Aim: To investigate whether the presence of left ventricular myocardial dysfunction (LVMD) assessed by Tei index (LVTX) impacts the outcomes of healthy infants with Respiratory Syncytial Virus Bronchiolitis (RSVB). To explore whether N-terminal pro-B-type natriuretic peptide (NT-proBNP) increases the accuracy of traditional clinical markers in predicting the outcomes. Methods: A single-centre, prospective, cohort study including healthy infants aged 1–12 months old admitted for RSVB between 1 October 2016 and 1 April 2017. All patients underwent clinical, laboratory and echocardiographic evaluation within 24 h of admission. Paediatric intensive care unit (PICU) admission was defined as severe disease. Results: We enrolled 50 cases of RSVB (median age of 2 (1–6.5) months; 40% female) and 50 age-matched controls. We observed higher values of LVTX in infants with RSVB than in controls (0.42 vs. 0.36; p = 0.008). Up to nine (18%) children presented with LVMD (LVTX > 0.5), with a higher incidence of PICU admission (89% vs. 5%; p < 0.001). The diagnostic performance of NT-proBNP in predicting LVMD was high (area under the receiver operator characteristic curve (AUC) 0.95, CI 95% 0.90–1). The diagnostic yield of the predictive model for PICU admission that included NT-proBNP was excellent (AUC 0.945, CI 95% 0.880–1), and significantly higher than the model without NT-proBNP (p = 0.026). Conclusions: LVMD could be present in healthy infants with RSVB who develop severe disease. NT-proBNP seems to improve traditional clinical markers for outcomes.

Dystrophin-deficient cardiomyopathy (DDC) is currently the leading cause of death in patients with dystrophinopathies. Targeting myocardial fibrosis (MF) has become a major therapeutic goal in order to prevent the occurrence of DDC. We aimed to review and summarize the current evidence about the role of the renin–angiotensin–aldosterone system (RAAS) in the development and perpetuation of MF in DCC. We conducted a comprehensive search of peer-reviewed English literature on PubMed about this subject. We found increasing preclinical evidence from studies in animal models during the last 20 years pointing out a central role of RAAS in the development of MF in DDC. Local tissue RAAS acts directly mainly through its main fibrotic component angiotensin II (ANG2) and its transducer receptor (AT1R) and downstream TGF-b pathway. Additionally, it modulates the actions of most of the remaining pro-fibrotic factors involved in DDC. Despite limited clinical evidence, RAAS blockade constitutes the most studied, available and promising therapeutic strategy against MF and DDC. Conclusion: Based on the evidence reviewed, it would be recommendable to start RAAS blockade therapy through angiotensin converter enzyme inhibitors (ACEI) or AT1R blockers (ARBs) alone or in combination with mineralocorticoid receptor antagonists (MRa) at the youngest age after the diagnosis of dystrophinopathies, in order to delay the occurrence or slow the progression of MF, even before the detection of any cardiovascular alteration.

This study aims to systematically review the incidence of myocardial strain detected by echocardiography in previously healthy infants with acute bronchiolitis and its role as a predictor for adverse outcomes in this setting. Methods: Pubmed/Medline, Excerpta Medica Data Base (EMBASE), and Cochrane Library were searched in April 2020 to identify original observational prospective studies that systematically performed echocardiography for the screening of myocardial strain in healthy infants with acute bronchiolitis. Pooled estimates were generated using random-effects models. Heterogeneity within studies was assessed using Cochran’s Q and I² statistics. Funnel plots and Egger´s regression method were constructed to evaluate publication bias. Sensitivity analyses were also conducted to evaluate potential sources of heterogeneity. Results: After a detailed screening of 305 articles, a total of 10 studies with 395 participants (mean of 40 participants per study) was included. Five of them were classified as high-quality studies. Up to 28% of cases presented adverse outcomes. The echocardiographic screening for myocardial strain was performed within the first 24 h of admission in 92% cases. Tissue Doppler imaging and Speckle-Tracking echocardiography were performed only in 20% of cases. The presence of pulmonary hypertension was evaluated with methods different from the tricuspid regurgitation jet in 64% of cases. Seven studies found some grade of myocardial strain with a pooled incidence of 21% (CI 95%, 11–31%), in the form of pulmonary hypertension (pooled incidence of 20% (CI 95%, 11–30%)), and myocardial dysfunction (pooled incidence of 5% (CI 95%, 1–9%)). The presence of these echocardiographic alterations was associated with adverse outcomes (pooled relative risk = 16; CI 95%, 8.2–31.5). After a subgroup analysis based on the echocardiographic techniques used, no significant heterogeneity across the studies was observed. There was no evidence of publication bias when assessed by Egger´s test. Cardiac biomarkers to assess myocardial strain were used in five studies. Only N-terminal-pro-brain natriuretic peptide accurately predicted the presence of myocardial strain by echocardiography. Conclusions: Myocardial strain is not infrequent in previously healthy infants with acute bronchiolitis, and it could be present at the early stages of the disease with prognostic implications. There is a need for sufficiently powered prospective studies with a similar methodology, preferably employing advanced imaging techniques, to conclusively address the usefulness of the assessment of myocardial strain in this setting.

Dystrophin-deficient cardiomyopathy (DDC) is currently the leading cause of death in patients with dystrophinopathies. Targeting myocardial fibrosis (MF) has become a major therapeutic goal in order to prevent the occurrence of DDC. We aimed to review and summarize the current evidence about the role of the renin-angiotensin-aldosterone system (RAAS) in the development and perpetuation of MF in DCC. We conducted a comprehensive search of peer-reviewed English literature on PubMed about this subject. We found increasing preclinical evidence from studies in animal models during the last 20 years pointing out a central role of RAAS in the development of MF in DDC. Local tissue RAAS acts directly mainly through its main fibrotic component angiotensin II (ANG2) and its transducer receptor (AT1R) and downstream TGF-b pathway. Also, it modulates the actions of most of the remaining pro-fibrotic factors involved in DDC. Despite limited clinical evidence, RAAS blockade constitutes the most studied, available and promising therapeutic strategy against MF and DDC. Conclusion: Based on the evidence reviewed, it would be recommendable to start RAAS blockade therapy through angiotensin converter enzyme inhibitors (ACEI) or AT1R blockers (ARBs) alone or in combination with mineralocorticoid receptor antagonists (MRa) at the youngest age after the diagnosis of dystrophinopathies, in order to delay the occurrence or slow the progression of MF, even before the detection of any cardiovascular alteration.