Key result
Sacubitril/valsartan improves renal function vs vehicle in post-MI cardiorenal syndrome, raising creatinine clearance ~13%.
Why the study?
Renal dysfunction in heart failure increases mortality and limits treatment, and ARNI may preserve renal function by modulating both the RAAS and natriuretic peptide systems.
Does sacubitril/valsartan preserve renal function and improve cardiac parameters in rats with cardiorenal syndrome after myocardial infarction?
Does sacubitril/valsartan preserve renal function and improve cardiac parameters in rats with cardiorenal syndrome after myocardial infarction?
Absolute Event Rate: 5.1% vs 4.5%
p-value: p=0.044
In a rat model of post-MI cardiorenal syndrome, sacubitril/valsartan provided similar renoprotection to valsartan alone but uniquely reduced left atrial dilatation, suggesting added structural benefits.
Should not change practice in cardiorenal syndrome; extends preclinical data on sacubitril/valsartan renoprotection.
Renal dysfunction in heart failure increases mortality, limits treatment options and blunts responses to therapy. Angiotensin receptor-blocker and neprilysin inhibitors (ARNI) may preserve renal function by modulating both the renin-angiotensin-aldosterone system and the natriuretic peptide system. We investigated the renal effects of the ARNI Sacubitril/valsartan (Sac/Val) in rats with systolic dysfunction secondary to myocardial infarction. Male Sprague-Dawley rats underwent surgical MI induction and were randomized to six weeks of treatment with vehicle, valsartan or Sac/Val, and compared to sham operated animals. Renal function was evaluated by creatinine clearance, mean arterial pressure (MAP) by tail-cuff measurements, and cardiac function by magnetic resonance imaging and echocardiography. Vehicle treated animals developed cardiorenal syndrome, with impaired cardiac systolic function and mild renal dysfunction. Both valsartan and Sac/Val preserved renal function compared to vehicle (creatinine clearance mL/min [median with interquartile range]; sham 5.4 [4.8-6.0], vehicle 4.5 [4.1-5.1], valsartan 5.1 [5.1-5.5], Sac/Val 5.1 [5.0-5.6]; vehicle vs valsartan p = 0.034 and vehicle vs Sac/Val p = 0.044). MAP was reduced by both treatments compared to sham and vehicle groups (MAP mmHg; sham 131 [116-138], vehicle 123 [115-132], valsartan 108 [99-112], Sac/Val 111 [99-119]; sham vs valsartan p < 0.001 and sham vs Sac/Val p = 0.003, vehicle vs valsartan p = 0.006 and vehicle vs Sac/Val p = 0.041). Only Sac/Val reduced left atrial dilatation (diameter mm; sham 4.1 [3.7-4.4], vehicle 4.6 [3.8-5.6], valsartan 4.6 [4.1-5.5], Sac/Val 3.9 [3.6-4.5]; vehicle vs Sac/Val p = 0.047, valsartan vs Sac/Val p = 0.017) despite no improvement in systolic function in either treatment group. Sac/Val initiated in the acute post-MI phase preserved renal function to the same extent as valsartan alone and uniquely reduced left atrial dilatation, suggesting additional benefits beyond renoprotection in the setting of persistent systolic dysfunction.
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Bergo et al. (2025) studied Cardiorenal syndrome after myocardial infarction (n=74). Sacubitril/valsartan vs. Vehicle was evaluated on Creatinine clearance (mL/min) (p=0.044). Sacubitril/valsartan preserved renal function compared to vehicle in rats with post-myocardial infarction cardiorenal syndrome, increasing median creatinine clearance (5.1 vs 4.5 mL/min, p=0.044).
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