated indices are given in Table 1. During both the first and the second baseline measurements, mean blood pressure decreased mildly during hyperemia compared with rest. Heart rate did not vary significantly. Resting average peak velocity, mean distal coronary pressure, and translesional pressure gradient were similar during the two baseline recordings. Hyperemia induced a similar increase in average peak velocity and translesional pressure gradient and a similar decrease in mean distal coronary pressure. The mean values of CFVR, IHDVPS, and FFRmyo did not change significantly between the two baseline measurements.
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The correlation between the first and the second baseline measurements are shown in Fig 3. The coefficient of variation observed between the first and the second measurements under baseline conditions was significantly larger for CFVR (10.5% [CI, 7.7% to 16.2%]) than for FFRmyo (4.8% [CI, 3.5% to 7.4%]). The variation coefficient observed between the first and the second measurements under baseline conditions of IHDVPS (27.7% [CI, 19.9% to 45.8%]) was significantly larger than for both CFVR and FFRmyo (Fig 4).
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Effects of Rapid Atrial Pacing
To investigate the effects of heart rate on CFVR, IHDVPS, and FFRmyo, these three indices were obtained in 13 stenoses, first during atrial pacing at 80 bpm and thereafter at 110 bpm. The hemodynamic changes induced by pacing tachycardia and the calculated indices are summarized in Table 2. During atrial pacing at 80 and 110 bpm, blood pressure was significantly lower during hyperemia than at rest. Resting average peak velocity, mean distal coronary pressure, and translesional pressure gradient were similar at 80 and 110 bpm. During hyperemia, average peak velocity and translesional pressure gradient increased and distal coronary pressure decreased to a similar level. CFVR decreased slightly but significantly from 1.85±0.45 at 80 bpm to 1.66±0.45 at 110 bpm (P<.05). The mean values of IHDVPS and FFRmyo at different heart rates were similar. The correlation between the various measurements performed at a heart rate of 80 versus 110 bpm is shown in Fig 5. The coefficient of variation performed at different heart rates was significantly lower for FFRmyo (4.0% [CI, 2.9% to 6.4%]) than for CFVR (14.9% [CI, 10.8% to 24.0%]) and IHDVPS (29.2% [CI, 20.4% to 51.3%]; both P<.05; Fig 4
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Effects of Nitroprusside
To study the effects of arterial pressure on CFVR, IHDVPS, and FFRmyo, these indices were measured in 10 stenoses at the spontaneous arterial pressure and after intravenous infusion of nitroprusside to obtain a decrease in systolic blood pressure of 20 mm Hg. The hemodynamic changes induced by nitroprusside infusion and the calculated indices are summarized in Table 3. Systolic blood pressure decreased from 136±12 mm Hg before nitroprusside infusion to 100±9 mm Hg during nitroprusside infusion (P<.01). No additional effect on blood pressure and heart rate was observed during administration of adenosine. A reflex tachycardia accompanied the nitroprusside-induced decrease in blood pressure. Nitroprusside infusion induced a mild decrease in resting flow velocity and a proportional decrease in hyperemic velocities. As a consequence, CFVR remained unchanged before and during nitroprusside. Resting and hyperemic distal coronary pressures were significantly lower during than before nitroprusside infusion. Translesional pressure gradients were similar during and before nitroprusside. The mean values of IHDVPS and FFRmyo remained unaltered before and during nitroprusside. The correlation between the values of CFVR, IHDVPS, and FFRmyo obtained before and during nitroprusside infusion is shown in Fig 6. The coefficient of variation observed between the measurements performed before and during infusion of nitroprusside was significantly lower for FFRmyo (3.3% [CI, 2.3% to 5.9%]) than for CFVR (13.6% [CI, 9.5% to 23.9%]) and IHDVPS (21.7% [CI, 14.9% to 39.6%]; both P<.05; Fig 4).
