Author + information
- Received January 26, 2015
- Revision received August 24, 2015
- Accepted September 8, 2015
- Published online November 1, 2015.
- Mauro Echavarría-Pinto, MD∗,†,‡∗ (, )
- Tim P. van de Hoef, MD∗,†,‡,
- Martijn A. van Lavieren, MSc‡,
- Sukhjinder Nijjer, MBChB§,
- Borja Ibañez, MD, PhD∗,†,
- Stuart Pocock, PhD†,
- Alicia Quirós, PhD∗,
- Justin Davies, MBBS, PhD§,
- Martijn Meuwissen, MD, PhD‖,
- Patrick W. Serruys, MD, PhD§,
- Carlos Macaya, MD, PhD∗,¶,
- Jan J. Piek, MD, PhD‡ and
- Javier Escaned, MD, PhD∗,†,¶
- ∗Cardiovascular Institute, Hospital Clínico San Carlos, Madrid, Spain
- †Centro Nacional de Investigaciones Cardiovasculares Carlos III (CNIC), Madrid, Spain
- ‡AMC Heart Centre, Academic Medical Centre—University of Amsterdam, Amsterdam, the Netherlands
- §International Centre for Circulatory Health, National Heart and Lung Institute, Imperial College London and Imperial College Healthcare National Health Service Trust, London, United Kingdom
- ‖Amphia Hospital, Breda, the Netherlands
- ¶Faculty of Medicine, Complutense University of Madrid, Madrid, Spain
- ↵∗Reprint requests and correspondence:
Dr. Mauro Echavarría-Pinto, Hospital Clinico San Carlos, Calle del Prof Martín Lagos, S/N, Madrid 28040, Spain.
Objectives This study sought to understand the physiological basis of baseline distal-to-aortic pressure ratio (Pd/Pa) and fractional flow reserve (FFR) agreement and discordance, using coronary flow reserve (CFR), stenosis resistance, and microcirculatory resistance measurements, and form there, to investigate the potential value of combining Pd/Pa with FFR in the diagnostic rationale.
Background Pd/Pa is always available before FFR assessment, and emerging data supports the notion that baseline indices can determine the ischemic potential of coronary stenosis in selected subsets.
Methods A total of 467 stenosed vessels from 363 patients were investigated with pressure and flow sensors during baseline and hyperemia: 168 vessels (135 patients) with thermodilution-derived flow, and 299 vessels (228 patients) with Doppler-derived flow.
Results Pd/Pa correlated more strongly with CFR than FFR (ρ difference = 0.129; p for ρ comparison <0.001). Although Pd/Pa and FFR were closely correlated (ρ = 0.798; 95% confidence interval: 0.767 to 0.828), categorical discordance was observed in 19.3% of total vessels. Such discordance was associated with the patients’ clinical profile and was characterized by contrastive changes in stenosis resistance, microcirculatory resistance, and the underlying CFR. Notably, all stenosis with Pd/Pa ≤0.83 (n = 74, 15.8%) progressed to FFR ≤0.80, and although no Pd/Pa cutoff was able to exclude the development of FFR ≤0.80 in the high end of values, only 15 (10.1%) vessels with Pd/Pa ≥0.96 (n = 149, 31.9%) developed FFR ≤0.80, from which none had definite ischemia, as defined by CFR ≤1.74.
Conclusions Combining baseline Pd/Pa with FFR seems to provide a more comprehensive physiological examination of stenosed coronary arteries and a closer pressure-based appraisal of the flow reserve of the downstream myocardial bed.
