Single-cell Multi-omics Analyses of OCT-diagnosed Plaque Subtypes in Coronary Artery Disease (MOOP-CAD)

Summary

The MOOP-CAD study program characterizes, for the first time, the pathophysiological processes and molecular mechanisms of coronary atherosclerotic plaque progression by combining in vivo intravascular imaging techniques with circulating immune single-cell multi-omics analysis. In this study, the investigators evaluate the imaging characteristics of coronary plaques by optical coherence tomography (OCT) and invasive angiography, and study the correlation between plaque characteristics and the multi-omics immune characteristic profiles.

Eligibility

Inclusion Criteria:

1. Male or female, Age ≥ 18 years and ≤ 85 years.
2. Ability to understand the requirements of the study and to provide informed consent.

Control group:

Patients with coronary angiographic diameter stenosis \<20%.

Stable plaque group:

1. Have been clinically stable for at least 6 months.
2. Presence of ≥1 lesion with angiographic diameter stenosis \>50% with no TCFA lesions in the most severely narrowed native coronary artery (target vessel). TCFA was defined as a lipidic plaque with the thinnest FCT \<75 mm and maximum lipid arc \>180°.
3. Rule out elevation of troponin or myocardial enzymology.

Vulnerable plaque group:

1. Have been clinically stable for at least 6 months.
2. Presence of ≥1 lesion with angiographic diameter stenosis \>50% with TCFA lesions in the most severely narrowed native coronary artery (target vessel).
3. Rule out elevation of troponin or myocardial enzymology.

Plaque rupture group:

1. Persistent chest pain for 30 minutes, arrival at the hospital within 24 hours from symptom onset. ST-segment elevation of \>0.1 mV in ≥2 contiguous leads or new-onset left bundle branch block, and high sensitive Troponin T or I or CK/CK-MB above upper reference value.
2. Exist clearly identified culprit lesion.
3. Plaque rupture was defined by the presence of a discontinuity of the fibrous cap with a cavity formed inside the plaque.

Plaque erosion group:

1. Persistent chest pain for 30 minutes, arrival at the hospital within 24 hours from symptom onset. ST-segment elevation of \>0.1 mV in ≥2 contiguous leads or new-onset left bundle branch block, and high sensitive Troponin T or I or CK/CK-MB above upper reference value.
2. Exist clearly identified culprit lesion.
3. Plaque erosion was defined by the presence of the attached thrombus overlying the intact fibrous cap of the atherosclerotic plaque, luminal surface irregularity at the culprit lesion in the absence of thrombus, or attenuation of the underlying plaque by thrombus without superficial lipid or calcium at the site of the thrombus.

Exclusion Criteria:

1. Cardiogenic shock or circulatory depression，life-threatening arrhythmia.
2. Known systolic heart failure with LVEF ≤30%.
3. Severe systemic diseases (end-stage renal disease, serious liver dysfunction, chronic active inflammatory diseases, active oncologic diseases, autoimmune diseases).
4. Septicemia, acute inflammatory event with fever.
5. Patients with organ transplants or patients on the waiting list for an organ transplant.
6. Previous CABG treatment, PCI treatment of the target vessel, and PCI treatment of non-target vessels within 1 year.
7. Thrombolysis before PCI.
8. Stenosis of the left main artery ≥50%.
9. Characteristics rendering high-quality OCT imaging unlikely such as chronic total occlusion, pronounced tortuosity, heavily calcified vessels.
10. Infarcted vessel with a diameter \>4mm or \<2.5mm.
11. "No-reflow" (TIMI 0-1) after thrombus aspiration or predilatation.
12. Other subjects deemed unsuitable for study by investigators.

Conditions2

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