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Effects of Dobutamine
To study the effects of left ventricular contractility on CFVR, IHDVPS, and FFRmyo, simultaneous pressure and flow velocity tracings were obtained in 14 stenoses before and after 5-minute intravenous infusion of dobutamine. The hemodynamic changes and the calculated indices are summarized in Table 4. During dobutamine infusion, resting and hyperemic mean blood pressure did not change significantly. Heart rate increased both at rest and during hyperemia. A marked increase in resting blood flow velocities was observed, while hyperemic blood flow velocities remained unchanged. As a result, the mean value of CFVR significantly decreased during dobutamine. Translesional pressure gradient increased during infusion of dobutamine. In contrast, hyperemic distal coronary pressure and translesional pressure gradient did not change significantly. The mean values of IHDVPS and FFRmyo did not change significantly during infusion of dobutamine. The correlation between the individual measurements of CFVR, IHDVPS, and FFRmyo before and during infusion of dobutamine is shown in Fig 7. The coefficient of variation observed between the measurements performed before and during infusion of dobutamine was significantly lower for FFRmyo (4.4% [3.2% to 6.9%]) than for both CFVR (26.7% [19.5% to 42.1%]) and IHDVPS (17.4% [12.2% to 30.5%]; both P<.05; Fig 4).
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Discussion |
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The present study compares side-by-side three invasive indices of coronary flow reserve, namely CFVR, IHDVPS, and FFRmyo, with respect to the easiness of their assessment in humans and to their dependence on hemodynamic changes. The measurements were made in a large range of stenosis severity, with special emphasis on lesions of "intermediate severity." The latter are usually the most difficult to gauge and therefore require functional evaluation for clinical decision making. The major findings of the study can be summarized as follows. (1) CFVR is easy to determine, is quite reproducible when hemodynamic conditions remain unchanged, but is highly sensitive to hemodynamic changes. (2) IHDVPS can be obtained in only 79% of cases and shows a large variability in the measurements even under baseline conditions. (3) FFRmyo is both very easy to obtain and almost independent from the prevailing hemodynamic conditions.
Coronary Flow Velocity Reserve
The recent development of Doppler velocity guide wires prompted the use of CFVR as a surrogate for absolute coronary flow reserve in humans. The present study indeed suggests that CFVR can easily be assessed whatever the heart rate, blood pressure, and contractile state. In 24% of measurements, the injection of intracoronary adenosine had to be repeated once or twice because the signal of the instantaneous blood flow velocity could not be detected with sufficient accuracy to rely on mean blood flow velocity. Our data, like others,16 17 show a rather good reproducibility of serial measurements of CFVR, provided that the conditions known to affect resting and hyperemic coronary flow remain constant. Previous animal and human studies have demonstrated significant reduction in coronary flow reserve (and CFVR) under the influence of tachycardia,6 16 17 18 volume loading,6 16 and increased contractility.6 Two studies conducted in humans did not show a significant change in CFVR accompanying changes in blood pressure because of proportional changes in coronary blood flow velocity so that their ratio remained similar.16 18 In the present study, no significant difference in CFVR was noted when blood pressure was lowered by nitroprusside. In contrast, when heart rate was increased by atrial pacing or when contractility increased under the influence of dobutamine, a significant decrease in CFVR occurred mainly as the result of an increase in resting coronary blood flow velocity. Moreover, the present study shows a high degree of variability of the values of CFVR under the influence of various hemodynamic changes. Although a large variability in CFVR measurements accompanied changes in hemodynamic conditions, two serial measurements under baseline conditions were quite reproducible, suggesting that the variability of CFVR measurements cannot be ascribed to technical factors. The hemodynamic dependence of CFVR is chiefly due to the fact that the concept is based on a ratio whose denominator is resting flow velocity, a parameter extremely sensitive to changes in myocardial oxygen consumption. Therefore, in clinical practice, serial measurements of CFVR are often difficult to compare and to interpret because of changes in prevailing myocardial oxygen consumption and secondary changes in basal and/or hyperemic coronary blood flow. Moreover, blood flow velocity is influenced not only by the severity of the epicardial lesion and by its consequences on myocardial resistance but also by the changes in dimensions of the vessel segment where the flow velocity measurements are taken. In the present study, however, these changes in vessel diameter are unlikely to play a major role because the coronary arteries were predilated with intracoronary nitrates. In addition, flow-induced vasodilatation of the epicardial vessel after a short-lasting hyperemia is expected to occur only 60 seconds later, at the time when coronary blood flow has already returned to normal.19
These results extend recent data showing a large variability of coronary flow velocity reserve measurements repeated after a 6-month interval.20 These authors pointed out that this variability can be reduced by normalization for the cross-sectional area at the site of the measurement (coronary flow) and for the aortic pressure at the time of the measurement (flow resistance).