Fractional flow reserve (FFR) has become the standard method to assess coronary stenosis severity in the catheterization laboratory following the demonstration that physiological rather than anatomical selection of stenosis candidates for revascularization results in better patient outcomes (1). This positive evidence has stimulated the interest in FFR and other physiology indices, and a desire for simplification has specifically boosted the attention to nonhyperemic indices (2). The baseline distal-to-aortic pressure ratio (Pd/Pa) is always available before FFR assessment, and several studies have shown that a Pd/Pa value close to 0.90 provides the best classification match with the clinically adopted 0.80 FFR cutoff, which is approximately 80% (3,4). This implies that most stenoses that will develop FFR ≤0.80 have already relatively low Pd/Pa values, and conversely, that most stenoses that will develop a final FFR >0.80 arise from high values of Pd/Pa. This also denotes, however, that in approximately 20% of the cases, Pd/Pa will not match dichotomously with FFR, because in some vessels an FFR value ≤0.80 will emerge from a near-normal Pd/Pa ratio, whereas in others, an FFR >0.80 will be preceded by an already fairly low Pd/Pa. Although this disagreement is used to stress the importance of standardizing measurements at hyperemia, its physiological basis is poorly described.
In this study, we investigated stenosed coronary arteries with combined intracoronary pressure and flow sensors because this allows selective interrogation of the epicardial stenosis resistance (SR), microcirculatory resistance (MR), and the coronary flow reserve (CFR) of the downstream vascular bed (5). We aimed firstly to explore the physiological basis of the agreement and discordance between baseline Pd/Pa and FFR and secondly to test whether adding baseline Pd/Pa to the diagnostic rationale conveys important information able to expand the physiological lone-FFR assessment.
Patients with a clinical indication for FFR interrogation of ≥1 intermediate coronary stenosis (40% to 70% diameter stenosis), investigated at Hospital Clinico San Carlos, Madrid, Spain, and the Academic Medical Centre, Amsterdam, the Netherlands, were prospectively studied. Patients with the following were excluded: myocardial infarction within 5 days; contraindications to adenosine; left ventricle ejection fraction <30%; left main disease; or significant valvular pathology; as well as vessels supplying previously known infarcted territories, with serial stenoses, marked diffuse narrowings, or with patent surgical grafts. All patients gave informed consent and approval from the institutional review boards was obtained according to local regulations.
Cardiac catheterization and hemodynamic measurements
Cardiac catheterization was performed according to standard practice. Angiographic views were obtained following intracoronary nitrates (0.2 mg) in a manner suitable for quantitative coronary angiography analysis. After diagnostic angiography, sensor-equipped guidewires were used to measure intracoronary pressure and flow according to described methodologies (6,7). Briefly, in Hospital Clinico San Carlos, coronary flow was assessed with the coronary thermodilution method (8). Resting and hyperemic thermodilution curves were obtained in triplicate, and CFR calculated as the ratio of average baseline mean thermodilution transit time (Tmn) to hyperemic Tmn. The inverse of baseline Tmn and hyperemic Tmn was computed and labeled as baseline and hyperemic flow, respectively (8). In the Academic Medical Centre, coronary flow velocity was assessed using Doppler sensors as described elsewhere (7). Baseline and hyperemic average peak flow velocities were recorded, and coronary flow velocity reserve was calculated as the ratio of hyperemic to baseline flow velocity. Because coronary flow velocity reserve and thermodilution-derived CFR are unitless and very strongly correlated (9), the term CFR was used and datasets merged. Indices of flow, SR, and MR were calculated as depicted in Table 1. Hyperemia was induced with adenosine, either by intravenous infusion through a central vein (140 μg/kg/min) at Hospital Clinico San Carlos, or intracoronary boluses (20 to 40 μg) at the Academic Medical Centre. Finally, FFR ≤0.80 and CFR <2 were used as cutoff values (1,7).
