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Dynamic Damping of the Aortic Pressure Trace During Hyperemia: The Impact on Fractional Flow Reserve Measurement

Tim Lockie, MBChB, PhD1,2, M. Cristina Rolandi, MSc3, Jan J. Piek, MD, PhD1

October 2013

Abstract: We report on two cases that illustrate an important caveat in the measurement of fractional flow reserve (FFR) in coronary arteries. To obtain accurate FFR measurements, two fundamental requirements must be fulfilled. One is to minimize microvascular resistance; the other is that there is no damping of the proximal aortic pressure trace. A problem with either of these requirements can be a source of serious error in the measurement of FFR. In each case we present here, despite a good aortic pressure trace at the start of the procedure, there is dynamic damping of the pressure trace during hyperemia, secondary to axial migration of the guiding catheter into the left main stem (LMS). In both cases, a normal aortic pressure trace (Pa) is present at baseline. After intracoronary adenosine injection, there was a fall in both mean Pa and distal coronary pressure (Pd) concomitant with damping of Pa, evidenced by loss of the dicrotic notch and ventricularization of the pressure trace. The resultant FFR value is underestimated. As hyperemia wears off, both pressure traces return to normal with good articulation of the dicrotic notch. When the procedure was repeated taking care to ensure that the guide did not move into the LMS during hyperemia, the Pa trace remained stable following intracoronary adenosine, while mean Pd decreased as before. In both cases, hemodynamically significant lesions were demonstrated that had been masked by the artifactual drop in Pa during the first attempt.

J INVASIVE CARDIOL 2013;25(10):549-550

Key words: fractional flow reserve, pressure tracing

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We report two cases that illustrate an important caveat in the measurement of fractional flow reserve (FFR) in coronary arteries. To obtain accurate FFR measurements, two fundamental requirements must be fulfilled. One is to minimize microvascular resistance, usually through either intracoronary injection or systemic venous infusion of adenosine to maximally vasodilate the microvascular bed.1,2 The other is that there is no damping of the proximal aortic pressure trace, most commonly transduced through the guiding catheter at the coronary ostium.3 A problem with either of these requirements can be a source of serious underestimation of the severity of FFR. To satisfy the second of these conditions, it is essential to position the guiding catheter correctly.

Case Descriptions

We report two cases where despite a good aortic pressure trace at the start of the procedure, there is damping of the dynamic pressure trace during hyperemia, secondary to axial migration of the guide into the left main stem (LMS). This is especially an issue with Q/CLS/EBU/Voda-shaped guiding catheters, which have more of a tendency to deeply intubate the LMS than Judkins-shaped guides. Both of the cases involved intermediate-severity left anterior descending (LAD) arterial stenoses in middle-aged, average-sized males presenting with stable angina (Figure 1). A 6 Fr CLS 3.5 guiding catheter and a standard 0.014˝ intracoronary pressure wire (Volcano PrimeWire) via the right radial approach were used. A total of 500 µg of intracoronary nitrates were administered beforehand and hyperemia was achieved with 48 µg intracoronary injections of adenosine, as is standard for our institution.  

It can be seen that in both cases a normal aortic pressure trace (Pa) is present at baseline with a clearly visible dicrotic notch (Figure 2, top panels). After intracoronary adenosine injection, there is a fall in both mean Pa and distal coronary pressure (Pd) concomitant with damping of Pa, evidenced by loss of the dicrotic notch and ventricularization of the pressure trace. The resultant FFR is underestimated, suggesting the lesion is not hemodynamically significant and would, therefore, not benefit from revascularization.4 As hyperemia wears off, both pressure traces return to normal with good articulation of the dicrotic notch. When the procedure was repeated, taking care to ensure that the guide did not move into the LMS during hyperemia, the Pa trace remained stable following intracoronary adenosine, while mean Pd decreased as before (Figure 2, bottom panels). Subsequently, in both cases, hemodynamically significant lesions were demonstrated with FFR values of 0.73 and 0.74, respectively; values that had been masked by the artifactual drop in Pa during the first attempt, and now falling into the category where revascularization would be beneficial.4 

Discussion

These pressure tracings reinforce the caveat that both proximal and distal pressure traces should be closely monitored throughout the period of FFR measurement and care taken that there is no forward axial movement of the guiding catheter during hyperemic flow that may give rise to erroneous FFR results. Ways to avoid this pitfall include backing the guiding catheter from the ostium immediately after adenosine injection, or using a continuous intravenous infusion of adenosine that does not require good catheter engagement, although care must still be taken to ensure that the guide does not move forward during hyperemia. 

Conclusion

Damping of the aortic trace is an important source of error in measuring FFR due to forward motion of the guiding catheter during hyperemic coronary blood flow. Normal pressure traces at the beginning and end of the case may be misleading and cause false reassurance.

References

  1. Kern MJ, Lerman A, Bech JW, et al. Physiological assessment of coronary artery disease in the cardiac catheterization laboratory: a scientific statement from the American Heart Association Committee on Diagnostic and Interventional Cardiac Catheterization, Council on Clinical Cardiology. Circulation. 2006;114(12):1321-1341.
  2. Pijls NH, De Bruyne B, Peels K, et al. Measurement of fractional flow reserve to assess the functional severity of coronary-artery stenoses. N Engl J Med. 1996;334(26):1703-1708.
  3. Pijls NH, Kern MJ, Yock PG, De Bruyne B. Practice and potential pitfalls of coronary pressure measurement. Catheter Cardiovasc Interv. 2000;49(1):1-16.
  4. Pijls NH, van Schaardenburgh P, Manoharan G, et al. Percutaneous coronary intervention of functionally nonsignificant stenosis: 5-year follow-up of the DEFER study. J Am Coll Cardiol. 2007;49(21):2105-2111.
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From the 1Department of Cardiology, Academic Medical Center, University of Amsterdam, Amsterdam, The Netherlands, 2King’s College London British Heart Foundation Centre of Excellence, and The Rayne Institute, St Thomas’ Hospital Campus, London, United Kingdom; 3Department of Biomedical Engineering and Physics, Academic Medical Center, University of Amsterdam, Amsterdam, The Netherlands.

Funding: Dr Lockie is supported by a grant from the British Heart Foundation; Dr Rolandi is supported by an AMC PhD Scholarship. 

Disclosure: The authors have completed and returned the ICMJE Form for Disclosure of Potential Conflicts of Interest. Dr Piek is a consultant for Miracor and on the board of Abbott Vascular. 

Manuscript submitted May 20, 2013, provisional acceptance given August 7, 2013, final version accepted August 14, 2013.

Address for correspondence: Professor J.J. Piek, Department of Cardiology, Academic Medical Center, Meibergdreef 9, Room B2-250, PO Box 22660, 1100 DD Amsterdam, The Netherlands. Email: j.j.piek@amc.uva.nl

 


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