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It is also unclear whether the hypertrophied right ventricle (RV) and left ventricle (LV) differ in their responsiveness to long\u2010term PDE5i and if this therapy affects renal function. The goal of this study was to elucidate the effect of PDE5i treatment in VO due to aorto\u2010caval fistula (ACF) and to compare PDE5i treatment with standard heart failure (HF) therapy with angiotensin\u2010converting enzyme inhibitor (ACEi). ACF\/sham procedure was performed on male HanSD rats aged 8\u2009weeks. ACF animals were randomized for PDE5i sildenafil, ACEi trandolapril, or placebo treatments. After 20\u2009weeks, RV and LV function (echocardiography, pressure\u2010volume analysis), myocardial gene expression, and renal function were studied. Separate rat cohorts served for survival analysis. ACF led to biventricular eccentric hypertrophy (LV: +68%, RV: +145%), increased stroke work (LV: 3.6\u2010fold, RV: 6.7\u2010fold), and reduced load\u2010independent systolic function (PRSW, LV: \u221254%, RV: \u221251%). Both ACF ventricles exhibited upregulation of the genes of myocardial stress and glucose metabolism. ACEi but not PDE5i attenuated pulmonary congestion, LV remodeling, albuminuria, and improved survival (median survival in ACF\/ACEi was 41\u2009weeks vs. 35\u2009weeks in ACF\/placebo, <jats:italic>p<\/jats:italic>\u2009=\u2009.02). PDE5i increased cyclic guanosine monophosphate levels in the lungs, but not in the RV, LV, or kidney. PDE5i did not improve survival rate and cardiac and renal function in ACF rats, in contrast to ACEi. VO\u2010induced HF is not responsive to PDE5i therapy.<\/jats:p>","DOI":"10.1002\/prp2.1172","type":"journal-article","created":{"date-parts":[[2024,1,29]],"date-time":"2024-01-29T09:26:41Z","timestamp":1706520401000},"update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":4,"title":["The impact of phosphodiesterase\u20105 inhibition or angiotensin\u2010converting enzyme inhibition on right and left ventricular remodeling in heart failure due to chronic volume overload"],"prefix":"10.1002","volume":"12","author":[{"ORCID":"https:\/\/orcid.org\/0000-0001-8434-0165","authenticated-orcid":false,"given":"Tereza","family":"Tykvartova","sequence":"first","affiliation":[{"name":"Institute for Clinical and Experimental Medicine\u2014IKEM  Prague Czech Republic"},{"name":"Department of Pathophysiology, Second Faculty of Medicine Charles University  Prague Czech 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Technology  Prague Czech Republic"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Michal","family":"Kolar","sequence":"additional","affiliation":[{"name":"Laboratory of Genomics and Bioinformatics Institute of Molecular Genetics of the Czech Academy of Sciences  Prague Czech Republic"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0003-1338-638X","authenticated-orcid":false,"given":"Jiri","family":"Novotny","sequence":"additional","affiliation":[{"name":"Laboratory of Genomics and Bioinformatics Institute of Molecular Genetics of the Czech Academy of Sciences  Prague Czech Republic"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0001-8921-7078","authenticated-orcid":false,"given":"Vojtech","family":"Melenovsky","sequence":"additional","affiliation":[{"name":"Institute for Clinical and Experimental Medicine\u2014IKEM  Prague Czech 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