Prehospital pulse-dose glucocorticoid on index of microvascular resistance in patients with ST-segment elevation myocardial infarction: a sub-study of the PULSE-MI trial.

IF 4.4 3区 医学 Q2 IMMUNOLOGY
Jasmine Melissa Marquard, Jacob Lønborg, Laust Emil Roelsgaard Obling, Rasmus Paulin Beske, Yan Zhou, Lars Nepper-Christensen, Niels Vejlstrup, Lia Evi Bang, Christian Hassager, Fredrik Folke, Lars Bredevang Andersen, Helle Collatz Christensen, Lene Holmvang, Frants Pedersen, Ole Ahlehoff, Reza Jabbari, Mikko Minkkinen, Rikke Sørensen, Hans-Henrik Tilsted, Thomas Engstrøm
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引用次数: 0

Abstract

Background: 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.

Results: 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).

Conclusions: 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.

Trial registration: http://www.

Clinicaltrials: gov ; Unique Identifier: NCT05462730.

院前脉冲剂量糖皮质激素对st段抬高型心肌梗死患者微血管抵抗指数的影响:PULSE-MI试验的一项亚研究
背景:st段抬高型心肌梗死(STEMI)患者微血管损伤发生率高达50%,但目前尚无治疗靶点。炎症直接导致STEMI的心肌损伤,也可能对微循环产生有害影响。这项预先指定的亚研究的目的是确定院前脉冲剂量糖皮质激素对微血管抵抗指数(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、盲法、安慰剂对照的临床试验,研究院前脉冲剂量糖皮质激素(甲基强的松龙250 mg)与安慰剂的心脏保护作用。在这个预先指定的亚研究中,我们研究了原发性PCI术后通过热稀释的微血管功能IMR和STEMI发病后24小时由c反应蛋白(CRP)定义的炎症。结果:在PULSE-MI试验纳入的530例患者中,295例(56%)进行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上平衡良好。糖皮质激素组的中位IMR为23(四分位间距(IQR), 11-38),安慰剂组的中位IMR为18 (IQR, 11-42) (p=0.49)。到达时的CRP在治疗组之间没有差异(p=0.81),但与安慰剂相比,糖皮质激素组24小时的CRP显着降低(结论:院前糖皮质激素对初次PCI后立即评估的IMR没有影响,尽管这种化合物在24小时的CRP水平上显示出显着的抗炎作用。试验注册:http://www.Clinicaltrials: gov;唯一标识符:NCT05462730。
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来源期刊
CiteScore
7.90
自引率
0.00%
发文量
18
审稿时长
>12 weeks
期刊介绍: Journal of Inflammation welcomes research submissions on all aspects of inflammation. The five classical symptoms of inflammation, namely redness (rubor), swelling (tumour), heat (calor), pain (dolor) and loss of function (functio laesa), are only part of the story. The term inflammation is taken to include the full range of underlying cellular and molecular mechanisms involved, not only in the production of the inflammatory responses but, more importantly in clinical terms, in the healing process as well. Thus the journal covers molecular, cellular, animal and clinical studies, and related aspects of pharmacology, such as anti-inflammatory drug development, trials and therapeutic developments. It also considers publication of negative findings. Journal of Inflammation aims to become the leading online journal on inflammation and, as online journals replace printed ones over the next decade, the main open access inflammation journal. Open access guarantees a larger audience, and thus impact, than any restricted access equivalent, and increasingly so, as the escalating costs of printed journals puts them outside University budgets. The unrestricted access to research findings in inflammation aids in promoting dynamic and productive dialogue between industrial and academic members of the inflammation research community, which plays such an important part in the development of future generations of anti-inflammatory therapies.
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