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Oxygenation-sensitive Cardiac MRI with Vasoactive Breathing Maneuvers for the Non-invasive Assessment of Coronary Microvascular Dysfunction
Published on: August 17, 2022
Biventricular dysfunction and blood oxygenation deficits in obstructive sleep apnea: a prospective study with
Jianping Wang1,2, Ziqian Cheng3,4, Jie Du2,4
1Capital Medical University, Beijing, 100069, China.
Background:
Conventional cardiac magnetic resonance imaging(CMR) metrics may remain normal in Obstructive Sleep Apnea (OSA) despite subclinical myocardial injury, limiting early risk stratification. This study aimed to evaluate whether biventricular function, mechanics, and tissue characteristics assessed by non-contrast CMR differ between patients with severe and non-severe OSA, and to explore their association with markers of nocturnal hypoxemia.
Methods:
Seventy-five newly diagnosed OSA patients(62 male; age 43.7 ± 9.3 years) were prospectively included and underwent polysomnography followed by non-contrast CMR, including cine imaging, native T1 and T2 mapping. Patients were stratified by apnea-hypopnea index (AHI) into non-severe (n = 21, 4 mild and 17 moderate cases) and severe (n = 54) groups. Biventricular parameters were compared and correlated with AHI and the oxygen desaturation index (ODI).
Results:
Compared with non-severe OSA group, severe OSA group exhibited higher left ventricular mass (LVM) and lower left ventricular global circumferential and radial strain (all p < 0.05). Right ventricular (RV) dysfunction was more pronounced, with significantly lower in global longitudinal, circumferential, and radial strain and strain rates (all p < 0.05). The RV end-systolic remodeling index (RVESRI) was higher in severe OSA (p = 0.002). The right ventricular blood pool T2 value (RVT2) was significantly lower in severe OSA than in the non-severe OSA group and moderately correlated with AHI (ρ=-0.435) and ODI (ρ=-0.425). Collectively, multiple CMR parameters showed weak‑to‑moderate correlations with AHI and ODI (ρ ranging from - 0.301 to 0.476), indicating that OSA severity is associated with a broad spectrum of subclinical biventricular alterations rather than a single dominant abnormality.
Conclusion:
Severe OSA is associated with subclinical biventricular dysfunction, disproportionately affecting the RV. Elevated RVESRI may indicate early systolic maladaptation, while lower RVT2 shows promise as a non-invasive imaging marker associated with hypoxemic burden, warranting further investigation. Non-contrast CMR enables detection of cardiac injury, offering valuable potential for risk stratification in OSA patients.
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