Key result
Levosimendan reduces focal loss of cross-striations ~75% versus control in human myocardial trabeculae.
Why the study?
The ability to limit ischemia-reperfusion injury remains largely unrealized, and whether levosimendan confers cardioprotection via an opioid-like mechanism in the human myocardium is unknown.
Does levosimendan reduce histological signs of ischemia-reperfusion injury in ex vivo human atrial trabeculae?
Does levosimendan reduce histological signs of ischemia-reperfusion injury in ex vivo human atrial trabeculae?
Levosimendan administered during re-oxygenation reduces histological signs of ischemia-reperfusion injury in isolated human atrial trabeculae.
Hypothesis-generating for levosimendan cardioprotection; prospective in vivo trials needed before clinical consideration.
The consequences of myocardial infarction (MI) are an increasing problem worldwide. Despite spectacular progress in the invasive treatment of ischemic heart disease, the ability to limit the ischemia-reperfusion (I/R) injury remains largely unrealized. Recent studies have shown that stimulation of opioid receptors may confer a cardioprotective effect against I/R injury. Levosimendan, the inodilator, is indicated for the short-term treatment of acutely decompensated heart failure. We tested the hypothesis that levosimendan may provide cardioprotection in the opioid-like mechanism in the human myocardium.
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Kunecki et al. (2022) studied Ischemia-reperfusion injury (n=10). Levosimendan vs. Control (ischemia-reperfusion protocol only) was evaluated on Focal loss of cross-striations (points) (p=0.012). Levosimendan significantly reduced the focal loss of cross-striations (2 vs. 8 points, p=0.012) and wavyform fibers (0 vs. 4 points, p=0.027) compared to control in human myocardial trabeculae.
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