Background: In patients with acute myocardial infarction, the one-year mortality remains at 7-15% despite successful interventional reperfusion. Thus, innovative treatment strategies beyond reperfusion are needed. In isolated perfused rat hearts, triiodothyronine (T3), when given during early reperfusion in a supraphysiological concentration, improves left ventricular function and reduces infarct size (Basic Res Cardiol 2021;116:27).

Aim: To investigate whether or not such acute, non-genomic effects of T3 also protect human myocardium.

Methods: We isolated right atrial trabeculae from patients undergoing routine coronary artery bypass grafting and investigated the effect of T3 on contractile function during hypoxia/reoxygenation. Trabeculae (≥ 3 mm length, ≤ 1 mm diameter) were isolated in cardioplegic buffer and transferred to Tyrode buffer. Electrically initiated (1 Hz) developed force of contraction (mN/mm²) was recorded for 10 min at baseline (95% O₂ – 5% CO₂, glucose). Hypoxia/reoxygenation (60 min/30 min) was induced by changing the buffer gas supply and composition and by increasing the stimulation rate (95% N₂ – 5% CO₂, choline chloride, 3 Hz) and returning back to baseline. T3 (500 µg/l) or NaOH (as solvent control), respectively, was administered A) during hypoxia and reoxygenation (n=11 vs. n=10) or B) 15 min before and during reoxygenation (n=12 vs. n=14).

Results: At baseline, before T3 or NaOH treatment, the contractile function of trabeculae was comparable (mN/mm²: 15.4±3.5, 13.8±4.4 in protocol A, and 14.5±4.1, 13.7±4.0 in protocol B, respectively). T3 improved the contractile function during reoxygenation, irrespectively of whether given continuously (A) or just before and during reoxygenation (B; see Figure).

Conclusion: T3 protects patient myocardium: contractile function is improved during reoxygenation in right atrial trabeculae. This bioassay will now permit an identification of causally involved cardioprotective signaling molecules of such non-genomic protection in human tissue by T3.