Etiology driven mortality in cardiogenic shock

Abstract Introduction Mortality in cardiogenic shock (CS) remains high. Recent studies have demonstrated that long-term mortality is greater in non–acute myocardial infarction (non-AMI)–related CS compared to AMI-induced CS. This disparity appears to be attributable to differences in comorbidities and distinct underlying pathophysiological mechanisms. Purpose This study aimed to identify and compare demographic, clinical, laboratory, echocardiographic, and therapeutic predictors of in-hospital mortality in patients with CS. Methods An observational cohort study was conducted on 160 patients hospitalized at our institute between January 2022 and June 2025 with a diagnosis of CS. CS was defined as systolic blood pressure 90mmHg with clinical signs of hypoperfusion and lactate levels ≥2mmol/l. Patients were categorized into two groups based on the etiology of CS: AMI-induced and non-AMI-induced CS. Results Among the 160 patients, 96 (60%) were male, and 123 (76.9%) had AMI as the cause of CS. The overall mortality was 43.1%. Mortality was significantly higher in the non-AMI compared to the AMI-CS group (67.6% vs. 35.8%, p=0.001) and non-AMI etiology was strongly associated with increased mortality (OR 3.74, 95% CI 1.71-8.17, p=0.001). A higher SCAI stage was identified as the sole independent predictor of in-hospital mortality (OR 17.18, 95% CI 7.29-40.49, p=0.001). At admission, patients with non-AMI CS more frequently presented with advanced CS stages (SCAI C, D, or E) (83.8% vs. 71.5%, p=0.004) and had a significantly higher heart rate (96 vs. 82bpm, p=0.017). The non-AMI group was also more likely to have a history of heart failure (73% vs. 24.4%, p=0.001) and a BMI 30kg/m² (37.8% vs. 20.3%, p=0.030). Out-of-hospital cardiac arrest occurred exclusively in the AMI-CS group (14.6% vs. 0%, p=0.014), while in-hospital cardiac arrest was significantly more common in the non-AMI group (78.4% vs. 46.3%, p=0.001). Echocardiographically, a left ventricular ejection fraction 35% was more frequent in the non-AMI group (58.3% vs. 38.3%, p=0.033). At admission, creatinine levels were significantly higher in the non-AMI group (172 vs. 116µmol/l, p=0.001), while high-sensitivity troponin was higher in the AMI-CS group (2306.05 vs. 339.30ng/mL, p=0.021). Revascularization was performed more frequently in the AMI-CS group (89.6% vs. 18.9%, p=0.001). There were no significant differences between the groups regarding the use of mechanical circulatory support (MCS), vasopressors, or inotropes, and MCS use did not improve in-hospital outcomes (OR 1.83, 95% CI 0.83-4.04, p=0.133). Conclusion Patients with non-AMI-induced CS represent a distinct cohort characterized by more chronic comorbidities, a more severe initial presentation, poorer renal function, and a substantially higher risk of in-hospital mortality compared to those with AMI-induced CS. The use of mechanical circulatory support did not confer a significant benefit in improving in-hospital outcomes.