Key result
Sleep fragmentation drives rapid transition from hypertrophy to dilated heart failure in preclinical HCM.
Why the study?
Sleep fragmentation disrupts biological rhythms and impacts cardiovascular health, but had never been shown to be a risk factor in the transition from cardiac hypertrophy to heart failure.
Does sleep fragmentation induce heart failure in a hypertrophic cardiomyopathy mouse model?
Does sleep fragmentation induce heart failure in a hypertrophic cardiomyopathy mouse model?
Sleep fragmentation accelerates the transition from cardiac hypertrophy to heart failure in a genetic mouse model of HCM by inducing mitochondrial dysfunction and altering redox metabolism.
May suggest sleep fragmentation as modifiable in HCM; leaves open whether interventions alter progression in patients.
Sleep fragmentation (SF) disrupts normal biological rhythms and has major impacts on cardiovascular health; however, it has never been shown to be a risk factor involved in the transition from cardiac hypertrophy to heart failure (HF). We now demonstrate devastating effects of SF on hypertrophic cardiomyopathy (HCM). We generated a transgenic mouse model harboring a patient-specific myosin binding protein C3 (MYBPC3) variant displaying HCM, and measured the progression of pathophysiology in the presence and absence of SF. SF induces mitochondrial damage, sarcomere disarray, and apoptosis in HCM mice; these changes result in a transition of hypertrophy to an HF phenotype by chiefly targeting redox metabolic pathways. Our findings for the first time show that SF is a risk factor for HF transition and have important implications in clinical settings where HCM patients with sleep disorders have worse prognosis, and strategic intervention with regularized sleep patterns might help such patients.
No takes yet. Share an insight, caveat, or question.
Bose et al. (2024) studied Hypertrophic Cardiomyopathy (HCM) and Heart Failure. Sleep fragmentation vs. Non-sleep fragmented mice (NSF) was evaluated on Transition to heart failure phenotypes (ejection fraction, fractional shortening, ventricular dilation). Sleep fragmentation induced a rapid transition from cardiac hypertrophy to a dilated heart failure phenotype in a genetically predisposed HCM mouse model by causing mitochondrial damage and redox stress.
Synapse has enriched 5 closely related papers on similar clinical questions. Consider them for comparative context: