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Ivabradine / Septic Shock · Phase 3 Trial
ClinicalTrials.gov · September 3, 2026
Early or partial results. Treat as a signal, not a conclusion.
This is a completed Phase 3 trial registration for ivabradine versus placebo in septic shock, but no results have been posted in this registry record. The trial enrolled 429 participants and measured heart rate control and 28-day mortality as primary outcomes, but the evidence of efficacy or harm cannot be evaluated until outcomes are reported.
Phase 3, Interventional, Randomized, Parallel, Double masking, Treatment purpose. Septic Shock; age from 18 Years. Intervention: Ivabradine (Low); Ivabradine (High). Compared with: Control — Placebo Comparator. n = 429. 1 site: France.
Primary outcomes measured: percentage of patients with heart rate 80–94 bpm at 48 hours and percentage dead at 28 days Trial enrolled 429 participants with completed recruitment status
No efficacy or safety data are presented; outcome values, effect sizes, and statistical significance are unavailable
If results support ivabradine, it could offer heart rate control in septic shock without the negative inotropic and blood pressure effects of beta-blockers, potentially improving outcomes in a condition with ~45% mortality. However, no clinical guidance can be drawn until results are published.
Phase 3 trial with completed enrollment but no results posted in this registry record; the study design is rigorous but outcome data are not yet reported, making this a planning/protocol document rather than evidence of efficacy.
As stated by the source record.
Quoted from the source exactly as published.
If results support ivabradine, it could offer heart rate control in septic shock without the negative inotropic and blood pressure effects of beta-blockers, potentially improving outcomes in a condition with ~45% mortality. However, no clinical guidance can be drawn until results are published.
Graded across the dimensions that decide whether you should act, each from what the source actually supports. There is no single score, and where a dimension was not assessed it says so.
Registry record from ClinicalTrials.gov (NCT04031573). This is a study registration, not published results. Lead sponsor: Assistance Publique - Hôpitaux de Paris. Recruitment status: COMPLETED. Phase: PHASE3. Study type: INTERVENTIONAL. Enrollment: 429 participants (ACTUAL). Conditions: Septic Shock. Interventions: DRUG: Ivabradine; DRUG: Ivabradine; DRUG: Placebo. Primary outcome measures: Percentage of patients with heart rate within the predefined threshold (80-94 bpm) at hour-48 , hour 48 after treatment; Percentage of patients dead at 28 days , 28 days. Brief summary: Septic shock is a major health problem, with several million cases annually worldwide and a mortality approaching 45%. Tachycardia is associated with excess mortality during septic shock. This pejorative effect could be related to the increase in cardiac metabolic demand, impaired cardiac diastolic function, and/or poorer tolerance of administered exogenous catecholamines. Recent studies suggest that controlling the heart rate with the use of beta blockers has beneficial effects on the morbidity and mortality of septic shock. However, the negative effects of beta-blockers on cardiac contractility and blood pressure complicate their use during septic shock, particularly because about one-half of patients exhibit a septic-associated systolic dysfunction, which often requires the use of inotropes. Ivabradine is a selective inhibitor of If channels in the sinoatrial node. It is a pure bradycardic agent with no deleterious effect on other aspects of cardiac function (contractility, conduction and repolarization) nor on blood pressure. Ivabradine can therefore alleviate sinus tachycardia without negative inotropic effects nor hypotension. Moreover, the improvement in diastolic function (ventricular filling) with ivabradine may increase stroke volume, even in case of severe impairment of systolic function. Controlling sinus tachycardia with ivabradine during septic shock would allow reducing cardiac metabolic demand (and potentially associated ischemic events) and improving the chronotropic tolerance of exogenous catecholamines. The effectiveness of ivabradine in controlling the heart rate was demonstrated in various clinical settings such as coronary artery disease, chronic heart failure and cardiogenic shock. Encouraging preliminary data are reported in critically ill patients.
Taken from the source record, never inferred. Follow any of these and new work involving them reaches your briefing.