We read with great interest the article Right ventriculoarterial coupling as a marker of subclinical myocardial damage in rheumatoid arthritis by Quezada et al.1 We commend the authors for studying this important and underexplored issue. However, we would like to offer several constructive comments to enhance the clarity and rigor of the manuscript.
Firstly, the acronym “DALYs” is used repeatedly throughout the manuscript without a clear definition. In public health, DALYs are widely recognized as Disability-Adjusted Life Years, a measure of disease burden. However, the authors seem to repurpose this acronym as an echocardiographic parameter. This unconventional usage risks confusion, especially since rheumatoid arthritis (RA) itself significantly contributes to global DALYs, as highlighted in the Global Burden of Disease Study 2021.2 We recommend clarifying this term explicitly to avoid ambiguity and maintain scientific precision.
Regarding the study design, this is a single-center study with a relatively small sample size, which limits generalizability. Nevertheless, it serves as a valuable pilot for larger future studies. Patient inclusion was based on the ACR/EULAR 2010 classification criteria.3 It is worth noting that the updated 2022 criteria enable earlier RA identification in patients without clinically evident synovitis, potentially influencing cardiovascular risk stratification and subclinical myocardial damage detection.4
The rationale for conducting echocardiograms in asymptomatic patients without clear cardiovascular risk factors needs clarification. While literature reports increased prevalence of subclinical myocardial dysfunction in RA,5 current professional guidelines do not recommend routine echocardiographic screening for asymptomatic patients.3 Imaging should be individualized based on symptoms or established risk factors.
The manuscript omits details on RA treatment regimens, which is a critical gap. Various therapies have differential cardiovascular effects. For instance, NSAIDs and glucocorticoids are associated with increased cardiovascular risk, including myocardial infarction and heart failure. Among disease-modifying antirheumatic drugs (DMARDs), methotrexate and most biologics reduce cardiovascular risk by controlling inflammation. However, tumor necrosis factor inhibitors (TNFi) such as etanercept and infliximab may worsen heart failure and are contraindicated in advanced stages (NYHA III/IV).6
Hydroxychloroquine, generally safe, has been linked to increased heart failure hospitalization risk in patients with prior cardiac dysfunction.7 Inclusion of treatment data would significantly enhance result interpretation.
The authors report 65% of RA patients had active disease based on clinical scores (PhsGA, PtGA, CDAI, SDAI, DAS28). Disease activity degree critically influences myocardial damage extent, even in asymptomatic individuals. Evidence indicates that higher inflammatory activity correlates with subclinical myocardial inflammation measured by PET-FDG,8 elevated high-sensitivity troponin, and reduced systolic function via global longitudinal strain. Achieving tight disease control may reduce myocardial injury risk.9
Regarding laboratory data, leukocyte count was mentioned but absent in comparative tables. Although leukocyte indices cannot replace validated activity scores or acute-phase reactants, they can serve as supplementary markers and should be consistently reported.
Notably, 65% of patients were anti-cyclic citrullinated peptide (anti-CCP) antibody positive. Anti-CCP positivity independently predicts increased cardiovascular risk and subclinical myocardial injury. It is linked to diastolic dysfunction, left ventricular hypertrophy, vascular remodeling, and coronary artery calcification.10 CCP status should be incorporated in analyses and interpretation.
Finally, reiterating the confusion regarding “DALYs,” it is essential that the authors clarify the term's use as an echocardiographic marker, distinct from the well-established public health metric. This will improve manuscript clarity and scientific rigor.
In conclusion, this study addresses a relevant and novel clinical question concerning subclinical myocardial dysfunction in RA patients. We encourage the authors to clarify the “DALYs” terminology, provide treatment data, and consider serological markers like anti-CCP antibodies. These steps will strengthen the findings’ interpretation and clinical applicability.
Institutional review board statementThe study was conducted in accordance with the Declaration of Helsinki.
Informed consent statementNo informed consent was necessary.
FundingThis research received no external funding.
Conflicts of interestThe authors declare no conflict of interest.
Data availability statementThe authors confirm that the data supporting the findings of this study are available from the corresponding author, upon reasonable request.


