Failure of the renin-angiotensin-aldosterone system is hypothesized to drive pathological vasodilation in a subset of cardiogenic shock patients, leading to a mixed shock phenotype.
Cardiogenic shock (CS) is a state of acute circulatory failure resulting from impaired myocardial function and reduced cardiac output, leading to inadequate tissue perfusion and subsequent organ dysfunction. In its early phase, CS is typically accompanied by systemic vasoconstriction as a compensatory response aimed at preserving mean arterial pressure and organ perfusion. However, an increasing body of evidence suggests that a subset of patients develop a mixed shock phenotype, characterized by superimposed vasodilation without evidence of concurrent sepsis, which portends a worse prognosis. Failure of the renin-angiotensin-aldosterone system (RAAS) may be a key driver of pathological vasodilation in CS, analogous to recent observations in septic shock. Specifically, RAAS dysfunction could lead to impaired angiotensin II signalling at the angiotensin II type 1 receptor level due to defective angiotensin II generation, enhanced peptide degradation, and/or receptor unavailability. Recognition of RAAS failure in CS could inform novel therapeutic strategies to restore vascular tone and improve outcomes in patients with mixed cardiogenic-vasodilatory shock.
Picod et al. (Thu,) conducted a other in Cardiogenic shock. Failure of the renin-angiotensin-aldosterone system is hypothesized to drive pathological vasodilation in a subset of cardiogenic shock patients, leading to a mixed shock phenotype.