Cardiac mechanical efficiency in patients with cardiogenic shock.
TL;DR
Early TTE-derived mCE was independently associated with short- and long-term mortality in CS, particularly in acute coronary syndrome-related CS, and captured the interaction between ventricular remodeling and mechanical performance underlying high-risk phenotypes.
Abstract
Background
Cardiogenic shock (CS) is characterized by impaired left ventricular (LV) mechanical performance and adverse remodeling. We evaluated whether transthoracic echocardiography (TTE)-derived modified cardiac efficiency (mCE), integrating stroke work and residual LV volume, is associated with short- and long-term mortality in CS and whether its prognostic value differs by shock etiology.
Methods
In this retrospective cohort study, consecutive adults admitted with CS to the cardiac intensive care unit at Mayo Clinic (2007-2018) were included if TTE was performed within 24 hours. mCE was calculated as (stroke volume × estimated LV end-systolic pressure) divided by LV end-systolic volume and categorized into quartiles. Primary outcome was in-hospital mortality; secondary outcome was 1-year mortality. Multivariable logistic and Cox models adjusted for illness severity, comorbidity burden, shock etiology, cardiac arrest, vasoactive therapy, and mechanical circulatory support.
Results
Among 667 patients, median mCE was 48 mmHg (IQR 32-74). In-hospital mortality was 28% and increased stepwise across decreasing mCE quartiles. The lowest quartile had a 2.5-fold higher adjusted odds of in-hospital death (OR 2.53; 95%CI: 1.49-4.37; P < 0.001). One-year mortality was 41%; the lowest quartile had a twofold higher adjusted hazard of death (HR 2.05; 95%CI: 1.45-2.89; P < 0.001). Associations were stronger in acute coronary syndrome-related CS (interaction P = 0.035 for in-hospital; P = 0.015 for 1-year). Within the lowest quartile, reduced systolic pressure further amplified mortality risk.
Conclusions
Early TTE-derived mCE was independently associated with short- and long-term mortality in CS, particularly in acute coronary syndrome-related CS, and captured the interaction between ventricular remodeling and mechanical performance underlying high-risk phenotypes.