Key result
Sacubitril/valsartan treatment improved cardiac structure in a rat model of hypertension-induced hypertrophic cardiomyopathy, increasing left ventricular internal diameter in systole (0.5 vs 0.22 cm, P<0.01).
Why the study?
The study evaluated the effect of sacubitril/valsartan on cardiac remodeling, molecular and cellular adaptations in an experimental rat model of hypertension-induced hypertrophic cardiomyopathy.
Does sacubitril/valsartan improve cardiac structure and function in an experimental rat model of hypertension-induced hypertrophic cardiomyopathy?
Does sacubitril/valsartan improve cardiac structure and function in an experimental rat model of hypertension-induced hypertrophic cardiomyopathy?
In a rat model of hypertension-induced hypertrophic cardiomyopathy, sacubitril/valsartan improved cardiac structure and hemodynamics while reducing oxidative stress and apoptosis.
Hypothesis-generating for sacubitril/valsartan in hypertrophic cardiomyopathy; leaves open translation from rat models to patients.
This study evaluated the effect of sacubtril/valsartan on cardiac remodeling, molecular and cellular adaptations in experimental (rat) model of hypertension-induced hypertrophic cardiomyopathy. Thirty Wistar Kyoto rats; 10 normal (control) and 20 rats with confirmed hypertension-induced hypertrophic cardiomyopathy (HpCM) were used for this study. The HpCM group was further subdivided into untreated, and sacubitril/valsartan treated group. Myocardial structure and function were assessed using echocardiography, Langendorff’s isolated heart experiment, blood sampling and qualitative polymerase chain reaction. Left ventricular internal diameter in systole (0.5 vs 0.22 cm, P < 0.01) and diastole (0.82 vs 0.50 cm, P < 0.01) were greater in treated compared to untreated HpCM rats. Interventricular septal wall thickness in end-systole was higher in untreated and treated HpCM rats compared to controls (0.22 vs 0.20 vs 0.16 cm, P < 0.05 respectively). Fractional shortening was lower in treated compared to untreated rats (34% vs 43%, P < 0.01). Systolic and diastolic blood pressures decreased by 58 and 37 mmHg (P < 0.01) respectively in treated compared to untreated rats. Similarly, sacubitril/valsartan treatment reduced oxidative stress and apoptosis (reduced expression of Bax and Cas3 genes) compared to untreated rats. There was a regular histomorphology of cardiomyocytes, interstitium, and blood vessels in treated rats compared to untreated HpCM rats which expressed hypertrophic cardiomyocytes, with polymorphic nuclei, prominent nucleoli and moderately dilated interstitium. In experimental model of hypertension-induced hypertrophic cardiomyopathy, sacubitril/valsartan treatment led to improved cardiac structure, haemodynamic performance, and reduced oxidative stress and apoptosis. Sacubitril/valsartan thus presents as a potential therapeutic strategy resulted in hypertension-induced hypertrophic cardiomyopathy.
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Jeremić et al. (2022) studied hypertension-induced hypertrophic cardiomyopathy (n=30). Sacubitril/valsartan vs. untreated was evaluated on Left ventricular internal diameter in systole (cm) (p=<0.01). Sacubitril/valsartan treatment improved cardiac structure in a rat model of hypertension-induced hypertrophic cardiomyopathy, increasing left ventricular internal diameter in systole (0.5 vs 0.22 cm, P<0.01).
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