ArticleThe British journal of cardiology2025
ACE inhibitors reduce the risk of myocardial fibrosis post-cardiac injury: a systematic review.
Article in The British journal of cardiology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
2 citing papers in PubMed.
- Article
- Inflammasomes as Potential Therapeutic Targets to Prevent Chronic Active Viral Myocarditis-Translating Basic Science into Clinical Practice.International journal of molecular sciences · 2025Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Myocardial fibrosis is a common pathological process associated with various cardiovascular diseases, contributing to adverse cardiac remodelling and increased morbidity. Angiotensin-converting enzyme inhibitors (ACEi) have been widely used for myocardial protection in high-risk patients. However, there are no clear recommendations for their use for the prevention of fibrosis after myocardial injury. On the other hand, procollagen type III amino-terminal propeptide (PIIIP) and procollagen type I propeptide (PIP) have been identified as effective biomarkers for predicting fibrotic change in the myocardium. It is important to evaluate the effects of ACEi by PIIIP and PIP levels to provide insights into the potential antifibrotic effects of ACEi. We assessed the effects of ACEi on the process of fibrosis in the myocardium through serum levels of PIIIP and PIP. Four databases were searched to identify relevant studies investigating the association between the use of ACEi and myocardial fibrosis marked by PIIIP and PIP levels. Animal and non-original research articles were excluded. Six studies with a total of 706 participants met the inclusion criteria. Three studies assessed the change of PIIIP and PIP levels in patients with hypertension, while the other three were in patients with heart failure, myocardial infarction and congenital heart diseases. The included studies demonstrated a significant reduction in PIIIP and PIP serum levels with ACEi therapy (p<0.05), except in patients with post-myocardial infarction. The mean reduction in serum PIIIP levels in all patients treated by ACEi was 20.8%. These results suggest that ACEi can effectively inhibit collagen synthesis and deposition in the myocardium, potentially preventing, or even reversing, the progression of myocardial fibrosis. This supports the idea that ACEi have potent antifibrotic effects and can contribute to improved clinical outcomes in cardiac conditions that are not currently indicated, including myocarditis.
Indexed as
Identifiers
What Socratic holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the Socratic graph.