Association between blood pressure and invasive hemodynamic measures in myocardial bridging
The dynamic nature of a myocardial bridge (MB) makes invasive hemodynamic assessment more complex than atherosclerotic coronary artery disease (CAD), and the influence of blood pressure (BP) on these measurements remains unclear. We investigated whether BP affects the hemodynamic significance of myocardial bridges (MBs), and compared this with CAD and normal vessels as a reference. We included 63 patients with an MB who underwent dobutamine resting full-cycle ratio (RFR) measurements, and compared them against reference groups of 85 patients with CAD and 45 patients with normal coronaries who underwent RFR and adenosine fractional flow reserve (FFR). Regression analyses were used to assess the relation between BP parameters and hemodynamic measurements. Higher systolic BP was associated with higher RFR values (i.e., less functionally significant lesions) in patients with an MB (0.03 RFR increase per 20 mmHg systolic blood pressure rise; <i>P</i> < 0.05) and in patients with CAD (0.01 RFR increase per 20 mmHg systolic blood pressure rise; <i>P</i> < 0.05). Pulse pressure showed the strongest association, with a 20 mmHg higher pulse pressure associated with a 0.05 higher dobutamine RFR in MBs and a 0.02 higher RFR in CAD (both <i>P</i> < 0.05). In patients with an MB, this relation was only present with low maximal MB compression (≤36%), and no relation was observed with more severe MB compression (<i>P</i><sub>interaction</sub> < 0.05). Higher procedural BP is associated with higher hemodynamic index values (i.e., less functionally significant lesions) in myocardial bridging, suggesting BP should be considered when interpreting measurements near treatment thresholds.<b>NEW & NOTEWORTHY</b> Higher procedural blood pressure (BP) is associated with less significant hemodynamic measures in myocardial bridging, suggesting BP should be considered when interpreting borderline hemodynamic measurements.
Authors
- Vedant Pargaonkar (ORCID: https://orcid.org/0000-0002-6765-6560)
- A. Yong (ORCID: https://orcid.org/0000-0002-6268-4300)
- Ingela Schnittger (ORCID: https://orcid.org/0000-0001-8476-2755)
- Luke P. Dawson (ORCID: https://orcid.org/0000-0003-3789-5808)
- Jennifer A. Tremmel (ORCID: https://orcid.org/0000-0001-6620-9139)
- Samit Shah (ORCID: https://orcid.org/0000-0002-3664-4102)
- Chinmay Khandkar (ORCID: https://orcid.org/0000-0002-0201-2262)
- William F. Fearon (ORCID: https://orcid.org/0000-0003-1799-1368)
- Christopher Wong (ORCID: https://orcid.org/0000-0002-0180-0072)
Institutions
- The University of Sydney (AU)
- Concord Hospital (US)
- Yale New Haven Hospital (US)
- VA Palo Alto Health Care System (US)
- Royal Prince Alfred Hospital (AU)
- Concord Repatriation General Hospital (AU)
- Australian Regenerative Medicine Institute (AU)
- Yale University (US)
- Palo Alto Veterans Institute for Research (US)
- Monash University (AU)
- Stanford University (US)
Publication Details
- Journal
- American Journal of Physiology-Heart and Circulatory Physiology
- Published
- 2025-11-10
- DOI
- https://doi.org/10.1152/ajpheart.00560.2025
- Primary Topic
- Coronary Artery Anomalies
- Type
- article
- Field-Weighted Citation Impact
- 0.00