Abstract 19177: Loss of Coronary Perfusion Efficiency in Microvascular Disease
Introduction: Coronary Microvascular Disease (MVD) is associated with an unfavorable prognosis, even in the absence of significant epicardial disease. The pathophysiological basis of increased cardiac events is unclear. The aim of this study was to characterize the forces that govern myocardial perfusion at rest and during stress.
Methods: Patients with chest pain syndromes requiring Fractional Flow Reserve (FFR) assessment were screened and those with a FFR>0.80 were included. MVD was defined by coronary flow reserve (CFR) < 2.0. Controls were those with CFR>2.0. Simultaneous intracoronary pressure (Pd) and flow velocity (U) recordings were made at rest and hyperemia. Microvascular Resistance (MR)= Pd/U. Wave intensity = dPd/dt x dU/dt and wave separation analysis was used to identify the waves that accelerate and decelerate flow. The proportional contribution of accelerating waves was assessed as an index of coronary perfusion efficiency.
Results: 39 consecutive patients were enrolled, 21 had MVD and 18 comprised controls. The groups were matched for atherosclerotic risk factors, rate-pressure-product and Pd. Coronary flow velocity in MVD patients was higher at rest (21.5±6.4 vs. 14.1±4.5cms-1, p < 0.001) but lower during hyperemia (28.3±13.0 vs. 45.1±13.1cms-1, p < 0.001) compared to controls. While resting MR was lower in MVD (501±162 vs. 755±262 mmHg.cm-1.s, p = 0.001), hyperemic MR was significantly lower in controls. At rest the magnitude of the accelerating waves was higher in the MVD group than controls. The percentage contribution of accelerating waves increased with hyperemia in controls but decreased in MVD patients (figure).
Conclusion: MVD manifests as resting microvascular dilation as well as diminished response to stress. While the normal heart has improved efficiency during hyperemia, in MVD efficiency decreases and as a result, flow augmentation is attenuated. These processes render the myocardium more susceptible to ischemia.
Author Disclosures: M. Lumley: None. M. Ryan: None. K. Asrress: None. R. Williams: None. S. Ari: None. H. Ellis: None. N. Briceno: None. S. Redwood: None. B. Clapp: None. M. Marber: None. D. Perera: None.
- © 2015 by American Heart Association, Inc.