Myocardial biomarkers in coronary microvascular dysfunction: Response to ranolazine

IF 1.3 Q3 CARDIAC & CARDIOVASCULAR SYSTEMS

American heart journal plus : cardiology research and practice Pub Date : 2025-02-21 DOI:10.1016/j.ahjo.2025.100513

Katherine E. Hampilos , Anum Asif , Puja K. Mehta , Daniel S. Berman , Galen Cook-Wiens , Michael D. Nelson , Carl J. Pepine , C. Noel Bairey Merz , Janet Wei

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Abstract

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.

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冠状动脉微血管功能障碍的心肌生物标志物：对雷诺嗪的反应

冠状动脉微血管功能障碍（CMD）患者发生保留射血分数（HFpEF）心力衰竭的风险增加。我们假设较高的心肌生物标志物（超高敏感性心肌肌钙蛋白I [u-hs-TnI]）和心室功能障碍（n端亲bnp [NT-proBNP]）可能与晚期钠通道抑制剂雷诺嗪对缺血的改善有关。方法：我们分析了基线心肌生物标志物随机分配到雷诺嗪或安慰剂组的CMD参与者（RWISE试验：NCT01342029）。缺血反应观察心肌灌注储备指数（∆MPRI）或西雅图心绞痛问卷（∆SAQ）的变化。结果在64名u-hs-TnI和40名NT-proBNP随机组中，较高的u-hs-TnI与雷诺嗪改善的∆MPRI相关（r = 0.26, p = 0.04），而与改善的∆SAQ无关（r = 0.03, p = 0.80）。与NT-proBNP无关。结论较高的u-hs-TnI表明雷诺嗪对缺血的改善作用更大。需要进一步的研究来评估CMD的缺血治疗，以开发潜在的HFpEF预防靶点。

本文章由计算机程序翻译，如有差异，请以英文原文为准。

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