Troponin I levels in permanent atrial fibrillation-impact of rate control and exercise testing

Anja Wiedswang Horjen1,2, Sara Reinvik Ulimoen3, Steve Enger3

  • 1Department of Medical Research, Baerum Hospital, Vestre Viken Hospital Trust, N-3004, Drammen, Norway. awhorjen@gmail.com.

Insights

Rate-controlling drugs significantly reduced high-sensitivity troponin I (hs-TnI) in atrial fibrillation patients. Verapamil showed a greater reduction in hs-TnI compared to hs-TnT, unlike other tested medications.

Area of Science:

  • Cardiology
  • Clinical Pharmacology

Background:

  • High-sensitivity troponin I (hs-TnI) and troponin T (hs-TnT) are biomarkers for cardiovascular risk in atrial fibrillation (AF).
  • Rate-controlling therapies are known to impact hs-TnT, but their effect on hs-TnI remains under-investigated.

Purpose of the Study:

  • To investigate the impact of four rate-controlling drug regimens on hs-TnI levels in patients with stable, permanent AF.
  • To compare the effects of these drugs on hs-TnI versus hs-TnT.

Main Methods:

  • A randomized crossover study involving 60 stable AF patients without heart failure or ischemic heart disease.
  • Patients received diltiazem, verapamil, metoprolol, or carvedilol daily for three weeks.
  • hs-TnI and hs-TnT were measured at rest and after maximal exercise at baseline and after each treatment period.

Main Results:

  • All tested drugs significantly reduced resting and peak exercise hs-TnI levels.
  • Verapamil demonstrated a greater reduction in hs-TnI compared to hs-TnT, unlike other regimens.
  • Exercise testing revealed a significantly larger relative increase in hs-TnI compared to hs-TnT across baseline and all treatment regimens.

Conclusions:

  • All four rate-controlling drug regimens effectively reduced hs-TnI in stable AF patients, both at rest and during exercise.
  • The reduction in hs-TnI and hs-TnT was similar for beta-blockers and calcium channel blockers, with verapamil showing a distinct effect on hs-TnI.
  • These findings highlight differential effects of rate-controlling agents on troponin isoforms in AF patients.
Abstract

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