Key result
Monocrotaline-induced pulmonary arterial hypertension in rats led to a 241.2% increase in right ventricle free wall thickness and a 24.3% reduction in left ventricle free wall weight at end-stage disease.
Why the study?
The study was conducted to assess changes in cardiac morphometric parameters at different stages of pulmonary arterial hypertension using a monocrotaline-induced rat model.
Does monocrotaline-induced pulmonary arterial hypertension alter cardiac morphometric parameters in Wistar rats?
Does monocrotaline-induced pulmonary arterial hypertension alter cardiac morphometric parameters in Wistar rats?
Effect estimate: 241.2% increase
Absolute Event Rate: 1.23% vs 0.51%
p-value: p=<0.001
In a rat model of pulmonary arterial hypertension, right ventricular hypertrophy and failure develop early, whereas left ventricular hypotrophy occurs in the end stages of the disease.
Animal model shows biventricular remodeling in PAH; leaves open translation to human disease and therapies.
BACKGROUND: Aim of this study was to assess changes in cardiac morphometric parameters at different stages of pulmonary arterial hypertension (PAH) using a monocrotaline-induced rat model. METHODS: Four groups were distinguished: I-control, non-PAH (n = 18); II-early PAH (n = 12); III-end-stage PAH (n = 23); and IV-end-stage PAH with myocarditis (n = 7). RESULTS: Performed over the course of PAH in vivo echocardiography showed significant thickening of the right ventricle free wall (end-diastolic dimension), tricuspid annular plane systolic excursion reduction and decrease in pulmonary artery acceleration time normalized to cycle length. No differences in end-diastolic left ventricle free wall thickness measured in echocardiography was observed between groups. Significant increase of right ventricle and decrease of left ventricle systolic pressure was observed over the development of PAH. Thickening and weight increase (241.2% increase) of the right ventricle free wall and significant dilatation of the right ventricle was observed over the course of PAH (p < 0.001). Reduction in the left ventricle free wall thickness was also observed in end-stage PAH (p < 0.001). Significant trend in the left ventricle free wall weight decrease was observed over the course of PAH (p < 0.001, 24.3% reduction). Calculated right/left ventricle free wall weight ratio gradually increased over PAH stages (p < 0.001). The reduction of left ventricle diameter was observed in rats with end-stage PAH both with and without myocarditis (p < 0.001). CONCLUSIONS: PAH leads to multidimensional changes in morphometric cardiac parameters. Right ventricle morphological and functional failure develop gradually from early stage of PAH, while left ventricle changes develop at the end stages of PAH.
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Hołda et al. (2020) studied Pulmonary arterial hypertension (n=60). Monocrotaline vs. Dulbecco's Phosphate Buffered Saline was evaluated on Right ventricle free wall thickness (241.2% increase, p=<0.001). Monocrotaline-induced pulmonary arterial hypertension in rats led to a 241.2% increase in right ventricle free wall thickness and a 24.3% reduction in left ventricle free wall weight at end-stage disease.
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