Key result
Sleep-disordered breathing linked to ~86% higher odds of vulnerable coronary plaque features.
Why the study?
Does sleep-disordered breathing increase the vulnerability of culprit coronary plaques in patients with coronary artery disease undergoing percutaneous coronary intervention?
Observational (n=289)
Observers (cardiologists) blinded to clinical/sleep data for IVUS analysis
No
Does sleep-disordered breathing increase the vulnerability of culprit coronary plaques in patients with coronary artery disease undergoing percutaneous coronary intervention?
Odds Ratio: 1.86 (95% CI 1.02–3.39)
Absolute Event Rate: 34.9% vs 22.6%
p-value: p=0.04
Sleep-disordered breathing is associated with larger atheroma volume and increased ultrasound attenuation, suggesting a mechanical link between SDB and increased plaque vulnerability in CAD patients.
SDB associated with vulnerable culprit plaques; hypothesis-generating, prospective trials needed before clinical adoption.
Background Sleep‐disordered breathing ( SDB ) is a novel cardiovascular risk factor. However, the coronary plaque characteristics of patients with SDB with coronary artery disease are still unclear. Methods and Results This study included 289 consecutive patients with coronary artery disease undergoing percutaneous coronary intervention. Plaque characteristics of the culprit lesion were assessed by preintervention intravascular ultrasound. The presence of SDB was defined as a 3% oxygen desaturation index of ≥15 events per hour measured by nocturnal pulse oximetry. Of 289 patients, the median 3% oxygen desaturation index was 9.6 (interquartile range, 5.1–16.6), and 88 patients (30.4%) were defined as having SDB . Compared with the no‐ SDB group, the SDB group had a larger total atheroma volume of the culprit lesion (224.5 mm 3 versus 190.8 mm 3 , P =0.05). The median maximum attenuation and calcification angle were 140° and 130°, respectively. Attenuated plaque with a maximum attenuation angle >140° was more frequently observed in the SDB group compared with the no‐ SDB group (34.9% versus 22.6%; P =0.03). However, there were no statistically significant differences between groups in the maximum calcium angle and the frequency of calcific plaques with a maximum calcium angle >130°. Multivariable logistic regression analysis showed that the presence of SDB was a significant predictor of a greater ultrasound attenuation angle (>140°) (odds ratio, 1.86; 95% confidence interval, 1.02–3.39; P =0.04). Conclusions SDB was associated with larger atheroma plaque volume and a greater ultrasound attenuation, which are discriminators of plaque vulnerability. Further studies are needed to clarify the effects of SDB treatment on coronary plaque lesions.
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Wada et al. (2018) conducted an observational in Coronary artery disease (CAD) requiring percutaneous coronary intervention (PCI) (n=289). Sleep-disordered breathing (SDB) vs. No sleep-disordered breathing was evaluated on Greater ultrasound attenuation angle (>140°) on preintervention IVUS (OR 1.86, 95% CI 1.02-3.39, p=0.04). The presence of sleep-disordered breathing was an independent predictor of a greater ultrasound attenuation angle (>140°) in coronary culprit lesions (OR 1.86, p=0.04), indicating increased plaque vulnerability.
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