Data was analyzed on per-patient basis for clinical characteristics and on per-vessel basis for the rest of calculations. For patient-level analyses, “center” was added as covariate to linear and logistic regression models in order to account for potential differences between the populations. Huber-White robust standard errors were used to adjust for additional variability of arteries from the same subject. From these models, adjusted means and prevalences with 95% confidence intervals (CI) are presented. For vessel-level analyses, we believed it was better to document the consistencies and the differences between the centers and their techniques to measure flow. Therefore, individual Doppler and Thermo findings are also provided in the tables and in the Online Appendix. Finally, because Pd/Pa, FFR, and CFR are vessel-specific indices that link upstream epicardial disease with the functionality and extension of the downstream microcirculatory bed, independence was assumed for vessel-level analyses. Continuous variables are presented as mean ± SD or median (quartiles 1 and 3, Q1-3) and categorical variables as counts and percentages. Normality and homogeneity of the variances were tested using Shapiro-Wilk and Levene tests, respectively. Continuous variables were compared with Student t or Mann-Whitney U tests, and categorical variables with chi-square or Fisher exact tests, as appropriate. Correlation coefficients (Pearson r, Spearman ρ) between physiology indices were calculated. For Pd/Pa dichotomization, receiver-operating characteristic analyses were used to determine its optimal cutoff against FFR ≤0.80, defined as that maximizing correct classification. Overall differences across Pd/Pa and FFR categories were compared with 1-way analysis of variance, Kruskal-Wallis, chi-square or Fisher exact tests, followed by post-hoc Student t tests, or Mann-Whitney U or Fisher exact tests with Bonferroni-adjusted significance level. In scatterplots, spherical controlled noise (“jitter”) was used to prevent overprinting of dots. Differences were considered significant at p < 0.05 (2-sided), and the STATA (version 12.1, StataCorp, College Station, Texas) software was used for all calculations.
Clinical, angiographic, and physiological characteristics of the study population are shown in Tables 2 and 3. In total, 467 stenosed vessels from 363 patients were investigated: 168 vessels (n = 135) with thermodilution-derived flow (Thermo) and 299 vessels (n = 228) with Doppler-derived flow (Doppler). Mean age was 62 ± 11 years and the majority of patients (n = 305, 84.0%) underwent catheterization because of stable symptoms. Overall, coronary stenoses were of intermediate severity, both angiographically (diameter stenosis: 52.7 ± 11.4%) and physiologically (median FFR = 0.81 [Q1-3: 0.72, 0.88]).
Relationship between Pd/Pa and FFR
Figure 1 shows the scatterplot of the Pd/Pa and FFR relationship. A moderate-to-strong correlation between Pd/Pa and FFR was observed in the overall population (ρ = 0.798; 95% CI: 0.767 to 0.828), which was similar between technologies (Online Figure 1): Thermo-vessels: ρ = 0.789 (95% CI: 0.724 to 0.839); Doppler-vessels: ρ = 0.821 (95% CI: 0.781 to 0.855); p for ρ comparison = 0.337. Using FFR ≤0.80 to define significant stenosis, receiver-operating characteristic analyses identified 0.91 as the optimal Pd/Pa cutoff, with an area under the curve of 0.882 (95% CI: 0.851 to 0.913) (Figure 1B). This 0.91 Pd/Pa cutoff classified correctly 80.7% of total stenoses, with a sensitivity of 68.9% and specificity of 91.7%. Consequently, Pd/Pa ≤0.91 (n = 201 [43.0%]) and FFR ≤0.80 (n = 225 [48.2%]) were used for further categorizations: A-vessels: both Pd/Pa and FFR are abnormal (Pd/Pa ≤0.91 and FFR ≤0.80, n = 166 [35.6%]); B-vessels: only FFR is abnormal (Pd/Pa >0.91 and FFR ≤0.80, n = 59 [12.6%]); C-vessels: only Pd/Pa is abnormal (Pd/Pa ≤0.91 and FFR >0.80, n = 35 [7.5%]); and D-vessels: both Pd/Pa and FFR are normal (Pd/Pa >0.91 and FFR >0.80, n = 207 [44.3%]); B-vessels and C-vessels are discordant-vessels.
Finally and with the aim to explore a perfect classification agreement between Pd/Pa and FFR on individual basis, no Pd/Pa cutoff was able to exclude the development of an FFR ≤0.80 in the high end of values, whereas, conversely, all stenosis with Pd/Pa ≤0.83 (n = 74, 15.8%) developed FFR ≤0.80.
