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    Optical coherence tomography derived differences of plaque characteristics in coronary culprit lesions between type 2 diabetic patients with and without acute coronary syndrome
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    Abstract:
    To compare optical coherence tomography (OCT)-derived plaque characteristics of coronary target lesions between diabetic patients with acute coronary syndrome (ACS) versus stable angina pectoris (SAP).In vivo assessment of plaque composition of coronary culprit lesions in a cardiovascular high-risk population with diabetes mellitus is incompletely elucidated.102 diabetic patients with coronary de novo lesions were enrolled and categorized into an ACS-group (40 patients) and a SAP-group (62 patients) according to their clinical presentation. Assessment of clinical data, angiographic, and OCT imaging including the analysis of plaque composition and lipid content of the target lesions were performed prior to percutaneous coronary intervention and compared between the two groups.Plaque characteristics of patients in the ACS-group compared with the SAP-group showed a higher incidence of lipid-rich plaque [33 (82.5%) vs. 25 (40.3%)], thin-capped fibroatheroma [29 (72.5%) vs. 10 (16.1%)], macrophage infiltration [32 (80.0%) vs. 21 (33.9%)], thrombus [23 (57.5%) vs. 2 (3.2%)], and plaque rupture [27 (67.5%) vs. 2 (3.2%)] (all P < 0.001). Moreover, there was a wider lipid arc (174.5 ± 33.8° vs. 122.9 ± 43.9°), a longer lipid plaque length (6.52 ± 2.04 mm vs. 3.73 ± 2.16 mm), a greater lipid volume index (1117.2 ± 349.9 vs. 504.8 ± 379.3), and a smaller minimal fibrous cap thickness (51.52 ± 9.14 µm vs. 80.33 ± 26.71 µm) within lipid-rich lesions of ACS patients (all P < 0.001).Diabetic patients with ACS exhibit more vulnerable plaque features in coronary culprit lesions compared with diabetic patients with SAP. This may provide rationale for a specific therapeutic strategy either by pharmacological plaque stabilization or coronary intervention in any lesion with vulnerable plaque morphology in patients with diabetes.
    Keywords:
    Fibrous cap
    Culprit
    Vulnerable plaque
    Unstable angina
    The types of lesion instability responsible for the majority of acute coronary events frequently include plaque disruption and plaque erosion with superimposed thrombosis. The term ‘vulnerable plaque' is used to describe atherosclerotic (ATS) plaques that are particularly prone to rupture and susceptible to thrombus formation, such as the thin‑cap fibroatheroma (TCFA). The aim of the present study was to assess the morphological and histological differences between plaques that are unstable and those that are vulnerable to instability. Carotid artery endarterectomy specimens were obtained from 26 patients with carotid artery stenosis, consisting of 20 men and 6 women (age range, 35‑80 years). Histological and morphometric methods were used to visualize and characterize the ATS plaques. Among the 26 carotid ATS plaques, 23% were stable, 23% were unstable and 54% were vulnerable. With regard to morphometric characteristics, the following mean values were obtained for the TCFA and unstable plaques, respectively: Fibrous cap thickness, 21.91 and 11.66 µM; proportion of necrotic core area in the total plaque area, 25.90 and 22.03%; and the proportion of inflammatory area in the total plaque area, 8.41 and 3.04%. No plaque calcification was observed in any of them. Since ATS coronary artery disease is considerably widespread and fatal, it is crucial to further study ATS lesions to obtain an improved understanding of the nature of vulnerable and unstable plaques. The methods used to detect plaque size, necrotic core area and fibrous cap thickness are considered to be particularly useful for identifying vulnerable and unstable plaques.
    Fibrous cap
    Vulnerable plaque
    Endarterectomy
    Atheroma
    Citations (23)
    Background: Plaque erosion can occur quietly without causing clinical symptoms, followed by a healing process resulting in healed plaque. This study aimed to assess culprit and non-culprit plaque characteristics of patients with acute myocardial infarction (AMI) caused by plaque erosion with vs. without healed phenotype at the culprit plaque using optical coherence tomography (OCT).
    Culprit
    Vulnerable plaque
    Citations (7)
    Vulnerable plaques are inflamed, active, and growing lesions which are prone to complications such as rupture, luminal and mural thrombosis, intraplaque hemorrhage, and rapid progression to stenosis. It remains difficult to assess what factors influence the biomechanical stability of vulnerable plaques and promote some of them to rupture while others remain intact. The rupture of thin fibrous cap overlying the necrotic core of a vulnerable plaque is the principal cause of acute coronary syndrome. The mechanism or mechanisms responsible for the sudden conversion of a stable atherosclerotic plaque to a life threatening athero-thrombotic lesion are not fully understood. It has been widely assumed that plaque morphology is the major determinant of clinical outcome [1, 2]. Thin-cap fibroatheroma with a large necrotic core and a fibrous cap of < 65μm was describes as a more specific precursor of plaque rupture due to tissue stress.
    Fibrous cap
    Vulnerable plaque
    Citations (0)
    Thrombosis is the main cause of acute coronary syndrome and myocardial infarction (Naghavi et al., 2003). The mechanism underlying thrombus formation is presently under debate, but several pathological conditions have been identified from human postmortem studies that correspond with the presence of thrombus. Of these conditions plaque rupture is the most common, but erosion of the endothelial layer and existence of calcified nodules without the existence of plaque rupture have also been identified. Plaques that have been ruptured have certain features in common (Falk, 1999; Virmani et al., 2002): (i) size of the lipid core (40% of the entire plaque), (ii) thickness of the fibrous cap (less than 65 µm), (iii) presence of inflammatory cells, (iv) amount of remodeling and extent of plaque-free vessel wall. Several terms have been identified focusing either on the pathological aspects ("thin-cap fibroatheroma") or on the possibility to rupture ("rupture-prone plaques") or on the possibility to induce thrombosis ("vulnerable plaque"). As vulnerable plaque is the term encompassing all other terms, therefore this term will be used throughout the chapter.
    Fibrous cap
    Vulnerable plaque
    Citations (1)