Prognostic value of microvascular resistance and its association to fractional flow reserve: a DEFINE-FLOW substudy

Ashkan Eftekhari1,2, Jelmer Westra3, Valérie Stegehuis4

  • 1Department of Cardiology, Aarhus University Hospital Skejby, Aarhus, Denmark asef@rn.dk.

Open Heart
|April 12, 2022
PubMed

Insights

Hyperemic microvascular resistance (HMR) did not predict adverse events in stable coronary artery disease patients. Fractional flow reserve (FFR) can be represented by the ratio of HMR to total resistance, linking epicardial and microvascular measures.

Area of Science:

  • Cardiovascular Medicine
  • Interventional Cardiology
  • Physiology

Background:

  • Coronary artery disease (CAD) management relies on assessing stenosis severity.
  • Fractional flow reserve (FFR) is a key metric, but microvascular function also impacts outcomes.
  • Understanding the interplay between epicardial stenosis and microvascular resistance is crucial for prognosis.

Purpose of the Study:

  • To investigate the prognostic value of hyperemic microvascular resistance (HMR).
  • To explore the relationship between HMR, hyperemic stenosis resistance (HSR), and FFR.
  • To determine if HMR predicts adverse clinical events in stable CAD.

Main Methods:

  • Substudy of the DEFINE-FLOW cohort (NCT02328820) including 430 patients.
  • Wire-based measurement of coronary pressure, flow, and resistance.
  • Combined assessment of FFR, coronary flow reserve (CFR), HMR, and HSR.

Main Results:

  • Mean FFR was 0.82±0.10 and mean CFR was 2.2±0.6.
  • HMR was highest in lesions with FFR>0.80 and CFR<2.0 (2.92±1.2 mm Hg/cm/s).
  • FFR correlated strongly with the HMR/(HMR+HSR) ratio (r²=0.98, p<0.0001).
  • Increased HMR did not correlate with higher rates of target vessel failure (HR 1.51, p=0.10).

Conclusions:

  • In stable CAD patients, elevated HMR was not associated with increased adverse clinical events.
  • FFR can be conceptually reformulated as HMR/(HMR+HSR), integrating epicardial and microvascular resistance.
  • This provides an alternative framework for understanding coronary lesion physiology.
Abstract