Clinical predictors of mortality in cardiogenic shock following acute myocardial infarction

Cardiogenic shock (CS) complicates acute myocardial infarction (AMI) in 3-13% of cases and has a mortality rate of approximately 40% within the first 30 days and 50% within the first year, making it the leading cause of death in AMI patients. AMI accounts for 81% of CS cases. Patients with elevated left ventricular end-diastolic pressure often present with an S3 gallop, tachypnea, and hypoxemia due to pulmonary edema, which may manifest with lung rales. CS patients post-AMI may present with hypotension, signs of hypoperfusion such as oliguria or cool extremities, indicators of increased intracardiac filling pressures (e.g., pulmonary edema, orthopnea, or elevated jugular venous pressure), or a combination of these.

This study aimed to identify clinical predictors of mortality in patients who develop CS following AMI.

We conducted a prospective cross-sectional study from March 20 to October 20, 2024. Patients admitted with acute coronary syndrome (STEMI or NSTEMI) were analyzed, and those who developed CS were included in the study. Participants were categorized into two groups based on outcomes: the mortality group and the survival group.

Among 1,166 patients admitted for acute coronary syndrome at the Clinic of Cardiology over the seven-month study period, 86 (7.4%) developed CS. Of these, 44 patients (51%) died. Table 1 compares baseline clinical parameters between the groups. Significant differences were found in blood pressure, 24-hour diuresis, and the presence of cool extremities. Parameters with statistical significance were included in a multiple regression model, which demonstrated an explanatory power of 30% (R² = 0.30) and statistical significance (p<0.001). This indicates that 24-hour urine output, systolic blood pressure, and cool extremities are significant clinical predictors of mortality in CS complicating acute coronary syndrome. Specifically, 24-hour urine output and cool extremities were identified as independent predictors, while lower systolic blood pressure was not (Table 2).