Gemmati Donato, Ctr. Hemostasis & Thrombosis, Hematology Section, Dpt. of Medical Sciences, University of Ferrara, Ferrara, Italy, Tel.: +39 0532 237291, Fax: +39 0532 209010, E-mail:
Thromb Haemost. 2015 Jul;114(1):123-32. doi: 10.1160/TH14-11-0952. Epub 2015 May 7.
After acute myocardial infarction (MI) the damaged heart has to be repaired. Factor XIII (FXIII) is considered a key molecule in promoting heart healing. FXIII deficiency was associated to cardiac rupture and anomalous remodelling in MI. During MI, FXIII contributes firstly to the intracoronary thrombus formation and shortly after to heal the myocardial lesion. To quantify the real contribution of FXIII in this process, and to explore its possible prognostic role, we monitored the FXIII-A subunit levels in 350 acute MI patients during the first six days (d0-d5) plus a control at 30-60 days (d30). A one-year follow-up was performed for all the patients. A transient drop in the FXIII-A mean level was noted in the whole cohort of patients (FXIII-Ad0 99.48 ± 30.5 vs FXIII-Ad5 76.51 ± 27.02; p< 0.0001). Interestingly, those who developed post-MI heart failure showed the highest drop (FXIII-Ad5 52.1 ± 25.2) and they already presented with low levels at recruitment. Similarly, those who died showed the same FXIII-A dynamic (FXIII-Ad5 54.0 ± 22.5). Conversely, patients who remained free of major adverse cardiac events, had lower consuming (FXIII-Ad0 103.6 ± 29.1 vs FXIII-Ad5 84.4 ± 24.5; p< 0.0001). Interestingly, the FXIII-A drop was independent from the amount of injury assessed by TnT and CKMB levels. The survival analysis ascribed an increased probability of early death or heart failure inversely related to FXIII-A quartiles (FXIII-A25th< 59.5 %; hazard ratio 4.25; 2.2-5.1; p< 0.0001). Different FXIII-A dynamics and levels could be utilised as early prognostic indicators during acute MI, revealing the individual potential to heal and suggesting tailored treatments to avoid heart failure or its extreme consequence.
急性心肌梗死后（MI），受损的心脏需要修复。因子 XIII（FXIII）被认为是促进心脏愈合的关键分子。FXIII 缺乏与 MI 中的心脏破裂和异常重塑有关。在 MI 期间，FXIII 首先有助于冠状动脉内血栓形成，然后不久后有助于修复心肌损伤。为了量化 FXIII 在这个过程中的实际贡献，并探索其可能的预后作用，我们在 350 名急性 MI 患者的前 6 天（d0-d5）期间监测了 FXIII-A 亚单位水平，并在 30-60 天（d30）时进行了对照。对所有患者进行了为期 1 年的随访。整个患者队列的 FXIII-A 平均水平出现一过性下降（FXIII-Ad0 99.48 ± 30.5 vs FXIII-Ad5 76.51 ± 27.02；p<0.0001）。有趣的是，发生 MI 后心力衰竭的患者下降幅度最大（FXIII-Ad5 52.1 ± 25.2），并且他们在招募时已经处于低水平。同样，死亡的患者也呈现出相同的 FXIII-A 动态（FXIII-Ad5 54.0 ± 22.5）。相反，没有发生主要不良心脏事件的患者，FXIII-A 消耗较低（FXIII-Ad0 103.6 ± 29.1 vs FXIII-Ad5 84.4 ± 24.5；p<0.0001）。有趣的是，FXIII-A 的下降与通过 TnT 和 CKMB 水平评估的损伤量无关。生存分析将与 FXIII-A 四分位数呈反比的早期死亡或心力衰竭的概率归因于 FXIII-A（FXIII-A25th<59.5%；危险比 4.25；2.2-5.1；p<0.0001）。不同的 FXIII-A 动力学和水平可作为急性 MI 期间的早期预后指标，揭示个体愈合的潜力，并提示采用针对性治疗以避免心力衰竭或其极端后果。
