Sleep fragmentation mimicking sleep apnea does not alter cardiac function in either control or heart failure mice

Background: Obstructive sleep apnea (OSA) has been associated with worsening heart failure. Sleep fragmentation (SF), one of the major hallmarks of OSA, induces inflammation, oxidative stress and sympathetic activation, and could potentially contribute to OSA-induced cardiovascular consequences. However, it remains unclear whether SF per se is deleterious to cardiac function. Aim: To evaluate the effect of SF mimicking OSA on echocardiographically-measured cardiac function (ECHO) in otherwise healthy mice and in a murine model of heart failure. Methods: Forty C57BL/6J male mice were randomized into 4 treatment groups: control sleep, sleep fragmentation (SF), isoproterenol-induced heart failure (HF), and SF+HF. ECHO was measured at baseline and after 30 days. Left ventricular end-diastolic diameter, end-systolic diameter, shortening fraction and left ventricular ejection fraction were recorded by a blinded investigator. Results: Isoproterenol treatment promoted significant left ventricular dilatation and reduced systolic function in HF and SF+HF groups (in all cases p Conclusion: SF, as occurs in OSA, does not appear to induce ECHO-detectable deleterious changes in heart structure and function.