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Abnormal circadian rhythms exacerbate dilated cardiomyopathy by reducing the ventricular mechanical strength

Hao Jia1, Hao Cui1, Zijie Zhao1

  • 1Beijing Key Laboratory of Preclinical Research and Evaluation for Cardiovascular Implant Materials, Animal Experimental Centre, National Centre for Cardiovascular Disease, Department of Cardiac Surgery, Fuwai Hospital, Chinese Academy of Medical Sciences and Peking Union Medical College, 167A Beilishi Road, Beijing 100037, China.

Cardiovascular Research
|September 13, 2024
PubMed

Insights

Sleep apnea is linked to more severe dilated cardiomyopathy (DCM) in patients, causing weaker heart walls and disrupted cellular patterns. This study investigates abnormal circadian rhythms (ACR) in DCM associated with sleep apnea (SA).

Area of Science:

  • Cardiovascular Research
  • Chronobiology
  • Genomics

Background:

  • Dilated cardiomyopathy (DCM) exhibits significant etiological and pathophysiological heterogeneity.
  • Abnormal circadian rhythms (ACR) are implicated in DCM development in animal models, but clinical data is limited.
  • Sleep apnea (SA) is a common condition associated with ACR, making it a relevant focus for studying ACR-DCM.

Purpose of the Study:

  • To investigate the relationship between sleep apnea (SA) and abnormal circadian rhythms (ACR) in patients with dilated cardiomyopathy (DCM).
  • To explore the molecular and structural changes in the heart associated with ACR-DCM in the context of SA.

Main Methods:

  • Included derivation (n=105) and validation (n=65) cohorts of DCM patients, categorized into SA and non-SA groups.
  • Utilized RT-qPCR to assess rhythm gene expression patterns in heart samples.
  • Employed single-nucleus RNA sequencing (snRNA-seq) to identify abnormal transcriptional patterns, with verification via pathological staining, atomic force microscopy (AFM), and knockout mouse models.

Main Results:

  • DCM patients with SA exhibited reduced amplitude in rhythm gene expression and more severe dilation of left heart chambers.
  • snRNA-seq revealed a loss of morning transcriptional patterns in ACR-DCM, characterized by disrupted cardiomyocyte actin cytoskeleton organization and aggravated hypertrophy.
  • Observed a decrease in activated fibroblasts and fibrotic area ratio in the SA group, supported by pathological and mechanical analyses.

Conclusions:

  • DCM patients with SA present with more severe left ventricular dilation and reduced structural integrity compared to non-SA patients.
  • Phenotypic alterations in cardiomyocytes and fibroblasts are key contributors to the structural weakness observed in ACR-DCM.
  • ACR-DCM is histopathologically defined by a structurally compromised ventricular wall, particularly in the presence of SA.
Abstract

Keywords:
Circadian rhythmCytoskeletonDilated cardiomyopathyFibrosisSleep apneaTranscriptome

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