Key result
Type I myocardial infarction in cardiogenic shock was not associated with a significantly higher incidence of adverse clinical outcomes compared to Type II MI (adjusted HR 1.63; 95% CI 0.96-2.77; P=0.07).
Why the study?
Type I and Type II myocardial infarction have different underlying mechanisms, but it is not understood whether patients experience different clinical outcomes in the setting of cardiogenic shock.
Does Type I myocardial infarction compared to Type II myocardial infarction result in different rates of the composite of all-cause in-hospital mortality, cardiac arrest, mechanical circulatory support, or RRT in patients with cardiogenic shock?
Cohort (n=103)
Does Type I myocardial infarction compared to Type II myocardial infarction result in different rates of the composite of all-cause in-hospital mortality, cardiac arrest, mechanical circulatory support, or RRT in patients with cardiogenic shock?
In patients with cardiogenic shock, there was no significant difference in 30-day adverse clinical outcomes between those with Type I versus Type II myocardial infarction, despite higher cardiac biomarker release in Type I.
Similar in-hospital outcomes for Type I vs Type II MI in cardiogenic shock; leaves open whether etiology should guide management.
IntroductionType I myocardial infarction (T1MI) or Type II MI (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.MethodsPatients from the CAPITAL-DOREMI trial presenting with acute myocardial infarction (AMI) associated CS (n=103) where 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 (RRT) at 30‐days. Secondary endpoints were evaluated as individual components of the primary endpoint.ResultsPatients with T1MI CS did not have a higher incidence of the primary composite endpoint when compared to T2MI CS (adjusted HR, 1.63; 95% CI, 0.96-2.77; P=0.07). Cardiac biomarkers including troponin I (p<0.001) and creatine kinase levels (p=0.001) were elevated in patients with T1MI CS when compared to T2MI. Furthermore, patients with T1MI CS presented with decreased urine output (p=0.01) when compared to T2MI. Predictors of T2MI CS included non-ischemic ventricular dysfunction (p=0.002), atrial fibrillation (p=0.02), and chronic obstructive pulmonary disease (p=0.002).ConclusionThere 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.
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Stotts et al. (2023) conducted a cohort in Acute myocardial infarction (AMI) associated cardiogenic shock (CS) (n=103). Type I myocardial infarction (T1MI) vs. Type II myocardial infarction (T2MI) was evaluated on Composite of all-cause in-hospital mortality, cardiac arrest, the need for mechanical circulatory support, or initiation of renal replacement therapy (RRT) at 30-days (adjusted HR 1.63, 95% CI 0.96-2.77, p=0.07). Type I myocardial infarction in cardiogenic shock was not associated with a significantly higher incidence of adverse clinical outcomes compared to Type II MI (adjusted HR 1.63; 95% CI 0.96-2.77; P=0.07).
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