Abdelaal Mohamed A, Allaithy Amany, Mustafa Taimor, Ashmawy Medhat
Cardiology, Aswan Heart Centre, Aswan, EGY.
Cardiology, Faculty of Medicine, Tanta University, Tanta, EGY.
Cureus. 2025 Jun 20;17(6):e86407. doi: 10.7759/cureus.86407. eCollection 2025 Jun.
Acute myocardial infarction (AMI) is a prevalent etiology of cardiogenic shock (CS). Microcirculatory dysfunction may continue even when hemodynamic factors improve in CS because the condition is hemodynamically diverse. Patients with CS associated with AMI have been advised to utilize vasopressors and inotropic medications. The study aims to assess the effects of mild therapeutic hypothermia (MTH) on vasopressors and inotropes in patients with CS due to AMI.
The study was carried out on a cohort of 60 individuals who had CS after AMI. CS was operationally defined as the condition characterized by a systolic blood pressure below 90 mm Hg for a duration beyond 30 minutes or the presence of inotropes required to sustain a systolic blood pressure over 90 mm Hg without any indications of hypovolemia. Vasopressor and inotrope use were guided by cardiac specialists using a predefined hemodynamic protocol. Cardiogenic shock was defined by hypotension or inotrope dependence with evidence of hypoperfusion. Mean arterial blood pressure (MAP) and lactate levels were monitored every two hours for 30 hours to ensure treatment was based on objective criteria.
Norepinephrine (NE) was significantly lower at four, six, eight, 10, 12, 14, 16, 18, and 20 hours in group I than in group II (p-value < 0.001) and was insignificantly different at 0, two, 22, 24, 26, 28, and 30 hours between both groups. The dobutamine dose was significantly higher at 10 hours in group I than in group II (p-value = 0.002) and was significantly lower at 14 hours in group I than in group II (p-value = 0.036) and was insignificantly different at 0, two, four, six, eight, 12, 16, 18, 20, 22, 24, 26, 28, and 30 hours between both groups.
Patients treated with MTH to 33°C for 24 to 36 hours were associated with reduced NE requirements and higher MAP, along with increased dobutamine doses, compared to those without MTH. Arterial lactate rose initially with MTH but later declined. However, complications, clinical outcomes, and 30-day mortality were comparable.
急性心肌梗死（AMI）是心源性休克（CS）的常见病因。即使CS患者的血流动力学因素有所改善，微循环功能障碍仍可能持续存在，因为该病症的血流动力学情况多样。已建议患有与AMI相关的CS的患者使用血管升压药和正性肌力药物。本研究旨在评估轻度治疗性低温（MTH）对因AMI导致CS的患者使用血管升压药和正性肌力药物的影响。
该研究针对60名AMI后发生CS的患者进行。CS在操作上被定义为收缩压低于90 mmHg持续超过30分钟，或存在维持收缩压超过90 mmHg所需的正性肌力药物且无血容量不足迹象的情况。血管升压药和正性肌力药物的使用由心脏科专家根据预定义的血流动力学方案指导。心源性休克由低血压或对正性肌力药物的依赖以及灌注不足的证据来定义。每两小时监测平均动脉血压（MAP）和乳酸水平，持续30小时，以确保治疗基于客观标准。
与第二组相比，第一组在4、6、8、10、12、14、16、18和20小时时去甲肾上腺素（NE）显著更低（p值<0.001），且在0、2、22、24、26、28和30小时时两组之间无显著差异。第一组在10小时时多巴酚丁胺剂量显著高于第二组（p值 = 0.002），在14小时时第一组显著低于第二组（p值 = 0.036），且在0、2、4、6、8、12、16、18、20、22、24、26、28和30小时时两组之间无显著差异。
与未接受MTH治疗的患者相比，接受MTH治疗至33°C持续24至36小时的患者NE需求量降低、MAP更高，同时多巴酚丁胺剂量增加。动脉乳酸水平最初随MTH升高，但随后下降。然而，并发症、临床结局和30天死亡率相当。
