Research progress on beta-blockers in the treatment of sepsis-induced cardiomyopathy: A mini review

Sepsis-induced cardiomyopathy (SCM), a frequent complication of septic shock with mortality exceeding 40%, arises from catecholamine-driven cardiotoxicity, sympathetic hyperactivity, and inflammation-mediated biventricular dysfunction. Short-acting β₁-blockers (esmolol, landiolol) offer a targeted therapeutic approach by reducing heart rate (target: 80–95 bpm), myocardial oxygen demand, and proinflammatory cytokines while improving diastolic perfusion—leveraging ultra-short half-lives (t₁/₂ = 4–9 min) for rapid reversibility during instability. Clinical evidence remains divergent: a landmark single-center RCT demonstrated significant 28-day mortality reduction (49.4% vs 80.5%; p < 0.001), improved hemodynamics, and reduced vasopressor requirements in hemodynamically stabilized patients, whereas premature termination of a multicenter trial revealed harm (increased vasopressor needs, mortality trend) when initiated during persistent hypoperfusion (lactate > 2 mmol/L). Current limitations include heterogeneous trial designs, small samples, and undefined benefiting phenotypes. Thus, cautious short-acting β-blockade is supported only for selected SCM patients with hemodynamic stability (MAP ⩾65 mmHg, normalized lactate, LVEF >35%), necessitating future precision trials with AI phenotyping to guide mechanism-targeted application.