Mohl Werner, Kiseleva Zlata, Jusic Alem, Bruckner Matthäus, Mader Robert M
Department of Cardiac Surgery, Medical University of Vienna, Vienna, Austria.
Department of Medicine I, Comprehensive Cancer Center of the Medical University of Vienna, Vienna, Austria.
Front Cardiovasc Med. 2023 May 9;10:1030842. doi: 10.3389/fcvm.2023.1030842. eCollection 2023.
Inducing recovery in myocardial ischemia is limited to a timely reopening of infarct vessels and clearing the cardiac microcirculation, but additional molecular factors may impact recovery.
In this scoping review, we identify the paradigm shifts decoding the branching points of experimental and clinical evidence of pressure-controlled intermittent coronary sinus occlusion (PICSO), focusing on myocardial salvage and molecular implications on infarct healing and repair.
The reporting of evidence was structured chronologically, describing the evolution of the concept from mainstream research to core findings dictating a paradigm change. All data reported in this scoping review are based on published data, but new evaluations are also included.
Previous findings relate hemodynamic PICSO effects clearing reperfused microcirculation to myocardial salvage. The activation of venous endothelium opened a new avenue for understanding PICSO. A flow-sensitive signaling molecule, miR-145-5p, showed a five-fold increase in porcine myocardium subjected to PICSO.Verifying our theory of "embryonic recall," an upregulation of miR-19b and miR-101 significantly correlates to the time of pressure increase in cardiac veins during PICSO ( = 0.90, < 0.05; = 0.98, < 0.03), suggesting a flow- and pressure-dependent secretion of signaling molecules into the coronary circulation. Furthermore, cardiomyocyte proliferation by miR-19b and the protective role of miR-101 against remodeling show another potential interaction of PICSO in myocardial healing.
Molecular signaling during PICSO may contribute to retroperfusion toward deprived myocardium and clearing the reperfused cardiac microcirculation. A burst of specific miRNA reiterating embryonic molecular pathways may play a role in targeting myocardial jeopardy and will be an essential therapeutic contribution in limiting infarcts in recovering patients.
心肌缺血的恢复仅限于及时重新开通梗死血管和清除心脏微循环，但其他分子因素可能会影响恢复情况。
在本范围综述中，我们确定了范式转变，解读压力控制间歇性冠状静脉窦闭塞（PICSO）的实验和临床证据的分支点，重点关注心肌挽救以及对梗死愈合和修复的分子影响。
证据报告按时间顺序构建，描述了该概念从主流研究到决定范式转变的核心发现的演变。本范围综述中报告的所有数据均基于已发表的数据，但也包括新的评估。
先前的研究结果将血流动力学PICSO效应清除再灌注微循环与心肌挽救联系起来。静脉内皮的激活为理解PICSO开辟了一条新途径。一种对血流敏感的信号分子miR-145-5p在接受PICSO的猪心肌中增加了五倍。验证我们的“胚胎回忆”理论，miR-19b和miR-101的上调与PICSO期间心脏静脉压力升高的时间显著相关（r = 0.90，P < 0.05；r = 0.98，P < 0.03），表明信号分子向冠状动脉循环的分泌与血流和压力有关。此外，miR-19b促进心肌细胞增殖以及miR-101对重塑的保护作用显示了PICSO在心肌愈合中的另一种潜在相互作用。
PICSO期间的分子信号传导可能有助于向缺血心肌进行逆向灌注并清除再灌注的心脏微循环。特定miRNA的爆发重复胚胎分子途径可能在靶向心肌危险中发挥作用，并且将是限制恢复患者梗死的重要治疗贡献。
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