Objective To investigate the therapeutic effects of a newly developed PDE5 inhibitor, CPD1, on pathological myocardial hypertrophy induced by abdominal aortic constriction (AAC) in rats, and its impact on the activation of the autophagy signaling pathway in myocardial tissue. Methods Male Sprague-Dawley (SD) rats weighing between 180 and 200 grams were randomly assigned to five groups: control group, the Sham surgery group, AAC model group, the CPD1 treatment group (5 mg/kg), and the sildenafil treatment group (20 mg/kg). The rats underwent blunt dissection of the abdominal aorta at the branch point of the left renal artery beside control group. The AAC model and treatment groups received constriction and ligation surgery, while the Sham group underwent dissection without ligation. After three days of modeling, the treatment group rats received either CPD1 or sildenafil via gavage, while control group, the sham group and model group were administered an equal volume of physiological saline by gavage once daily for eight weeks. Small animal ultra-high-resolution echocardiography and left ventricular catheterization were employed to assess left heart function in rats, calculate the heart mass index, and evaluate the expression of the hypertrophy factor atrial natriuretic peptide (ANP), the key autophagy pathway factor p62, and LC3A/B in rat left heart tissue using Western blot and RT-PCR techniques. Results Abdominal aortic stenosis leads to damage in left heart function in rats, characterized by an increase in cardiac mass index and a significant enlargement of myocardial cell cross-sectional area. The expression of ANP in left heart tissue is significantly elevated (P < 0.05). Additionally, autophagy signaling activity is diminished, with a notable accumulation of LC3-I protein and a reduced conversion to LC3-II. Furthermore, the expression of p62 protein is significantly increased. CPD1 and sildenafil significantly improved left ventricular function in AAC rats, reduced cardiac hypertrophy, inhibited the expression of hypertrophic factors ANP and p62 protein (P < 0.05), activated autophagy signaling, and promoted the conversion of LC3-I to LC3-II. Notably, low-dose CPD1 treatment is equivalent to high-dose sildenafil. Conclusions CPD1 promotes the activation of the autophagy signaling pathway in left heart tissue, inhibits the expression of p62 and ANP, reduces the cross-sectional area of myocardial cells, and improves pathological myocardial hypertrophy as well as left heart function impairment caused by abdominal aortic constriction. Additionally, CPD1 has the advantage of a lower effective dose compared to sildenafil, offering a new option for the treatment of pathological myocardial hypertrophy.