Left ventricular diastolic dysfunction markers (LAVI and E/e') were not significantly correlated with ventilatory control instability (loop gain) (R=0.21, p=0.37 and R=-0.15, p=0.51, respectively).
Observational (n=21)
Is worse left ventricular diastolic dysfunction associated with greater ventilatory control instability in patients with obstructive sleep apnea?
Left ventricular diastolic dysfunction does not appear to be significantly associated with greater ventilatory control instability in patients with obstructive sleep apnea.
Effect estimate: R = 0.21 (LAVI); R = -0.15 (E/e')
p-value: p=0.37 (LAVI); 0.51 (E/e')
Abstract Introduction Systolic dysfunction of the left ventricle may contribute to the pathogenesis of obstructive sleep apnea (OSA) by destabilizing ventilatory control. However, the role of left ventricular diastolic dysfunction (LVDD) in OSA pathogenesis is relatively underexplored. We hypothesized that worse LVDD would be associated with greater ventilatory control instability (higher loop gain). Methods We prospectively recruited adult patients with 1) known untreated OSA or suspected OSA given snoring and/or daytime sleepiness and 2) known LVDD or at risk for LVDD given age ≥55 years or the presence of obesity, hypertension, or diabetes. Recruited participants underwent in-lab polysomnography (PSG) and transthoracic echocardiography (TTE) with measurement of diastolic parameters. PSGs were scored according to American Academy of Sleep Medicine recommendations. OSA endotypes were estimated with Phenotyping Using Polysomnography (PUP) and included loop gain (LG1), collapsibility (Vpassive and Vmin), arousal threshold (ArTH), and muscular compensation (Vcomp). Results Of 32 participants who consented to the study, 21 (14 male) completed PSG and TTE and were aged 58.7±10.3 years, with body mass index 33.6±6.3 kg/m2, and AHI3A 29±16.6 events/hr. LG1 was not correlated with markers of LVDD, including left atrial volume index (LAVI) or E/e’ (R = 0.21, p = 0.37 and R = -0.15, p = 0.51, respectively). Neither did LG1 increase with increased LVDD grade (Kruskal-Wallis p = 0.71) or in the presence of elevated left atrial pressure (LAP) by lateral E/e’12 (Wilcoxon p = 0.25). Secondary, exploratory analyses suggested that rising E/e’ is associated with increasing Vmin (R = 0.39, p = 0.079) and decreasing ArTH (R = -0.41, p = 0.068), though correlations were not statistically significant. Elevated LAP was associated with increased Vmin (57±28 vs 33.6±25.4 %Veupnea, p = 0.029). Elevated LAP was also associated with lower ArTH, but the difference was not statistically significant (124.3±30.6 vs 152.3±44.4 %Veupnea, p = 0.110). Conclusion Greater LVDD by left atrial size or pressure elevation according to TTE indices was not significantly associated with greater ventilatory control instability by PUP-estimated LG1. However, LAP elevation may be associated with easier arousal from sleep and relatively preserved upper airway collapsibility. Support (if any) American Academy of Sleep Medicine Physician-Scientist Training Award, T32HL160511.
Tolbert et al. (2026) conducted an observational in Obstructive Sleep Apnea (n=21). Left ventricular diastolic dysfunction was evaluated on Correlation between loop gain (LG1) and markers of LVDD (LAVI or E/e') (R = 0.21 (LAVI); R = -0.15 (E/e'), p=0.37 (LAVI); 0.51 (E/e')). Left ventricular diastolic dysfunction markers (LAVI and E/e') were not significantly correlated with ventilatory control instability (loop gain) (R=0.21, p=0.37 and R=-0.15, p=0.51, respectively).