Instantaneous Hyperemic Diastolic Velocity-Pressure Slope
To overcome the limitations of coronary flow reserve, Mancini et al4 introduced the instantaneous hyperemic flow–versus–pressure slope index, which has been shown to correlate most closely with subendocardial coronary conductance.5 It is determined by calculating the slope of the linear diastolic segment of the relation between instantaneous aortic pressure and hyperemic coronary flow. During this part of diastole, compressive forces of the ventricle are minimal and coronary flow is exclusively related to the severity of the lesion and to the driving pressure. The steeper the slope, the milder the coronary lesion. To some extent this index can be compared with the Doppler pressure–half-time used to evaluate the severity of mitral stenoses. The instantaneous hyperemic flow–versus–hyperemic pressure slope incorporates aortic pressure and showed no significant hemodynamic dependence on left ventricular end-diastolic pressure, heart rate, or contractility in an open chest animal model.6 17 This concept was recently simplified (IHDVPS) and applied to humans by Di Mario et al.7 The IHDVPS, also used in this study, differs from the originally proposed index with at least two respects: first, distal flow velocity measurements were used instead of proximal absolute coronary blood flow normalized for myocardial mass. Second, maximal coronary blood flow velocity was used instead of left ventricular high-fidelity pressure measurements to detect the diastolic interval of interest for analysis. Although in Di Mario's study interobserver and intraobserver reproducibility of IHDVPS was excellent, the latter index could only be obtained in 77% of cases with angiographically proven coronary stenosis. Failed measurements were related to poor quality of the Doppler signal. This is very similar to the findings of the present study. Di Mario et al7 did not find a higher specificity of IHDVPS than CFVR in discriminating between normal and diseased coronary arteries (diameter stenosis >30%). Moreover, our data demonstrate a large variability of two consecutive values of IHDVPS taken under baseline conditions, while this variability did not seem to increase further with changing hemodynamic conditions. This suggests that technical factors rather than fluctuating hemodynamics are responsible for the observed variability. In addition, at heart rates usually encountered in the catheterization laboratory, the duration of diastole is often too short to reliably calculate the slope of the instantaneous relationship between flow velocity and pressure.
Myocardial Fractional Flow Reserve
Like IHDVPS, FFRmyo has the conceptual advantage of relying only on measurements performed during maximal hyperemia. FFRmyo is defined as the maximal myocardial blood flow in the presence of an epicardial coronary stenosis expressed as a fraction of the expected normal maximal myocardial blood flow, ie, hyperemic flow in the hypothetical case that the epicardial coronary artery were normal. FFRmyo can be calculated as the ratio of mean distal coronary pressure to mean aortic pressure recorded during maximal pharmacological vasodilatation. FFRmyo takes into account the collateral contribution to maximal myocardial blood flow. By definition, its normal value is unequivocally equal to 1 (or 100%) for any vessel under study, whatever the myocardial mass supplied by the lesion. The theoretical basis of the concept has been validated in an open chest animal model.8 The feasibility in humans and the accuracy of pressure-derived FFRmyo have been demonstrated by comparison with positron emission tomographic assessment of myocardial blood flow measurements.9 Recently we established threshold values of FFRmyo, above which no electrocardiographic signs of myocardial ischemia could be elicited during exercise.21 22 The present study demonstrates the hemodynamic independence of FFRmyo measurements in humans. Tachycardia, changes in arterial pressure, and changes in contractility induced significantly smaller variability in FFRmyo measurements than in both CFVR and IHDVPS measurements. This is probably related to the combination of the following factors: (1) FFRmyo is unaffected by changes in resting conditions; (2) the index incorporates mean arterial pressure, therefore correcting for the changes in driving coronary pressure; (3) the mean coronary pressure as recorded in this study through thin fluid-filled column appears to be an extremely stable signal devoid of artifacts that often obscure the velocity tracings in humans; and (4) distal coronary pressure integrates all possible changes in vessel diameter that could accompany changes in absolute coronary blood flow.23 In addition, our data show that FFRmyo as derived from pressure measurements is obtainable in all cases.