Clinical characteristics across the Pd/Pa and FFR categories
Table 2 depicts the clinical characteristics of the study population. Some were different across the Pd/Pa and FFR categories. The more significant differences were age and the prevalence of hypertension: B-vessels were more frequently observed in younger patients, whereas C-vessels were more prevalent in elderly and hypertensive patients.
Relationship of Pd/Pa and FFR with measurements of flow
Pd/Pa (ρ = 0.474; 95% CI: 0.401 to 0.542, p < 0.001) and FFR (ρ = 0.344; 95% CI: 0.261 to 0.442, p < 0.001) were both significantly correlated with CFR (Figure 2), although Pd/Pa correlated more strongly (ρ difference = 0.129; 95% CI: 0.066 to 0.243, p for ρ comparison < 0.001). Overall, coronary flow increased with hyperemia a median of +116% (Q1-3: +54%, +172%). However, the increase in flow (Tables 3 and 4, Figure 3) was significantly different across Pd/Pa and FFR categories (p for overall comparison <0.001). The smallest and largest increases in flow were observed in A-vessels (median: +60% [Q1-3: +25%, +120%]) and D-vessels (median: +140% [Q1-3: +91%, +192%]), respectively. C-vessels exhibited moderate increases of flow (median: +97% [Q1-3: +45%, +154%]), whereas, notably, the increase in flow of B-vessels was high (median: +144% [Q1-3: +95%, +201%]) and did not statistically differ (p = 0.977) from that observed in the most normal D-vessels. Similar trends were observed when the percentage of vessels with exhausted flow reserve (CFR <2) was investigated across Pd/Pa and FFR categories (Figure 2B). If baseline Pd/Pa was >0.91 (n = 266, 57%), the prevalence of exhausted CFR was low (n = 82, 30.8%), and did not statistically differ (p = 0.425) whether final FFR was ≤0.80 (B-vessels: n = 32, 35.6%) or >0.80 (D-vessels: n = 61, 29.5%). Conversely, if Pd/Pa was ≤0.91 (n = 201, 43%), the prevalence of exhausted CFR was high (n = 201, 63.7%), and only marginally statistically different (p = 0.053) whether final FFR was ≤0.80 (A-vessels: n = 111, 66.9%) or >0.80 (C-vessels: n = 17, 48.6%).
Stenosis resistance across Pd/Pa and FFR categories
Baseline and hyperemic SR values were significantly different across the Pd/Pa and FFR categories (Table 2). The highest SR were observed in A-vessels, the lowest in D-vessels, and discordant-vessels exhibited intermediate SR values. Hyperemia increased SR a median of +11% (Q1-3: -21%, +62%) in the total vessel population. However, the modification in SR induced by hyperemia was very different across Pd/Pa and FFR categories. As shown in Table 3 and Figure 3, in concordantly abnormal and normal vessels, SR was only slightly modified by hyperemia, as it only increased a median of +6% (Q1-3: -15%, +23%) in A-vessels and +17% (Q1-3: -22%, +79%) in D-vessels. In discordant-vessels, however, the modification in SR with hyperemia was more substantial, as it increased a median of +72% (Q1-3: +25%, +160%) in B-vessels, whereas it decreased a median of -33% (Q1-3: -46%, -16%) in C-vessels. Consistency in this finding was observed in both Thermo-vessels and Doppler-vessels (Table 4, Figure 3).
Microcirculatory resistance across Pd/Pa and FFR categories
In the total population, hyperemia decreased MR a median of -61% (Q1-3: -70%, -50%) (Table 3). The reduction in MR was largest in B-vessels (median: -68% [Q1-3: -77%, -59%]) and smallest in A-vessels (median: -54% [Q1-3: -65%, -38%]) and C-vessels (median: -54% [Q1-3: -70%, -43%]). In Doppler-vessels, the minimum MR was not statistically different across the Pd/Pa and FFR categories, whereas in Thermo-vessels, an overall significant difference was observed, being lower and higher in B-vessels and D-vessels, respectively (Table 2, Figure 3).
