Diastolic dysfunction in men with severe obstructive sleep apnea syndrome but without cardiovascular or oxidative stress-related comorbidities

Abstract

Background: We aimed to evaluate whether the severity of obstructive sleep apnea syndrome (OSAS) per se affects the prevalence of left ventricular (LV) diastolic dysfunction in patients without comorbidities.

Methods: A total of 42 patients with first-diagnosed severe OSAS [apnea-hypopnea index (AHI) > 30] and 25 controls (AHI < 5), having been referred for snoring to the Sleep Laboratory Department of our tertiary Hospital, were enrolled in the study. Inclusion criteria were absence of any cardiovascular or oxidative stress-related comorbidities, and age between 20 and 70 years. Clinical, laboratory, echocardiographic, and polysomnographic data were recorded prospectively. Diastolic dysfunction diagnosis and grading was based on 2016 ASE/EACVI recommendations.

Results: Severe OSAS was associated with significantly increased prevalence and degree of diastolic dysfunction (26/42; 61.9%) compared with controls (7/25; 28%) (p = 0.007). AHI ⩾ 55 (dichotomous value of severe OSAS subset) was also characterized by greater prevalence and degree of diastolic dysfunction compared with 30 < AHI < 55 patients (p = 0.015). In the severe OSAS subset, age >45 years-old, height <1.745 m, body-mass index (BMI) >27.76 kg m^-2, OSAS severity (AHI > 57.35), oxidative stress (overnight reduction of reduced to oxidized glutathione ratio < 18.44%), and BMI/height ratio > 16.155 kg m^-3 (an index describing 'dense', short-heavy patients) presented significant diagnostic utility in identifying diastolic dysfunction in ROC-curve analysis (0.697 ⩾ AUC ⩾ 0.855, 0.001 ⩽ p ⩽ 0.018). In binary logistic regression model, advanced age (OR 1.23, 95% CI 1.025-1.477; p = 0.026) and AHI (OR 1.123, 95% CI 1.007-1.253; p = 0.036) showed independent association with diastolic dysfunction in severe OSAS.

Conclusions: The present prospective study may suggest that severe OSAS is significantly associated with LV diastolic dysfunction; OSAS clinical severity exerts a positive influence on (and possibly constitutes an independent risk factor of) LV diastolic dysfunction. The reviews of this paper are available via the supplementary material section.

Keywords: GSH; GSSG; comorbidity; diastolic dysfunction; obstructive sleep apnea syndrome; oxidative stress.

Figure 1.

Incidence and grading of diastolic dysfunction in our severe OSAS patients (n = 42) compared with controls (n = 25). OSAS, obstructive sleep apnea syndrome.

Figure 2.

Incidence and grading of diastolic dysfunction in patients with more critical severe OSAS (AHI ⩾ 55; n = 21) compared with those with less critical severe OSAS (30 < AHI < 55; n = 21). OSAS, obstructive sleep apnea syndrome.

Figure 3.

Overnight changes (%) in oxidative stress biomarkers in the subset of severe OSAS patients (n = 42), divided into patients without (open bars, n = 16) and with (closed bars, n = 26) diastolic dysfunction. Bars and vertical lines represent mean and standard deviation values, respectively. OSAS, obstructive sleep apnea syndrome.