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The Relationship Between Corrected TIMI Frame Count and Myocardial Fractional Flow Reserve
March 2002
Thrombolysis in myocardial infarction (TIMI) frame count (TFC) is a reproducible, objective and quantitative index of coronary flow that allows standardization of TIMI flow grades.1 The quality of coronary flow restored by percutaneous coronary interventions (PCI) mainly depends on the success of the mechanical intervention. TIMI grade flow achieved in infarct-related arteries (IRA) after PCI is directly related to the degree of improvement in minimal luminal diameter and residual stenosis. After myocardial infarction (MI), coronary blood flow decreases in the infarct region due to residual stenosis and increased resistance in the microvasculature subtended by this IRA. PCI can markedly diminish residual stenosis, normalizing resistance to flow and pressure gradients across the lesion sites. The functional severity of this residual lesion can be determined by using the intracoronary pressure measurement technique, which also has considerable complementary value in the evaluation of the PCI results.2,3 From this physiological point of view, myocardial fractional flow reserve (FFRmyo) is a lesion-specific index for epicardial stenosis and provides important data about the functional severity of the intracoronary lesion.4–6 PCI produces changes in vessel wall geometry that maximize acute gain and decrease residual stenosis; this can be translated into improvement of the coronary flow together with intracoronary hemodynamics. In this study, we hypothesized that the improvements in FFRmyo (determined by intracoronary pressure measurement) achieved by PCI would translate into improvements in coronary blood flow (as measured with TFC). Therefore, the aim of this study was to investigate the relationship between improvement of the corrected TFC (CTFC) and change in FFRmyo after PCI in patients with recent MI who underwent late mechanical revascularization to the IRA.
METHODS
Patient population. We studied 41 consecutive patients who presented with their first acute MI and were referred to our institution between December 1998 and August 2000 and met the following criteria: 1) treatment with thrombolytic therapy within 12 hours of symptom onset; 2) > 60% stenosis in the IRA at the coronary angiography, which was performed routinely 5–7 days after uncomplicated acute MI; and 3) stent implantation performed for this culprit lesion. Patients who had more than one stenotic lesion in the IRA were excluded. In the coronary care unit, all patients received conventional drug therapy in accordance with guidelines for treatment of acute MI (Table 1).7 Written informed consent was obtained from all patients, and study protocol was approved by our institutional review board.
Intracoronary pressure measurements and angiographic analysis. Cardiac catheterization was performed 5–7 days after acute MI. Left and right coronary angiography and left ventriculography were performed in all patients. Angiography was recorded at 25 frames per second and injections were performed by hand. The first frame used for TFC was defined by a column of contrast extending across >= 70% of the arterial lumen and the last frame counted was that in which contrast first appeared in the distal pre-defined landmark branches for each vessels. Corrected TFC (CTFC) was calculated for the left anterior descending coronary artery (LAD) by dividing TFC of the LAD by a factor of 1.7. Quantitative coronary angiographic analyses (QCA), all coronary pressure measurements and assessments of CTFC were performed both before and after the revascularization procedures. Percentages of the improvement in the CTFC, FFRmyo and infarct-related stenosis after PCI were calculated for each lesion. QCA was performed on all patients by a computer-assisted program (Philips Integris Angiographic Systems). The angiographic projection showing maximal severity of the diameter narrowing was used for assessment of stenosis severity, with the guiding catheter used as a scaling device. Percent diameter stenosis of the target lesion was calculated. After coronary angiography, a fiber-optic pressure monitoring guidewire (0.014 inch Pressure wire, RADI Medical Systems, Uppsala, Sweden) was set at zero, calibrated and advanced through the guiding catheter and positioned distal to the stenosis to be dilated. The same wire was used as a guidewire for the angioplasty catheter. Proximal aortic (Pa) and distal pressures (Pd) were simultaneously recorded under baseline and hyperemic conditions. Pd was recorded from the pressure wire and proximal pressure was recorded from the guiding catheter. Adenosine was the hyperemic agent used; a dose of 20 µg intracoronary bolus was given for the left system and 15 µg was given for the right coronary artery (RCA) and repeated if necessary. FFRmyo was calculated under adenosine hyperemia as the ratio of mean distal coronary pressure (Pd) to mean aortic pressure (Pa).
Statistical analysis. Statistical analyses were performed using SPSS 10.0 for Windows. Data were expressed as means ± standard deviation and a p-value Study limitations. Several limitations of this study should be considered. First, our study population is relatively small and more patients may be required to obtain conclusive results. Second, it has been reported that FFRmyo measurements may not be valid for the determination of stenosis significance in the IRA.17 However, we considered improvement of the FFRmyo after revascularization and this situation to be valid for each patient enrolled in this study.
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