Background Galectin-3, considered as a new inflammatory marker; it is increased in cardiovascular disease. We investigated Galectin-3 in relation to heart damage in patients with OSA and its role in inflammation, based on the Neutrophil-to-Lymphocyte Ratio (NLR). Methods Sixty-three consecutive patients (45 males, 18 females, 58.60±12.28 years old) were studied. According to the Apnoea-Hypopnoea Index (AHI) patients were divided into Group 1 – non-severe (AHI <30) (17 males and 10 females, 59.89 ± 10.62 years old) and Group 2 - severe (AHI ≥30) (29 males and 6 females, aged 57.53 ± 13.30 years old) OSA. All patients underwent morning blood gas analysis, laboratory tests, nocturnal polygraphy, and echocardiography. Results Galectin-3 was significantly increased in Group 2 (p=0.027) patients. Moreover, it was directly related to left ventricle (LV) mass, left ventricle hypertrophy and LV posterior wall diameter. Tissue Doppler septal velocity (e’), that measures wall motion, was inversely correlated to Galectin-3. Furthermore, a direct association to diastolic dysfunction, evaluated as E/e’ ratio, was observed. In line with these data, a direct correlation between Galectin-3 and left atrium volume was also found. Galectin-3 and percentage of total registration time with nocturnal oxygen saturation <90% (TST90) were directly correlated (p=0.0003), while Galectin-3 and mean nocturnal SpO2 were negatively correlated (p=0.0045). We found a direct correlation between Galectin-3 and NLR (p=0.011). Finally, Galectin-3 was able to predict 3-yr mortality with a specificity of 83.33% and a sensitivity of 91.84%. Conclusion Galectin-3 showed a direct association to nocturnal respiratory indices and to cardiac remodelling in patients with OSA. OSA-induced inflammation may play an important role in the pathogenesis of heart damage.

Galectin-3 and Neutrophil-to-Lymphocyte ratio are indicative of heart remodelling and disease severity in patients with Obstructive Sleep Apnoea

Sebastiano Cicco
;
Giorgio Castellana;Lorenzo Marra;Valentina Di Lecce;Pierluigi Carratù;Marcella Prete;Giuseppe Ranieri;Onofrio Resta;Giovanna Elisiana Carpagnano;Vito Racanelli;Silvano Dragonieri;Angelo Vacca
2021

Abstract

Background Galectin-3, considered as a new inflammatory marker; it is increased in cardiovascular disease. We investigated Galectin-3 in relation to heart damage in patients with OSA and its role in inflammation, based on the Neutrophil-to-Lymphocyte Ratio (NLR). Methods Sixty-three consecutive patients (45 males, 18 females, 58.60±12.28 years old) were studied. According to the Apnoea-Hypopnoea Index (AHI) patients were divided into Group 1 – non-severe (AHI <30) (17 males and 10 females, 59.89 ± 10.62 years old) and Group 2 - severe (AHI ≥30) (29 males and 6 females, aged 57.53 ± 13.30 years old) OSA. All patients underwent morning blood gas analysis, laboratory tests, nocturnal polygraphy, and echocardiography. Results Galectin-3 was significantly increased in Group 2 (p=0.027) patients. Moreover, it was directly related to left ventricle (LV) mass, left ventricle hypertrophy and LV posterior wall diameter. Tissue Doppler septal velocity (e’), that measures wall motion, was inversely correlated to Galectin-3. Furthermore, a direct association to diastolic dysfunction, evaluated as E/e’ ratio, was observed. In line with these data, a direct correlation between Galectin-3 and left atrium volume was also found. Galectin-3 and percentage of total registration time with nocturnal oxygen saturation <90% (TST90) were directly correlated (p=0.0003), while Galectin-3 and mean nocturnal SpO2 were negatively correlated (p=0.0045). We found a direct correlation between Galectin-3 and NLR (p=0.011). Finally, Galectin-3 was able to predict 3-yr mortality with a specificity of 83.33% and a sensitivity of 91.84%. Conclusion Galectin-3 showed a direct association to nocturnal respiratory indices and to cardiac remodelling in patients with OSA. OSA-induced inflammation may play an important role in the pathogenesis of heart damage.
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Utilizza questo identificativo per citare o creare un link a questo documento: https://hdl.handle.net/11586/367251
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