Author + information
- Nils P. Johnson, MD, MS∗ (, )
- Richard L. Kirkeeide, PhD and
- K. Lance Gould, MD
- ↵∗Weatherhead PET Center, McGovern Medical School at UTHealth, 6431 Fannin Street, Room MSB 4.256, Houston, Texas 77030
We are relieved that Härle et al. (1) conclude that the laws of nature hold in their laboratory. Although an elaborate experimental setup was not strictly necessary to estimate hydrostatic effects, their results confirm hundreds of years of fundamental physics, as well as decades of coronary physiology (2). The consequences for intracoronary pressure measurements, however, require a few clarifications.
First, as agreed by the authors in their discussion, the hydrostatic effect is usually <5 mm Hg, given typical cardiac dimensions that limit the height difference between the coronary ostium and distal pressure sensor. Because a fractional flow reserve (FFR) value below the 0.75 to 0.80 grey zone has an absolute gradient of about 20 to 30 mm Hg, depending on aortic pressure, a 5 mm Hg offset will not cross from <0.75 to >0.80 or vice versa. As such, hydrostatic effects join a host of other minor factors (central venous pressure, drift, obstruction from the guide, test/retest of adenosine) that contribute to a non-zero, but clinically excellent, FFR imprecision (3). However, because instantaneous wave-free ratio values below 0.90 usually have a 10 mm Hg gradient, the same 5 mm Hg offset causes a much larger relative effect.
Second, daily experience contradicts their statement that “further research is advisable on how to perform corrections for the deviations in the values of both indices attributable to variations in relative sensor height.” Whatever correction for hydrostatic forces applied when supine in the catheterization laboratory (or derived from a supine computed tomography angiogram) does not apply when angina occurs during upright exertion.
Third, quantitation invalidates their statement that the “findings of our study provide an alternative explanation to the gradual loss of pressure observed in longitudinal pressure pullbacks.” Although clearly a minor contribution, a 5 mm Hg or smaller hydrostatic effect cannot account for the vast majority of a 31 mm Hg gradient as observed in a subject in that study or the 8% of its subjects with an FFR <0.75 (4). Significant, longitudinal pressure gradients exist in some patients due to the presence of severe, diffuse atherosclerotic disease, not trivial hydrostatic forces.
Finally, clinical studies relating FFR to noninvasive testing and clinical outcomes from observational and randomized trials have neglected hydrostatic gradients yet demonstrated a profound benefit from FFR assessment, attesting to the clinically insignificant impact of hydrostatic forces.
Therefore, the results from Härle et al. (1) confirm that hydrostatic effects are not important for invasive FFR assessment—don’t let the pressure get to your head!
Please note: The authors have received internal funding from the Weatherhead PET Center for Preventing and Reversing Atherosclerosis; and have an institutional licensing and consulting agreement with Boston Scientific for the smart minimum FFR algorithm. Dr. Johnson has received significant institutional research support from St. Jude Medical (CONTRAST, NCT02184117) and Volcano/Philips Corporation (DEFINE-FLOW, NCT02328820) for studies using intracoronary pressure and flow sensors. Dr. Gould is the 510(k) applicant for CFR Quant (K113754) and HeartSee (K143664) software packages for cardiac positron emission tomography image processing, analysis, and absolute flow quantification.
- 2017 American College of Cardiology Foundation
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- Meyer S.,
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