Marquard Jasmine Melissa, Lønborg Jacob, Obling Laust Emil Roelsgaard, Beske Rasmus Paulin, Zhou Yan, Nepper-Christensen Lars, Vejlstrup Niels, Bang Lia Evi, Hassager Christian, Folke Fredrik, Andersen Lars Bredevang, Christensen Helle Collatz, Holmvang Lene, Pedersen Frants, Ahlehoff Ole, Jabbari Reza, Minkkinen Mikko, Sørensen Rikke, Tilsted Hans-Henrik, Engstrøm Thomas
Department of Cardiology, Rigshospitalet, Copenhagen University Hospital, Inge Lehmanns Vej 7, Copenhagen, 2100, Denmark.
Department of Clinical Medicine, University of Copenhagen, Copenhagen, Denmark.
J Inflamm (Lond). 2025 Mar 18;22(1):12. doi: 10.1186/s12950-025-00440-2.
Microvascular injury in patients with ST-segment elevation myocardial infarction (STEMI) occurs in up to 50%, yet no therapeutic target exists. Inflammation contributes directly to myocardial damage in STEMI and may also cause deleteriously effects on the microcirculation. The aim of this prespecified sub-study was to determine the effect of prehospital pulse-dose glucocorticoid on the microcirculation determined by index of microvascular resistance (IMR) and its relation to inflammation. The PULSE-MI trial was a 1:1 randomized, blinded, placebo-controlled clinical trial in patients with STEMI transferred for primary percutaneous coronary intervention (PCI) investigating the cardioprotective effects of prehospital pulse-dose glucocorticoid (methylprednisolone 250 mg) compared with placebo. In this prespecified sub-study, we investigated microvascular function as IMR by thermodilution after primary PCI and inflammation defined by C-reactive protein (CRP) at 24 hours after onset of STEMI.
Of 530 patients included in the PULSE-MI trial, 295 (56%) were assessed with coronary physiology of whom 142 (48%) were treated with glucocorticoid and 153 (52%) with placebo. Baseline characteristics were overall well-balanced in both groups. The median IMR in the glucocorticoid group was 23 (interquartile range (IQR), 11-38) and 18 (IQR, 11-42) in the placebo group (p=0.49). CRP upon arrival did not differ between treatment groups (p=0.81), but CRP at 24 hours was significantly lower in the glucocorticoid group compared to placebo (p<0.001).
Prehospital glucocorticoid did not impact IMR assessed immediately after primary PCI, albeit this compound, demonstrated significant anti-inflammatory effects as determined by CRP levels at 24 hours.
gov ; Unique Identifier: NCT05462730.
ST段抬高型心肌梗死（STEMI）患者中微血管损伤发生率高达50%，但尚无治疗靶点。炎症直接导致STEMI患者的心肌损伤，也可能对微循环产生有害影响。这项预先设定的亚研究旨在确定院前脉冲剂量糖皮质激素对通过微血管阻力指数（IMR）测定的微循环的影响及其与炎症的关系。PULSE-MI试验是一项1:1随机、双盲、安慰剂对照的临床试验，纳入因行直接经皮冠状动脉介入治疗（PCI）而转诊的STEMI患者，研究院前脉冲剂量糖皮质激素（甲泼尼龙250mg）与安慰剂相比的心脏保护作用。在这项预先设定的亚研究中，我们在初次PCI后通过热稀释法测定IMR来评估微血管功能，并在STEMI发病24小时后通过C反应蛋白（CRP）来定义炎症。
在PULSE-MI试验纳入的530例患者中，295例（56%）接受了冠状动脉生理学评估，其中142例（48%）接受糖皮质激素治疗，153例（52%）接受安慰剂治疗。两组的基线特征总体平衡。糖皮质激素组的IMR中位数为23（四分位数间距（IQR），11 - 38），安慰剂组为18（IQR，11 - 42）（p = 0.49）。入院时CRP在治疗组之间无差异（p = 0.81），但糖皮质激素组24小时时的CRP显著低于安慰剂组（p < 0.001）。
院前糖皮质激素对初次PCI后立即评估的IMR无影响，尽管该化合物在24小时时通过CRP水平显示出显著的抗炎作用。
gov；唯一标识符：NCT05462730。
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