Key result
Remifentanil applied during reperfusion significantly improved the contractile function of human ischemic cardiomyocytes compared to control (42.7% vs. 26.9% at 60 minutes), whereas sufentanil showed no cardioprotective effect.
Why the study?
Animal models suggested delta-opioid receptor signaling drives opioid cardioprotection, leading investigators to hypothesize that mu-opioid receptor activation protects human heart muscle.
Does remifentanil or sufentanil improve contractility in human ischemic heart muscle in vitro?
Does remifentanil or sufentanil improve contractility in human ischemic heart muscle in vitro?
Absolute Event Rate: 42.7% vs 26.9%
p-value: p=0.04
Remifentanil, but not sufentanil, induces a cardioprotective effect on human right atria muscle in vitro, manifested as increased contraction amplitude during reperfusion.
Does not support clinical use of remifentanil for cardioprotection; leaves open translation from in vitro human cardiomyocytes to patient outcomes.
BACKGROUND: Previous studies on animal models have suggested that δ-opioid receptor (OR) signaling is the primary pathway responsible for opioids' cardioprotective effect. We hypothesize that the μ-OR's activation protects the human heart muscle. METHODS: We performed the experiments on muscular trabeculae obtained from the right atrial appendages of 104 consecutive patients subjected to coronary artery bypass surgery. Two trabeculae from each patient were studied simultaneously and exposed to 60 min of hypoxia with subsequent 60 min of reoxygenation. Remifentanil (5 μM or 50 μM) or sufentanil (40 μM or 400 μM) was used from the time of reoxygenation. Trabeculae contractility was assessed as the maximal amplitude of the contraction at baseline, after 60 min of hypoxia, during reoxygenation, and after norepinephrine application. RESULTS: During reperfusion, the application of remifentanil improved cardiomyocytes' function as compared to the control group (time from reperfusion: 15 min: 39.8% vs. 21.7%, p = 0.01; 30 min: 41.4% vs. 21.8%, p = 0.01; 60 min: 42.7% vs. 26.9%, p = 0.04; after norepinephrine: 64.7% vs. 43.2%, p = 0.03). The application of sufentanil did not influence cardiomyocyte function as can be seen when comparing the results of the experimental and control group. CONCLUSIONS: Remifentanil, but not sufentanil, induces a cardioprotective effect on human right atria muscle in in vitro conditions, manifested as the increased amplitude of their contraction during reperfusion after 60 min of ischemia.
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Kunecki et al. (2023) studied Ischemic heart disease (n=104). Remifentanil vs. Control (hypoxia protocol only) was evaluated on Maximal amplitude of contraction at 60 minutes of reperfusion (% of baseline) (p=0.04). Remifentanil applied during reperfusion significantly improved the contractile function of human ischemic cardiomyocytes compared to control (42.7% vs. 26.9% at 60 minutes), whereas sufentanil showed no cardioprotective effect.
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