Stotts Cameron, Jung Richard G, Prosperi-Porta Graeme, Di Santo Pietro, Abdel-Razek Omar, Parlow Simon, Ramirez F Daniel, Simard Trevor, Labinaz Marino, Morgan Baylie, Robinson Lisa, Mathew Rebecca, Hibbert Benjamin
CAPITAL Research Group, University of Ottawa Heart Institute, Ottawa, Ontario, Canada.
Vascular Biology and Experimental Medicine Laboratory, University of Ottawa Heart Institute, Ottawa, Ontario, Canada.
CJC Open. 2023 Oct 16;6(2Part A):122-132. doi: 10.1016/j.cjco.2023.10.011. eCollection 2024 Feb.
Type I myocardial infarction (T1MI) or type II myocardial infarction (T2MI) have different underlying mechanisms; however, in the setting of cardiogenic shock (CS), it is not understood if patients experience resultantly different outcomes. The objective of this study was to determine clinical features, biomarker patterns, and outcomes in these subgroups.
Patients from the CAPITAL-DOREMI trial presenting with acute myocardial infarction-associated CS (n = 103) were classified as T1MI (n = 61) or T2MI (n = 42). The primary endpoint was a composite of all-cause in-hospital mortality, cardiac arrest, the need for mechanical circulatory support, or initiation of renal replacement therapy at 30 days. Secondary endpoints were evaluated as individual components of the primary endpoint.
Patients with T1MI CS did not have a higher incidence of the primary composite endpoint compared with T2MI CS (adjusted hazard ratio [HR], 1.63; 95% confidence interval [CI], 0.96-2.77; = 0.07). Cardiac biomarkers including troponin I ( < 0.001), and creatine kinase levels ( = 0.001) were elevated in patients with T1MI CS compared with T2MI. Furthermore, patients with T1MI CS presented with decreased urine output ( = 0.01) compared with T2MI. Predictors of T2MI CS included nonischemic ventricular dysfunction ( = 0.002), atrial fibrillation ( = 0.02), and chronic obstructive pulmonary disease ( = 0.002).
There were no differences in adverse clinical outcomes between patients with T1MI and T2MI CS, although the events were numerically increased, and the sample size was small. Overall, this study provides a hypothesis-generating analysis regarding the clinical and biochemical outcomes in T1MI vs T2MI CS.
I型心肌梗死（T1MI）和II型心肌梗死（T2MI）具有不同的潜在机制；然而，在心源性休克（CS）的情况下，尚不清楚患者的预后是否会因此而有所不同。本研究的目的是确定这些亚组患者的临床特征、生物标志物模式和预后。
来自CAPITAL-DOREMI试验的急性心肌梗死相关CS患者（n = 103）被分为T1MI组（n = 61）或T2MI组（n = 42）。主要终点是30天时全因住院死亡率、心脏骤停、机械循环支持需求或肾脏替代治疗启动的综合指标。次要终点作为主要终点的各个组成部分进行评估。
与T2MI CS患者相比，T1MI CS患者的主要复合终点发生率没有更高（调整后风险比[HR]，1.63；95%置信区间[CI]，0.96 - 2.77；P = 0.07）。与T2MI患者相比，T1MI CS患者的心脏生物标志物包括肌钙蛋白I（P < 0.001）和肌酸激酶水平（P = 0.001）升高。此外，与T2MI患者相比，T1MI CS患者的尿量减少（P = 0.01）。T2MI CS的预测因素包括非缺血性心室功能障碍（P = 0.002）、心房颤动（P = 0.02）和慢性阻塞性肺疾病（P = 0.002）。
T1MI和T2MI CS患者的不良临床结局没有差异，尽管事件数量在数值上有所增加且样本量较小。总体而言，本研究提供了一项关于T1MI与T2MI CS临床和生化结局的假设生成分析。
