Key result
MR16-1 reduces LVEF by ~20% versus control following ischemia-reperfusion.
Why the study?
Does IL-6R inhibition with MR16-1 improve cardiac function and prevent adverse remodeling in a murine model of myocardial ischemia-reperfusion?
RCT (n=36)
null
null
No
Does IL-6R inhibition with MR16-1 improve cardiac function and prevent adverse remodeling in a murine model of myocardial ischemia-reperfusion?
Effect estimate: null (95% CI null)
Absolute Event Rate: 28% vs 35%
p-value: p=0.02
Continuous blockade of the IL-6 receptor with MR16-1 for four weeks after ischemia-reperfusion injury in mice worsened left ventricular ejection fraction and did not prevent adverse cardiac remodeling.
IL-6R blockade worsened LVEF post-I/R in mice; hypothesis-generating and should not yet inform clinical practice.
Blockade of the IL-6R receptor by the monoclonal MR16-1 antibody for four weeks started directly after I/R injury did not prevent the process of cardiac remodeling in mice, but rather associated with a deterioration in the process of adverse cardiac remodeling.
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Hartman et al. (2016) conducted an RCT in myocardial ischemia-reperfusion (n=36). MR16-1 vs. control IgG was evaluated on Left ventricular ejection fraction (LVEF) (null, 95% CI null, p=0.02). MR16-1 treatment after ischemia-reperfusion resulted in a reduced left ventricular ejection fraction of 28% compared to 35% in the control IgG group (p = 0.02).
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