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-ter...
Saved in:
| Main Authors: | , , , , , , , , |
|---|---|
| Format: | Article |
| Language: | English |
| Published: |
Elsevier
2025-04-01
|
| Series: | American Heart Journal Plus |
| Subjects: | |
| Online Access: | http://www.sciencedirect.com/science/article/pii/S2666602225000163 |
| Tags: |
Add Tag
No Tags, Be the first to tag this record!
|
| Summary: | 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. |
|---|---|
| ISSN: | 2666-6022 |