- Journal
- CATHETERIZATION AND CARDIOVASCULAR INTERVENTIONS
- Année
- 2025
- Volume
- 106
- Numéro
- 7
- Pages
- 3588-3596
- Mois
- DEC
- DOI
- 10.1002/ccd.70268
Abstract
Background and Objectives: Fractional flow reserve (FFR) is a validated tool for assessing epicardial coronary stenosis. In myocardial infarction (MI), microvascular dysfunction may impair hyperemic flow, potentially affecting the interpretation of FFR measurement. The FLOVITA Study (NCT04818918) aimed to assess the impact of prior myocardial necrosis on absolute coronary blood flow and resistance using pressure wire-based continuous thermodilution. Methods: This prospective pilot study included 40 patients undergoing coronary physiological assessment of the left anterior descending (LAD) artery between May 2021 and February 2024. Patients were stratified into two groups: recent anterior ST-elevation MI (n = 23) and controls without history or imaging evidence of MI (n = 17). Absolute coronary blood flow and microvascular resistance were measured using pressure wire-derived continuous thermodilution. This novel technique allows direct, operator-independent quantification of coronary flow and microvascular resistance, offering high reproducibility. Multivariable linear regression identified factors associated with absolute coronary blood flow. Results: LAD absolute blood flow was significantly lower in the MI group compared to controls (0.169 +/- 0.005 vs. 0.215 +/- 0.05 L/min; p = 0.006), despite similar FFR values and macrovascular resistance. Infarct size and microvascular resistance were independently associated with reduced flow. Each 10% increase in infarct size was associated with a 0.01 L/min reduction in LAD flow (p = 0.026), while a 100 WU increase in microvascular resistance corresponded to a 0.02 L/min decrease (p < 0.001). Conclusion: The FLOVITA study is a proof-of-concept analysis suggesting that MI significantly reduces coronary blood flow through increased microvascular resistance. These findings underscore the importance of accounting for microvascular dysfunction when interpreting post-MI coronary physiology.