Left ventricular end-diastolic pressure affects measurement of fractional flow reserve

Abstract

Background Fractional flow reserve (FFR), the hyperemic ratio of distal (Pd) to proximal (Pa) coronary pressure, is used to identify the need for coronary revascularization. Changes in left ventricular end-diastolic pressure (LVEDP) might affect measurements of FFR. Methods and Materials LVEDP was recorded simultaneously with Pd and Pa during conventional FFR measurement as well as during additional infusion of nitroprusside. The relationship between LVEDP, Pa, and FFR was assessed using linear mixed models. Results Prospectively collected data for 528 cardiac cycles from 20 coronary arteries in 17 patients were analyzed. Baseline median Pa, Pd, FFR, and LVEDP were 73 mmHg, 49 mmHg, 0.69, and 18 mmHg, respectively. FFR < 0.80 was present in 14 arteries (70%). With nitroprusside median Pa, Pd, FFR, and LVEDP were 61 mmHg, 42 mmHg, 0.68, and 12 mmHg, respectively. In a multivariable model for the entire population LVEDP was positively associated with FFR such that FFR increased by 0.008 for every 1-mmHg increase in LVEDP (beta = 0.008; P < 0.001), an association that was greater in obstructed arteries with FFR < 0.80 (beta = 0.01; P < 0.001). Pa did not directly affect FFR in the multivariable model, but an interaction between LVEDP and Pa determined that LVEDP’s effect on FFR is greater at lower Pa. Conclusions LVEDP was positively associated with FFR. The association was greater in obstructive disease (FFR < 0.80) and at lower Pa. These findings have implications for the use of FFR to guide revascularization in patients with heart failure. Summary for Annotated Table of Contents The impact of left ventricular diastolic pressure on measurement of fractional flow reserve (FFR) is not well described. We present a hemodynamic study of the issue, concluding that increasing left ventricular diastolic pressure can increase measurements of FFR, particularly in patients with FFR < 0.80 and lower blood pressure.

Low Coronary Microcirculatory Resistance Associated With Profound Hypotension During Intravenous Adenosine Infusion

“…41 It remains uncertain whether the marked fall in microcirculatory resistance in patients with profound hypotensive responses to intravenous adenosine obeys to an exacerbated response to adenosine-potentially triggered by impaired sympathetic autonomic or adenosine A 1 receptor function-or a decrease in zero flow pressure as a result of decreased left ventricular end-diastolic pressure, which has been reported to influence FFR interrogation. 42,43 Nevertheless, the potential contribution of this phenomenon to overestimation of coronary stenosis severity is supported by the obtained CFR measurements in our study because the observed proportion of vessels with CFR values >2 despite FFR ≤0.80 was significantly higher during profound hypotensive responses. This is of particular relevance because it has been proposed that patients in this quadrant of the FFR-CFR classification should not be treated on the grounds of documented preserved myocardial flow.…”

The FAME Trials: Impact on Clinical Decision Making

“…Regarding the secondary endpoints, while the reduction of all-cause mortality rates (1.8 versus 3.0 %; p=0. 19), and reduction in MI rates (5.7 versus 8.7 %; p=0.07) were not significant, the reduction in the rates of the combined endpoints-a non prespecified secondary endpoint-(7.3 versus 11.1 %; p=0.04) was statistically significant. Collateral benefit of the FFR strategy was a decrease in the number of stents, a decrease in the amount of contrast and radiation time, resulting in a decrease in procedurerelated costs.…”

Clinical Application of Fractional Flow Reserve–Guided Percutaneous Coronary Intervention for Stable Coronary Artery Disease

“…It is essential to confirm lack of a pressure drop in such scenarios [37]. Similarly in patients with elevated left ventricular diastolic pressure, the FFR can be elevated especially in low blood pressures [38]. Caffeine has been shown to prevent adenosine-induced hyperemia [39].…”