Notwithstanding the limitations of considering a “true“ baseline (8) and a “true“ maximal hyperemic state (10), in this work we explored the possibility of expanding with simplicity the physiological assessment of coronary stenosis by combining Pd/Pa with the standard FFR. This is important at a time when randomized trials have moved optimal guidance of coronary revascularization from angiography to physiology (1) and emerging data supports the notion that hyperemia-free indices can accurately determine the ischemic potential of coronary stenosis in selected subsets (2–4).
We observed that a baseline Pd/Pa value of 0.91 classified correctly the majority (80.7%) of the stenosis against that clinically adopted 0.80 FFR cutoff. Furthermore, we observed that Pd/Pa was more closely correlated with CFR than FFR, and that the Pd/Pa and FFR discordance was associated with the patients’ clinical profile and characterized by contrastive changes in SR, MR, and the underlying CFR. The combination of baseline Pd/Pa with FFR seems hence to provide a more comprehensive physiological examination of stenosed coronary arteries and a closer pressure-based appraisal of the flow reserve of the downstream myocardial bed.
Combining baseline Pd/Pa with FFR in the assessment of coronary stenosis severity
From a broad perspective, intracoronary physiology has pursued standardized hyperemic stress to assess coronary stenosis severity, largely neglecting the information readily available during the baseline state. This rationale contrasts with that of all the other noninvasive tests aimed to detect electrical, contractile, or perfusional manifestations of ischemia, in which hyperemic findings are always weighted against those observed during baseline. Nevertheless, interventionalists are accustomed to witness modifications of variable magnitude in the Pd/Pa ratio, from the time they cross the stenosis during baseline to the moment of achievement of hyperemia. For example, an FFR value of 0.70 may develop from a near-normal baseline Pd/Pa of 0.99, or from a frankly abnormal Pd/Pa of 0.80. This Pd/Pa value, however, is conventionally not considered worthwhile—even though it is always readily accessible—and therefore all stenoses reaching the same FFR value are currently pondered alike. Our findings suggest that the physiological assessment of epicardial stenosis severity with the standard FFR is augmented by the simple incorporation of the baseline Pd/Pa, because the CFR underlying a low (≤0.80) or a high (>0.80) FFR value was largely dependent on the initial Pd/Pa value (Figure 4). We documented that most vessels with near-normal (>0.91) Pd/Pa values exhibited concomitant nonischemic CFR values, even if a final FFR ≤0.80 was achieved (Figure 5A). Conversely, a significant percentage of vessels with abnormal (≤0.91) Pd/Pa exhibited moderately to highly exhausted CFR values, even if a final FFR >0.80 was only achieved (Figure 5A). Therefore, the combination of baseline Pd/Pa with FFR seems physiologically incremental and practically appealing. In the same line, our findings substantiate the observed better correlation of the underlying CFR with baseline rather than hyperemic pressure-indices (11), which provides further support to the clinical use of the baseline state. Finally and comparable with previous studies (3,4), we observed that Pd/Pa and FFR dichotomously disagreed in approximately 20% of vessels. In the following paragraphs, these hemodynamic patterns are discussed in detail.
