Sepsis-Induced Cardiomyopathy Reviewed: The Case for Early Consideration of Mechanical Support.

Sepsis-induced cardiomyopathy (SCM) is an increasingly recognized problem encountered in critical care medicine. It generally is characterized as a decrease in left, right, or biventricular ejection fraction followed by a recovery of function over a period of days to weeks. Venoarterial extracorporeal membrane oxygenation (ECMO) has been used for the treatment of adults with various etiologies of shock, including cardiogenic and septic shock. This review summarizes current pathophysiologic mechanisms leading to SCM and provides a detection and treatment algorithm for SCM, as well as a discussion about the rationale and recent clinical data surrounding the use of ECMO and other forms of mechanical circulatory support for SCM.

Early Activation of Growth Pathways in Mitral Leaflets Exposed to Aortic Regurgitation: New Insights from an Animal Model.

BACKGROUND AND AIM OF THE STUDY: Mitral leaflet enlargement in patients with chronic aortic regurgitation (AR) has been identified as an adaptive mechanism potentially able to prevent functional mitral regurgitation (FMR) in response to left ventricular (LV) dilatation. The timing of valve enlargement is not known, and the related mechanisms are largely unexplored. METHODS: AR was induced in 58 rats, and another 54 were used as sham controls. Animals were euthanized at different time points after AR creation (48 h, one week, and three months), and AR severity, FMR and LV dilatation were assessed using echocardiography. Mitral valves were harvested to document the reactivation of embryonic growth pathways. RESULTS: AR animals had increased LV dimensions and mitral annulus size. No animal developed FMR. No change in leaflet length or thickness was seen at 48 h; however, anterior mitral leaflets were longer and thicker in AR animals at one week and three months. Molecular changes were present early (at 48 h and at one week), with positive staining for transforming growth factor-b1 (TGF-b1), Alpha-smooth muscle actin (α-SMA) and matrix metalloproteinase-2 (MMP-2), which suggested active matrix remodeling. Increased gene expression for collagen 1, TGF-ß1, α-SMA and MMP-2 was found in the mitral valve at 48 h and at one week, but after three months their expression had returned to normal. CONCLUSIONS: This model of AR induces active expansion and thickening of the mitral leaflets. Growth signals are expressed acutely, but not at three months, which suggests that most of this enlargement occurs at an early stage. The stimulation of valvular growth could represent a new strategy for the prevention of FMR.