Abstract 9697: Relation Between Measures of Ventricular Volume/Pressure and Myocardial Damage and Coronary Microvascular Dysfunction Response to Ranolazine

Abstract

Introduction: Late sodium channel inhibition with ranolazine may beneficially impact coronary microvascular dysfunction (CMD). We hypothesized that markers of ventricular volume/pressure (N-terminal -pro BNP [NT-proBNP]) and myocardial damage (ultra-high sensitivity cardiac troponin I [u-hs-TnI]) are related to therapeutic response. Methods: We analyzed CMD response in a randomized, double-blind, crossover trial of ranolazine vs. placebo using invasive coronary function testing or non-invasively cardiac magnetic resonance imaging (cMRI) myocardial perfusion reserve index (MPRI). NT pro-BNP and u-hs-TnI values were available in subgroups prior to trial enrollment. Treatment response was change in MPRI (Δ MPRI) or Seattle Angina Questionnaire, angina stability change (ΔSAQ). Spearman correlations and Wilcoxon Rank Sum test were used. Results: Among 128 participants, 12 had NT pro-BNP and 20 had u-hs-TnI available. Median NT pro-BNP and u-hs-TnI were (66 pg/mL) and (0.71 pg/mL), respectively. Higher u-hs-TnI (0.87pg/mL) positively correlated with improved ΔMPRI (Table), but not ΔSAQ (r= 0.03 p=0.80). No significant correlations between NT pro-BNP and ΔMPRI (r= -0.09, p=0.58) or ΔSAQ (r=0.005, P=0.976) were observed. Conclusion: Our study finds that higher u-hs-TnI, a measure of myocardial damage, related to improved cMRI perfusion reserve to the late-sodium channel blocker ranolazine. These results suggest that CMD accompanied by existing myocardial damage, likely secondary to ischemia, may have more favorable response to anti-ischemic therapy. Further studies are needed to validate these results in a larger cohort.