Coronary Artery Disease, Obstructive Sleep Apnea of Adult
Conditions
Keywords
Coronary artery disease, Obstructive sleep apnea, Optical coherence tomography, Vascular response
Brief summary
Obstructive sleep apnea (OSA) is an increasingly common chronic disorder in adults. Compared to the general population, OSA occurs more often in patients with coronary artery disease (CAD), with a reported prevalence of 38% to 65%. Emerging evidence indicates OSA initiates and exacerbates coronary atherosclerosis. Moreover, several observational studies indicate the presence of OSA was associated with higher rate of restenosis and repeat revascularization (mainly attributed non-culprit lesion revascularization) after percutaneous coronary intervention (PCI). OSA might initiate endothelial injury by repetitive bursts of sympathetic activity that occur with apneas and hypopneas. Moreover, untreated OSA reduces endothelial repair capacity. Whether OSA could exacerbate neointimal proliferation and plaque progression in the non-culprit lesion after drug-eluting stent (DES) implantation remains less studied. The investigators aimed to evaluate neointimal proliferation and strut coverage within stent segment as well as changes of plaque volume and morphology in the non-culprit lesion by optical coherence tomography (OCT) in patients with versus without OSA at 12-month follow-up.
Interventions
OTHEROSA
Patients with OSA (apnea hypopnea index ≥15) based on sleep study
OTHERNon-OSA
Patients without OSA (apnea hypopnea index \<15) based on sleep study
Sponsors
Beijing Anzhen Hospital
Study design
Observational model
COHORT
Time perspective
PROSPECTIVE
Eligibility
Sex/Gender
ALL
Age
18 Years to 80 Years
Healthy volunteers
No
Inclusion criteria
1. 18 to 80 years old 2. Patients undergoing PCI with stenting in at least one de novo lesion in a native coronary artery 3. 3-vessel OCT was available visually (at least one pullback/vessel) 4. Written informed consent
Exclusion criteria
1. Predominantly central sleep apnea (CSA, ≥50% central events or central apnea hypopnea index ≥10/h) 2. Previous or current use of continuous positive airway pressure (CPAP) 3. Cardiogenic shock (systolic arterial pressure \<90mmHg), congestive heart failure (NYHA or Killip≥3) 4. STEMI within 1 week 5. Prior PCI or CABG 6. Chronic kidney disease \[eGFR\<60ml/(min\*1.73m2)\] 7. Aortic-coronary ostial lesion 8. Left main lesion 9. Chronic total occlusion 10. In-stent restenotic lesion 11. A tortuous vessel and/or severely calcified lesion or severe stenosis and the OCT catheter could not pass across the lesion 12. Massive residual thrombus on angiography despite thrombus aspiration or thrombectomy 13. Planned elective PCI within 12 months 14. Severe comorbidities: eg. malignancy (life expectancy \<2 years) 15. Known or planned pregnancy
Design outcomes
Primary
| Measure | Time frame |
|---|---|
| Relative proliferation volume within stent segment (% of stent volume) | 12 months |
Secondary
| Measure | Time frame | Description |
|---|---|---|
| Maximum area stenosis within stent segment | 12 months | Defined as minimal lumen area divided by the mean of reference lumen area |
| Change of total lipid volume index in the non-culprit lesion | 12 months | — |
| Total proliferation volume within stent segment | 12 months | — |
| Maximum proliferation area within stent segment | 12 months | — |
| Minimal lumen area within stent segment | 12 months | — |
| Prevalence of uncovered struts, uncovered and apposed struts, malapposed struts | 12 months | — |
| Prevalence of neoatherosclerosis | 12 months | — |
| Total lipid volume index | Baseline | Defined as the averaged lipid angle multiplied by lipid length; including culprit and non-culprit lesions |
| Prevalence of TCFA | Baseline | In the culprit and non-culprit lesions |
| Prevalence of plaque rupture | Baseline | In the culprit and non-culprit lesions |
| Rate of major adverse cardiac events (cardiac death, myocardial infarction, or ischemic-driven repeat revascularization) | 12 months | — |
Other
| Measure | Time frame | Description |
|---|---|---|
| Macrophage volume | Baseline | — |
| Correlation of total lipid volume index with AHI | Baseline | — |
| Correlation of total lipid volume index with lowest SpO2 | Baseline | — |
| Correlation of total lipid volume index total time with SpO2 <90% | Baseline | — |
| Total lipid volume index stratified by sex in both groups | Baseline | — |
| Total lipid volume index stratified by obesity in both groups | Baseline | — |
| Total lipid volume index stratified by diabetes in both groups | Baseline | — |
| Rate of individual cardiovascular events | 12 months | Including all-cause death, cardiac death, myocardial infarction, target vessel revascularization, target lesion revascularization, non-target vessel revascularization, hospitalization for unstable angina |
| Calcium volume | Baseline | — |
| Maximum lipid angle | Baseline | — |
Countries
China
Contacts
Primary ContactShao-Ping Nie, MD, PhD
Backup ContactXiao Wang, MD
Outcome results
None listed