Study Limitations
In the present study, lowering blood pressure by nitroprusside infusion was accompanied by a reflex tachycardia. The infusion of dobutamine in addition to an increase in left ventricular contractility also induced an increase in heart rate. Although not specifically monitored in the present study, an increase in heart rate is known to increase left ventricular contractility.24 Hence, the specific influence of heart rate, blood pressure, and contractility were not really divorced from one another. However, the study protocol closely mimics alterations in hemodynamic parameters that are likely to occur in humans during interventional procedures during which changes in heart rate, blood pressure, contractility, and volume loading are closely interrelated and do not fluctuate independently from one another.
The use of intracoronary adenosine to induce maximal hyperemia may introduce a bias in evaluating the easiness of measuring CFVR and IHDVPS. Indeed, a longer-lasting hyperemia as obtained by intravenous adenosine or by intracoronary papaverine would have allowed repositioning of the Doppler wire during the hyperemic phase. This could have led to a higher success rate in computing IHDVPS. In addition, steady-state hyperemia could have diminished the variability related to quick changes in pressures sometimes associated with the administration of intracoronary adenosine. Yet, intracoronary adenosine at the dosages used in the present study induces a maximal hyperemia and has a very short half-live.13 These characteristics contribute to the safety and to the easiness of use of the vasodilatory drug. The easiness and rapidity with which measurements can be obtained are nonnegligible characteristics for new indices to be used in interventional catheterization laboratories.
Clinical Implications
Temporary changes in heart rate, arterial pressure, and myocardial contractile state are likely to occur in the setting of catheterization and even more so in the setting of interventional cardiology. Prolonged episodes of myocardial ischemia might even limit the return to truly basal hemodynamic conditions and coronary flow. Therefore, methods proposed for gauging the physiological impact of epicardial stenoses or to evaluate the results of an intervention should provide similar results whatever the prevailing hemodynamic conditions so as to be interpretable and thus useful for clinical decision making. In addition, in the era of interventional cardiology, all indices should be simple, safe, and swift to obtain. FFRmyo, by combining easiness and high reproducibility, appears to be superior to both CFVR and IHDVPS in providing information on the consequences of an epicardial lesion on the perfusion of the underlying myocardium.
Received October 10, 1995; revision received April 30, 1996; accepted May 6, 1996.
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W. Aarnoudse, M. van't Veer, N. H.J. Pijls, J. ter Woorst, S. Vercauteren, P. Tonino, M. Geven, M. Rutten, E. van Hagen, B. de Bruyne, et al. Direct Volumetric Blood Flow Measurement in Coronary Arteries by Thermodilution J. Am. Coll. Cardiol., December 11, 2007; 50(24): 2294 - 2304. [Abstract] [Full Text] [PDF]
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M. A. Leesar, T. Abdul-Baki, N. I. Akkus, A. Sharma, T. Kannan, and R. Bolli Use of fractional flow reserve versus stress perfusion scintigraphy after unstable angina: Effect on duration of hospitalization, cost, procedural characteristics, and clinical outcome J. Am. Coll. Cardiol., April 2, 2003; 41(7): 1115 - 1121. [Abstract] [Full Text] [PDF]
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M. Albertal, E. Regar, G. Van Langenhove, S.G. Carlier, J.J. Piek, B. de Bruyne, C. di Mario, D. Foley, K. Kozuma, M.A. Costa, et al. Value of coronary stenotic flow velocity acceleration in prediction of angiographic restenosis following balloon angioplasty Eur. Heart J., December 1, 2002; 23(23): 1849 - 1853. [Abstract] [Full Text] [PDF]
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M. Meuwissen, M. Siebes, S. A.J. Chamuleau, B. L.F. van Eck-Smit, K. T. Koch, R. J. de Winter, J. G.P. Tijssen, J. A.E. Spaan, and J. J. Piek Hyperemic Stenosis Resistance Index for Evaluation of Functional Coronary Lesion Severity Circulation, July 23, 2002; 106(4): 441 - 446. [Abstract] [Full Text] [PDF]
