Myocardial biomarkers in coronary microvascular dysfunction: Response to ranolazine

Introduction

Patients with coronary microvascular dysfunction (CMD) are at increased risk of developing heart failure with preserved ejection fraction (HFpEF). We hypothesized that higher myocardial biomarkers (ultra-high sensitivity cardiac troponin I [u-hs-TnI]) and ventricular dysfunction (N-terminal pro-BNP [NT-proBNP]) would be related to greater ischemia improvement on the late sodium channel inhibitor ranolazine.

Methods

We analyzed CMD participants with baseline myocardial biomarkers randomized to ranolazine or placebo (RWISE trial: NCT01342029). Ischemia response was change in global myocardial perfusion reserve index (∆MPRI) or Seattle Angina Questionnaire (∆SAQ).

Results

Among 64 randomized participants with u-hs-TnI and 40 with NT-proBNP, higher u-hs-TnI related to improved ∆MPRI (r = 0.26, p = 0.04), but not ∆SAQ (r = 0.03, p = 0.80) on ranolazine. There was no relation with NT-proBNP.

Conclusions

These findings suggest that higher u-hs-TnI signals greater ischemia improvement on ranolazine. Further studies evaluating ischemia therapies in CMD are needed to develop potential HFpEF prevention targets.