Hemodynamic Patterns in Septic Cardiomyopathy: Insights From Echocardiographic Parameters and Biomarker Analysis.
Rabia Jaffar, Ahmed Jamal Chaudhary, Marium Nadeem Khan, Hamza Wakil, Muhammad Waseem Hussain, Mohammad Ibrahim Rasool, Taha Nasim, Muhammad Haris Khan, Ali Raza
Abstract
Open AccessIntroduction Septic cardiomyopathy (SCM) refers to an acute, reversible impairment of cardiac performance. This study aimed to evaluate hemodynamic patterns in SCM using echocardiographic parameters and cardiac biomarkers in critically ill patients. Materials and methods A 12-month prospective observational study was conducted at a single tertiary care center in Peshawar, Pakistan. Adult ICU patients with sepsis or septic shock underwent transthoracic echocardiography (TTE) within 48 hours of admission, with a repeat study on day 5 or earlier if clinically indicated. Left ventricular (LV) and right ventricular (RV) systolic and diastolic functions were assessed, including global longitudinal strain (GLS) and RV free-wall strain. High-sensitivity troponin I (hs-TnI) and N-terminal pro-B-type natriuretic peptide (NT-proBNP) were measured on days 1 and 3. Associations between cardiac dysfunction and in-hospital mortality were analyzed using multivariable logistic regression after adjusting for age, sex, Acute Physiology and Chronic Health Evaluation II (APACHE II) score, and vasopressor use. Results Among 122 patients, the prevalence of SCM, defined by LV GLS > -17%, was high, with concurrent RV dysfunction observed in a significant proportion. Elevated hs-TnI and NT-proBNP levels correlated with impaired GLS and adverse outcomes. After multivariable adjustment, GLS impairment and elevated NT-proBNP remained independently associated with in-hospital mortality. Conclusions In this South Asian cohort with sepsis or septic shock, combined strain-based echocardiography and biomarker profiling revealed distinct patterns of myocardial dysfunction associated with early mortality. While these findings highlight the prognostic utility of GLS and NT-proBNP, they should be interpreted as associations rather than causal effects. Larger multicenter studies with extended follow-up and incorporation of additional biomarkers and advanced imaging are needed to validate these observations and clarify underlying pathophysiological mechanisms.