We commend Jamschid S et al. for their contribution to exploring the association between sleep disorders and subsequent heart failure (HF). The study investigates whether HF patients with sleep disorders experience poorer prognoses compared to those without sleep disorders. Patients with HF frequently exhibit sleep-related breathing disturbances, yet the causal relationship between sleep disorders and HF onset remains unclear. Therefore, early screening for high-risk populations with sleep disorders is of particular importance [1]. However, the article has certain limitations that, if addressed through revisions, could more effectively guide disease management and enhance its contribution to clinical practice.
First, the study did not account for the diagnostic delay effect in HF, where the actual onset of HF may precede the first recorded diagnosis. Such delays may obscure the true association between sleep disorders and HF. Early diagnosis of HF is critical, as the initial clinical confirmation of chronic HF often occurs much later than the actual disease progression. For instance, 50 % of all AF patients present with moderate-to-severe sleep disorders [2]. If diagnostic delays exist, the observed strong association between sleep disorders and HF in the original study might partially reflect sleep disturbances caused by early HF symptoms (e.g., dyspnea, nocturnal cough) rather than sleep disorders directly contributing to HF pathogenesis. Second, the article lacks analysis of psychiatric comorbidities (e.g., bipolar disorder, post-traumatic stress disorder) that may independently increase both sleep disorders and cardiovascular risks. Psychiatric conditions such as bipolar disorder or major depressive disorder (MDD) are known to elevate the prevalence of sleep disturbances and concurrently heighten cardiovascular risks. For example, Zhao et al. demonstrated that insomnia is associated with higher risks of certain subtypes of cardiovascular disease, partially mediated by MDD [3]. Failure to adjust for psychiatric comorbidities may lead to overestimation or confounding of the observed association between sleep disorders and HF. Third, the study did not incorporate genetic background or family history of patients, potentially confounding the assessment of sleep disorder- or HF-related risks and limiting the accuracy of individualized risk stratification. Recent genetic epidemiological research by Dashti et al. revealed that specific genetic variants (e.g., alleles in HCRTR1 rs2271933, HCRTR2 rs2653349, and missense variants in TRPC6) may jointly predispose individuals to both sleep disorders and HF [4]. Without accounting for genetic factors, the observed sleep disorder-HF association might not reflect pure causality but could instead be driven by shared genetic risk factors.
In conclusion, while this systematic review provides valuable insights into the relationship between sleep disorders and HF, future research designs should rigorously evaluate diagnostic delay effects and incorporate assessments of psychiatric comorbidities and genetic susceptibility. Addressing these limitations would enhance the clinical applicability of the findings and further improve patient prognoses.
| Research design | Description of limitations | Potential impact | |
|---|---|---|---|
| 1 | The study did not fully explore the diagnostic delay effect in HF. | HF may precede the first recorded diagnosis. | Early HF symptoms may directly contributing to HF pathogenesis. |
| 2 | The analysis did not incorporate the assessment of psychiatric comorbidities. | It may independently increase both sleep disorders and cardiovascular risks. | It may overestimation the association. |
| 3 | The investigation lacks genetic background or family history of patients. | It potentially confounding the assessment of sleep disorder-or HF-related risks. | The association might instead be driven by shared genetic risk factors. |
CRediT authorship contribution statement
Qiulu Wang: Writing – original draft. Ying Hai: Writing – review & editing.
Funding
We claim that the study was independently conducted without specific financial support from funding agency in public, commercial, or not-for-profit sectors.
Declaration of competing interest
The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper.
Acknowledgments
We sincerely acknowledge all participants for their value time and effort in this study.
Disclosure.
This study was conducted in no commercial collaborations or financial relationships existed throughout the research process that could lead to potential conflicts of interest.
References
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