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N. H.J. Pijls, B. De Bruyne, L. Smith, W. Aarnoudse, E. Barbato, J. Bartunek, G. J. W. Bech, and F. Van De Vosse Coronary Thermodilution to Assess Flow Reserve: Validation in Humans Circulation, May 28, 2002; 105(21): 2482 - 2486. [Abstract] [Full Text] [PDF]
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D. Brosh, S. T. Higano, M. J. Slepian, H. I. Miller, M. J. Kern, R. J. Lennon, D. R. Holmes Jr, and A. Lerman Pulse transmission coefficient: a novel nonhyperemic parameter for assessing the physiological significance of coronary artery stenoses J. Am. Coll. Cardiol., March 20, 2002; 39(6): 1012 - 1019. [Abstract] [Full Text] [PDF]
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W. F. Fearon, J. Luna, H. Samady, E. R. Powers, T. Feldman, N. Dib, E. M. Tuzcu, M. W. Cleman, T. M. Chou, D. J. Cohen, et al. Fractional Flow Reserve Compared With Intravascular Ultrasound Guidance for Optimizing Stent Deployment Circulation, October 16, 2001; 104(16): 1917 - 1922. [Abstract] [Full Text] [PDF]
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M. J. Kern and B. Meier Evaluation of the Culprit Plaque and the Physiological Significance of Coronary Atherosclerotic Narrowings Circulation, June 26, 2001; 103(25): 3142 - 3149. [Full Text] [PDF]
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M. Abe, H. Tomiyama, H. Yoshida, and N. Doba Diastolic Fractional Flow Reserve to Assess the Functional Severity of Moderate Coronary Artery Stenoses : Comparison With Fractional Flow Reserve and Coronary Flow Velocity Reserve Circulation, November 7, 2000; 102(19): 2365 - 2370. [Abstract] [Full Text] [PDF]
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W. J. Cantor, E. D. Peterson, J. J. Popma, J. P. Zidar, M. H. Sketch Jr., J. E. Tcheng, and E. M. Ohman Provisional stenting strategies: systematic overview and implications for clinical decision-making J. Am. Coll. Cardiol., October 1, 2000; 36(4): 1142 - 1151. [Abstract] [Full Text] [PDF]
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B. De Bruyne, N. H. J. Pijls, G. R. Heyndrickx, D. Hodeige, R. Kirkeeide, and K. L. Gould Pressure-Derived Fractional Flow Reserve to Assess Serial Epicardial Stenoses : Theoretical Basis and Animal Validation Circulation, April 18, 2000; 101(15): 1840 - 1847. [Abstract] [Full Text] [PDF]
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M. J. Kern Coronary Physiology Revisited : Practical Insights From the Cardiac Catheterization Laboratory Circulation, March 21, 2000; 101(11): 1344 - 1351. [Abstract] [Full Text] [PDF]
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A. Jeremias, S. D. Filardo, R. J. Whitbourn, R. S. Kernoff, A. C. Yeung, P. J. Fitzgerald, and P. G. Yock Effects of Intravenous and Intracoronary Adenosine 5'-Triphosphate as Compared With Adenosine on Coronary Flow and Pressure Dynamics Circulation, January 25, 2000; 101(3): 318 - 323. [Abstract] [Full Text] [PDF]
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A. Takagi, Y. Tsurumi, Y. Ishii, K. Suzuki, M. Kawana, and H. Kasanuki Clinical Potential of Intravascular Ultrasound for Physiological Assessment of Coronary Stenosis : Relationship Between Quantitative Ultrasound Tomography and Pressure-Derived Fractional Flow Reserve Circulation, July 20, 1999; 100(3): 250 - 255. [Abstract] [Full Text] [PDF]
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C. E. E. Hanekamp, J. J. Koolen, N. H. J. Pijls, H. R. Michels, and H. J. R. M. Bonnier Comparison of Quantitative Coronary Angiography, Intravascular Ultrasound, and Coronary Pressure Measurement to Assess Optimum Stent Deployment Circulation, March 2, 1999; 99(8): 1015 - 1021. [Abstract] [Full Text] [PDF]
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M. Ferrari, B.a. Schnell, G. S. Werner, and H. R. Figulla Safety of deferring angioplasty in patients with normal coronary flow velocity reserve J. Am. Coll. Cardiol., January 1, 1999; 33(1): 82 - 87. [Abstract] [Full Text] [PDF]
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