Abstract 12649: Can Coronary Wave Intensity Analysis Predict Infarct Size in Acute Coronary Syndromes?
INTRODUCTION: Microvascular dysfunction is the most important predictor of infarct size. Wave intensity analysis (WIA) distinguishes and quantifies the origin and nature of energy transfer in the coronary circulation. In stable coronary disease, flow is predominantly driven by a diastolic, microvascular-derived “suction” wave (backward expansion wave, BEW) and a systolic, aortic-driven forward compression wave (FCW) (Fig 1a). The utility of WIA in acute coronary syndromes (ACS) is unknown.
METHODS: NSTEMI and late-presenting STEMI patients within 7-days of their index event had simultaneous intra-coronary (IC) pressure-Doppler measurements following PCI in the infarct-related artery (IRA) and in a remote reference vessel (REF), during IC adenosine-induced hyperemia. Exclusions were prior MI, hemodynamic instability, and occluded IRA. Pearson regression analysis was used to correlate the magnitude of predominant waves with Troponin T (TnT) and quantitative late-gadolinium enhancement (LGE) Cardiac Magnetic Resonance (CMR) scar mass, defined as a 5 standard deviation increase in signal intensity compared to normal myocardium (Fig 1b).
RESULTS: 18 patients (56 ± 11 years) underwent IRA (44% LAD, 22% Cx, 33% RCA) and REF interrogation (44% Cx, 33% LAD, RCA 22%) at 90±51 hours post MI. 12-hour TnT was 1.61±1.59 µg/L. Predominating waves were BEW and FCW (-3.19 W m-2 s-2 and +2.64 W m-2 s-2 respectively). Peak BEW magnitude in the IRA showed a strong inverse correlation with both TnT (R2 = 0.53 p = 0.0004) and LGE-CMR infarct mass (n=11, R2 = 0.56 p = 0.0007) (Fig 1 c & d). BEW in the REF only weakly correlated with TnT and LGE, R2=0.36, p=0.01 and R2=0.34, p=0.03 respectively. FCW in the IRA also correlated with infarct size (R2 = 0.43, p = 0.002).
CONCLUSION: Coronary WIA in ACS correlates with the magnitude and location of myocardial infarction. BEW is most sensitive to infarction, which is likely to be a manifestation of microvascular dysfunction in the infarcted territory.
- © 2011 by American Heart Association, Inc.