Vessels with baseline Pd/Pa > 0.91 and FFR ≤ 0.80
Stenosed coronary arteries exhibiting mild pressure drops at baseline (Pd/Pa >0.91) that significantly worsened (FFR≤0.80) during hyperemia represented 12.6% of the total population and most (62.8%) of the Pd/Pa and FFR disagreement. Physiologically, this pattern was characterized by low baseline SR that significantly increased during hyperemia (+73%), achieving final intermediate magnitudes, large increases in flow (+140%), and the largest drops (-68%) in MR. Because pressure loss due to friction predominates during baseline and pressure loss due to separation predominates during hyperemia (12), it seems reasonable to speculate that in this type of vessels, friction energy losses are small whereas separation energy losses are more substantial. Although the mechanisms leading to the observed large hyperemic rise in SR in this vessels’ subgroup are unclear, it seems plausible to suggest that these stenoses are prone to separation losses, either due to their fixed anatomical components or to hyperemic changes in their functional geometry (13), such as the partial collapsing as described by Brown et al. (13) and Siebes et al. (14) (“dynamic stenosis“) or hyperemic vasodilation at the exit throat (“D” losses) as proposed by Gould (12). Importantly and in spite of achieving final FFR values ≤0.80, the increase in flow in these vessels was high and did not statistically differ from that observed in the most normal (Pd/Pa >0.91 and FFR >0.80) D-vessels. This could be explained by the fact that SR only reached intermediate levels at hyperemia. Finally, the sizable drop in MR possibly indicates preserved autoregulation and microcirculatory function. Altogether, these findings help to justify why these hemodynamic patterns were more likely observed in younger subjects and in patients where hypertension was less likely, because hypertension (15) and increasing age (16) have been associated with a decrease in the hyperemic response. From a clinical point of view, our data suggest that the underlying CFR of most vessels with FFR ≤0.80 values arising from near-normal Pd/Pa values will not be exhausted by the stenosis. Figure 6 shows in-depth analyses of this assumption, where B-vessels (Pd/Pa >0.91 and FFR ≤0.80) were further examined according to more clinically meaningful CFR ischemic thresholds (1,17,18). Notably the same figure illustrates how among all vessels with Pd/Pa ≥0.96 (n = 149, 31.9%), only 15 (10.1%) developed FFR ≤0.80 (Figure 6), from which none had definite ischemia, as defined by CFR ≤1.74, and only 5 (3.4%) had mild to moderate ischemia, as defined by CFR >1.74 to <2.0 (1,17,18). Because substantial data support the notion that the risk of future adverse events is low when the CFR is preserved (1,17,18), it seems reasonable to question whether the small proportion of FFR ≤0.80 vessels arising from Pd/Pa values ≥0.96 will receive significant benefit from revascularization.
Vessels with baseline Pd/Pa ≤0.91 and FFR >0.80
Vessels exhibiting fairly important pressure drops at baseline (Pd/Pa ≤0.91) that did not significantly worsened during hyperemia (FFR >0.80) were the scarcest (7.5%). Herein, the increase in flow was moderate (+97%), and the drop (-54%) in MR was low. Because most of the energy loss during baseline is explained by viscous friction (12), it can be hypothesized that in these vessels, the fairly important pressure loss at baseline and the absence of a significant worsening (FFR ≤0.80) during hyperemia could suggest meaningful friction but small separation energy losses, findings compatible with predominant diffuse atherosclerosis (1,12). The concomitantly small drop in MR could alternatively suggest microcirculatory dysfunction as the cause of the moderately exhausted CFR (19). Interestingly, in this hemodynamic pattern, SR was intermediate at baseline and was significantly reduced (-33%) to low levels in hyperemia. The reduction in SR from baseline to hyperemia is a poorly described phenomenon, suggested by Brown et al. (13) and appraised invasively in humans by Sambuceti et al. (20). Although the mechanisms underlying this hyperemic decrease in SR are unclear, it seems plausible to suggest that diffuse atherosclerosis or less likely paradoxical hyperemic epicardial vasoconstriction (by modifying the functional geometry of the stenosis and decreasing separation losses at the exit throat) could lead to this condition (21,22). Finally, almost one-half of these vessels (48.6%) presented an exhausted CFR. Because a diminished CFR conveys a significant risk for future adverse events (1,18), it seems reasonable to question whether this subgroup of vessels might carry a worse prognosis in spite of an FFR value above 0.80.
