Vascular Responses After Percutaneous Coronary Intervention With Stenting In Patients With Obstructive Sleep Apnea

• Conditions: Obstructive Sleep Apnea of Adult; Coronary Artery Disease
• Interventions: Other: OSA; Other: Non-OSA

• Registration Number: NCT04022824
• Lead Sponsor: Beijing Anzhen Hospital

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.

Detailed Description

Not available

Study Timeline

• Study Start: 2018-04-18
• Study First Submitted: 2019-07-01
• Study First Submitted QC: 2019-07-14
• Study First Posted: 2019-07-17
• Primary Completion: 2019-11-12
• Status Verified: 2021-09
• Last Update Submitted: 2021-09-02
• Last Update Posted: 2021-09-05
• Study Completion: 2021-10-31

Recruitment & Eligibility

• Status: UNKNOWN
• Sex: All
• Target Recruitment: 84

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

Study & Design

• Study Type: OBSERVATIONAL
• Study Design: Not specified

Arm && Interventions

Group	Intervention	Description
OSA	OSA	-
Non-OSA	Non-OSA	-

Primary Outcome Measures

Name	Time	Method
Relative proliferation volume within stent segment (% of stent volume)	12 months

Secondary Outcome Measures

Name	Time	Method
Rate of major adverse cardiac events (cardiac death, myocardial infarction, or ischemic-driven repeat revascularization)	12 months
Minimal lumen area within stent segment	12 months
Maximum area stenosis within stent segment	12 months	Defined as minimal lumen area divided by the mean of reference lumen area
Total proliferation volume within stent segment	12 months
Prevalence of TCFA	Baseline	In the culprit and non-culprit lesions
Change of total lipid volume index in the non-culprit lesion	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 uncovered struts, uncovered and apposed struts, malapposed struts	12 months
Prevalence of plaque rupture	Baseline	In the culprit and non-culprit lesions
Maximum proliferation area within stent segment	12 months

Trial Locations

Locations (1)

Beijing Anzhen Hospital, Capital Medical University; 🇨🇳 Beijing, China