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Angiographic No-Reflow in Patients With Acute Coronary Syndrome Caused by Calcified Nodules
Yuichi Ozaki1, Hironori Kitabata1, Ryo Hikida1
1Department of Cardiovascular Medicine, Wakayama Medical University, Wakayama, Japan.
Insights
Calcified nodules (CNs) causing acute coronary syndrome (ACS) are linked to the no-reflow phenomenon. High lipid content in CNs worsens outcomes, indicating underlying lipidic components are key.
Area of Science:
- Cardiology
- Interventional Cardiology
- Biomedical Imaging
Background:
- Acute coronary syndrome (ACS) from calcified nodules (CNs) has a poor prognosis.
- The no-reflow phenomenon in CNs is poorly understood.
- Investigating plaque components in CNs is crucial for understanding ACS outcomes.
Purpose of the Study:
- To determine the incidence of the no-reflow phenomenon in ACS patients with CNs.
- To evaluate the relationship between no-reflow and plaque components in CNs.
- To compare clinical outcomes based on plaque morphology and components.
Main Methods:
- 355 ACS patients with de novo culprit lesions were assessed using optical coherence tomography (OCT) and near-infrared spectroscopy-intravascular ultrasound (NIRS-IVUS).
- Patients were grouped by OCT findings (plaque rupture, plaque erosion, or CNs).
- NIRS-IVUS assessed lipid core burden (maxLCBI4mm), with a cutoff of 400.
Main Results:
- maxLCBI4mm was higher in plaque rupture and erosion than in CNs.
- In CN patients, higher maxLCBI4mm correlated with the no-reflow phenomenon (p=0.027).
- Patients with CNs and maxLCBI4mm ≥400 had significantly higher major adverse cardiovascular events (p=0.024).
Conclusions:
- Lipidic components are associated with the no-reflow phenomenon in CNs.
- CNs with large lipid cores predict worse long-term outcomes post-PCI in ACS.
- Understanding plaque composition is vital for managing ACS caused by CNs.
Abstract:
Acute coronary syndrome (ACS) caused by calcified nodules (CNs) has a poor prognosis. The no-reflow phenomenon in CNs has not been well studied. We investigated the incidence of the no-reflow phenomenon, evaluated the relationship between the no-reflow phenomenon and plaque components in patients with ACS caused by CNs, and compared the clinical outcomes on the basis of plaque morphology and components. This study enrolled 355 ACS patients who had de novo culprit lesions in a native coronary artery. The culprit lesions were assessed by both optical coherence tomography (OCT) and near-infrared spectroscopy-intravascular ultrasound (NIRS-IVUS). The patients were classified into 3 groups according to OCT findings (plaque rupture [PR], plaque erosion [PE], or CN), and then respectively divided into 2 groups using a maximum lipid core burden index in 4 mm (maxLCBI4mm) cutoff value of 400 on NIRS-IVUS. The maxLCBI4mm in the infarct-related lesion was greater in patients with PR (641 [461-772]) than in those with PE (vs 533 [373 to 713], p = 0.004) and CN (vs 479 [342 to 639], p = 0.002). In patients with CN, the maxLCBI4mm was significantly greater in patients with the no-reflow phenomenon than in those without (p = 0.027). The incidence of major adverse cardiovascular events was significantly higher in patients with CN and a maxLCBI4mm ≥400 than in those with other plaque features (p = 0.024). Underlying lipidic components are associated with the no-reflow phenomenon in CNs. CNs and a large lipid core provide worse long-term clinical outcomes after percutaneous coronary intervention in ACS.
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