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.

Anthracyclines remain a cornerstone of cancer therapy but are associated with a spectrum of cardiovascular toxicity, ranging from subclinical myocardial injury to overt heart failure (HF). Despite strong biological rationale, the role of universal pharmacologic prophylaxis remains uncertain. In this context, the recent meta-analysis by Pizzi et al. provides a timely synthesis of randomized evidence evaluating angiotensin-converting enzyme inhibitors (ACEi) for the prevention of anthracycline-related cardiotoxicity. The analysis demonstrates a statistically significant attenuation of left ventricular ejection fraction decline with ACEi prophylaxis, although the absolute effect size is modest and accompanied by substantial heterogeneity. Importantly, the magnitude of benefit appears to be context-dependent, with more consistent effects observed in higher-risk settings, such as combined anthracycline and trastuzumab exposure or in patients with early markers of myocardial injury. Contemporary data suggest that declining event rates and improved supportive care may limit the ability of prophylaxis trials to detect clinically meaningful differences in low-risk populations. Furthermore, the absence of significant effects on clinical endpoints underscores the limitations of current surrogate markers and trial design. Emerging evidence supports a more nuanced, risk-adapted approach, integrating early detection strategies such as global longitudinal strain and biomarker-guided intervention. Within this framework, ACEi prophylaxis may be most appropriately targeted to patients with higher baseline risk or early evidence of myocardial injury, rather than applied universally. Future studies should prioritize risk enrichment, standardized imaging protocols, and clinically meaningful outcomes to better define the role of cardioprotective strategies in cardio-oncology.

This study explored the association between enalapril-folic acid treatment and the likelihood of developing cardiovascular disease (CVD) in patients with hemorrhagic stroke combined with H-type hypertension. This prospective study involved 799 patients diagnosed with hemorrhagic stroke and H-type hypertension (defined as total homocysteine levels ≥ 10 μmol/L). Patients were instructed to take a daily regimen of enalapril (10 mg) and folic acid (0.8 mg) and were monitored for a median duration of 9.6 months. Adherence to the treatment was classified as either high (≥ 70%) or low (< 70%). The study's primary endpoint comprised a combination of CVD events, such as cardiovascular mortality, nonfatal myocardial infarction, and nonfatal stroke. The relationship between adherence to treatment and clinical outcomes was analyzed using Cox proportional hazards models, controlling for confounding factors. Subgroup analyses investigated interactions within stratifications of sex, age (< 65 vs ≥ 65 years), body mass index (< 24 vs ≥ 24 kg/m2), seated blood pressure (< 160 vs ≥ 160 mm Hg), total cholesterol (< 4.6 vs ≥ 4.6 mmol/L), and total homocysteine (< 13.7 vs ≥ 13.7 μmol/L). During the follow-up, 40 participants (5.0%) developed CVD, and 21 participants (2.6%) experienced recurrent hemorrhagic stroke. Patients with high adherence to enalapril-folic acid therapy exhibited significantly reduced risks of CVD (hazard ratio [HR]: 0.16; 95% confidence interval [CI]: 0.06-0.45), recurrent hemorrhagic stroke (HR: 0.21; 95% CI: 0.07-0.67), and all-cause mortality (HR: 0.14; 95% CI: 0.05-0.41) when compared to those with low adherence. Greater compliance with enalapril-folic acid therapy was associated with decreased CVD and recurrent hemorrhagic stroke incidence in hypertensive individuals with elevated homocysteine levels. The results indicated that folic acid supplementation may be a promising strategy for secondary stroke prevention. Nonetheless, further randomized controlled trials are required to confirm its efficacy.

High-protein fermented milks are promising vehicles for delivering probiotics and bioactive compounds, contributing to health promotion, particularly in the context of healthy aging. This study evaluated the effect of fermenting dairy formulations with different protein profiles using Lacticaseibacillus rhamnosus, with a focus on bioactive potential and peptide bioaccessibility. Milk was supplemented with calcium caseinate (CC) or whey protein isolate (WPI) to obtain distinct protein profiles. Fermented and non-fermented formulations were submitted to in vitro gastrointestinal digestion under older adults' conditions, followed by the assessment of probiotic viability, bacterial growth-promoting effect, angiotensin-converting enzyme (ACE) inhibitory activity, and peptide bioaccessibility. L. rhamnosus remained highly viable after intestinal digestion (7.27 log CFU/mL). Fermentation also exerted a positive effect on L. rhamnosus growth-promoting potential, particularly in the WPI-supplemented formulation. Furthermore, formulations containing WPI exhibited greater ACE inhibition. The peptide profile revealed sequences derived from caseins, especially the β-casein fraction, including peptides previously described as bioactive. Overall, these findings highlight the combined role of fermentation by L. rhamnosus and protein profile in modulating the bioactive potential of high-protein fermented milks. The results also support their potential as multifunctional matrices capable of delivering bioaccessible peptides with biological relevance, contributing to the development of products aimed at promoting health during aging.