First, Pd/Pa and FFR were used in a dichotomous fashion. Whereas this approach oversimplifies the continuum of risk, it also increases clinical applicability, and is currently advocated for FFR use. Second, different hyperemic routes and doses of adenosine were used, as well as methodologies to measure intracoronary flow. However, consistency in individual findings was noted between Doppler-vessels and Thermo-vessels, which we believe strengthens the external validity and implications of our observations. Third, investigated stenoses were of intermediate angiographic severity, so the generalization of our findings to other ranges of disease is unclear. Fourth and most importantly, clinical inference remains speculative, particularly in the light of the well-documented clinical benefit of FFR guidance of coronary revascularization as compared with that of angiography. Finally and even if initial invasive data is encouraging (7), it should be acknowledged that most of CFR prognostic information comes from noninvasive studies (1,18). Hence, caution should be urged when translating the powerful risk stratification of CFR to the invasive sphere. The DEFINE-FLOW (Combined Pressure and Flow Measurements to Guide Treatment of Coronary Stenoses) study (NCT02328820) is currently evaluating the safety of PCI deferral in vessels with low FFR but preserved CFR and will shed further lights on the topic.
In this work we sought to understand the physiological basis of baseline Pd/Pa and FFR agreement and discordance with combined pressure and flow measurements. Although Pd/Pa and FFR were closely correlated, discordance was observed in 19.3% of vessels. Such discordance was associated with the patient’s clinical profile and characterized by contrastive changes in SR, MR, and the underlying CFR. All stenosis with Pd/Pa ≤0.83 (n = 74, 15.8%) progressed to FFR ≤0.80, and although no Pd/Pa cutoff was able to exclude the development of an FFR ≤0.80 in the high end of values, only 15 vessels (10.1%) with Pd/Pa ≥0.96 (n = 149, 31.9%) developed FFR ≤0.80, from which none had definite ischemia, as defined by CFR ≤1.74. Combining baseline Pd/Pa with FFR seems thus to provide a more comprehensive physiological examination of stenosed coronary arteries.
WHAT IS KNOWN? Baseline Pd/Pa is always accessible before FFR assessment, and emerging data support the notion that baseline indices can determine the ischemic potential of coronary stenosis in selected subsets.
WHAT IS NEW? Discordance between baseline Pd/Pa and FFR is associated with the patients’ clinical profile and is characterized by contrastive changes in SR, MR, and CFR. CFR underlying a low or a high FFR is largely dependent on the initial Pd/Pa value. Combining baseline Pd/Pa with FFR seems to provide a more comprehensive physiological examination of stenosed coronary arteries.
WHAT IS NEXT? Future studies should focus now on the possible role of baseline physiology indices in the clinical decision-making process.
For a supplemental figure, please see the online version of this article.
Dr. Echavarría-Pinto has received speaking honoraria for educational events organized by St. Jude Medical and Volcano Corporation; and has received a clinical scholarship from Fundación Interhospitalaria Investigacion Cardiovascular. Dr. van de Hoef has received speaking honoraria for educational events organized by Boston Scientific, St. Jude Medical, and Volcano Corporation. Dr. Davies has received consulting fees, a research grant, and intellectual property royalties from Volcano Corporation. Dr. Piek serves on the advisory board of Abbott Vascular; and has received consulting fees from Mircacor. Dr. Escaned has received consulting fees and/or speaking honoraria for educational events organized by St. Jude Medical and Volcano Corporation. All other authors have reported that they have no relationships relevant to the contents of this paper to disclose. Drs. Echavarría-Pinto and van de Hoef contributed equally to this work.
- Abbreviations and Acronyms
- both baseline distal-to-aortic pressure ratio and fractional flow reserve are abnormal
- only fractional flow reserve is abnormal
- coronary flow reserve
- confidence interval(s)
- only baseline distal-to-aortic pressure ratio is abnormal
- both baseline distal-to-aortic pressure ratio and fractional flow reserve are normal
- fractional flow reserve
- microcirculatory resistance
- baseline distal-to-aortic pressure ratio
- quartile 1, quartile 3
- stenosis resistance
- thermodilution transit time
- Received January 26, 2015.
- Revision received August 24, 2015.
- Accepted September 8, 2015.
- American College of Cardiology Foundation
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