Soluble neprilysin levels tracked anthracycline-induced myocardial damage, suggesting it may predict benefits from ARNI in cardio-oncology.
Does sacubitril/valsartan prevent left ventricular ejection fraction decline in patients receiving anthracycline-based cancer therapy?
While preclinical models suggest soluble neprilysin tracks anthracycline-induced cardiotoxicity, the neutral results of the PRADA II trial highlight a translational gap, emphasizing the need for biomarker-driven stratification and more sensitive endpoints in cardio-oncology trials.
Absolute Event Rate: 0% vs 0%
In cardio-oncology, the gap between mechanistic studies and pharmacological trials impedes the delineation of effective cardioprotective strategies. The angiotensin-receptor/neprilysin inhibitor (ARNI) have shown beneficial effects in patients with heart failure with reduced ejection fraction, but failed to show significant benefit in cardio-oncology. In a preclinical model, soluble neprilysin levels (sNEP) tracked anthracycline-induced myocardial damage and systolic dysfunction and sNEP levels may predict benefits of ARNI. The neutral results of clinical trials testing sacubitril/valsartan in this setting underscore the challenge of bridging pre-clinical knowledge to patients' management and call for clinical trials in precision medicine approaches in which biomarkers (i.e. sNEP) may guide treatment (i.e. ARNI).
Camilli et al. (Thu,) reported a other. Soluble neprilysin levels tracked anthracycline-induced myocardial damage, suggesting it may predict benefits from ARNI in cardio-oncology.
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