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Difference in inflammation, atherosclerosis, and platelet activation between coronary artery aneurysm and coronary
Wei Wei1, Xingxu Wang1, Zhenghao Huang1
1Department of Cardiovascular Medicine, East Hospital, Tongji University School of Medicine, Shanghai, China.
Insights
Coronary artery aneurysm (CAA) is linked to atherosclerosis, while coronary artery ectasia (CAE) is associated with inflammation. Both conditions show platelet activation, suggesting antiplatelet therapy is beneficial for managing these coronary dilatations.
Area of Science:
- Cardiology
- Vascular Biology
- Immunology
Background:
- Coronary artery aneurysm (CAA) and coronary artery ectasia (CAE) are distinct forms of coronary artery dilatation with unclear origins.
- Understanding their etiological differences is crucial for effective management.
Purpose of the Study:
- To compare the distinct characteristics of CAA and CAE.
- To investigate the underlying pathogenesis of both conditions.
- To determine the necessity of antiplatelet therapy in patients with CAA and CAE.
Main Methods:
- A comparative study included 100 patients each with CAA, CAE, and normal coronary arteries (NCA).
- Evaluated ankle-brachial index (ABI), pulse wave velocity, carotid ultrasonography, and various blood parameters.
- Assessed vascular inflammatory markers, platelet activation, and aggregation after antiplatelet drug withdrawal.
Main Results:
- CAE showed elevated inflammatory markers (ANCA, TNF-α, MPO) and endothelial dysfunction.
- CAA was associated with higher low-density lipoprotein/high-density lipoprotein ratios and carotid artery thickening, indicating atherosclerosis.
- Both CAA and CAE exhibited increased platelet activation markers and aggregation rates, with specific differences in response to arachidonic acid and adenosine 5'-diphosphate.
Conclusions:
- CAE pathogenesis is closely linked to inflammation.
- CAA pathogenesis is closely linked to atherosclerosis.
- Platelet activation is a common feature in both CAA and CAE, supporting the recommendation for antiplatelet therapy.
Background:
Coronary artery aneurysm (CAA) and coronary artery ectasia (CAE) may be two different types of coronary artery dilatation with unknown etiology. This study aimed to compare the differences between CAA and CAE and to investigate their pathogenesis and the necessity of antiplatelet therapy.
Methods:
One hundred patients each with confirmed CAA, CAE, and normal coronary artery (NCA) from September 2017 to July 2019 were included. All patients completed examinations of the ankle-brachial index (ABI), pulse wave rate, and carotid ultrasonography; and were tested for routine blood, lipid, and immune parameters. Blood samples were collected 1 week after the withdrawal of antiplatelet drugs, and vascular inflammatory indexes, platelet activation indexes, thromboelastography, and the platelet aggregation rate were measured. Analysis of variance and the chi-square or Fisher exact test were used for statistical analysis.
Results:
The perinuclear anti-neutrophil cytoplasmic antibody (ANCA), endothelial-1, matrix metalloproteinase-9, and tumor necrosis factor-α were significantly higher in CAE than in NCA, while cytoplasmic ANCA was appreciably higher in CAE than in CAA (P<0.05). Myeloperoxidase and growth/differentiation factor-15 were significantly higher in CAE than in CAA and NCA (P<0.05). ABI was significantly lower in CAA and CAE than in NCA (P<0.05), low-density lipoprotein/high-density lipoprotein was significantly higher in CAA than in NCA (P<0.05), and the detection rate of carotid artery thickening was significantly higher in CAA than in CAE and NCA (P<0.05). The Gensini and SYNTAX scores were significantly higher in CAA than in CAE (P<0.05). The percentages of CD62P and PAC-1 were higher in CAA and CAE than in NCA (P<0.05). The arachidonic acid aggregation rate in CAA and adenosine 5'-diphosphate aggregation rate in CAE were significantly higher than in NCA (P<0.05). The values of thrombin formation time and reaction time were significantly lower in CAE than in NCA (P<0.05), and the α angle was significantly higher in CAE than in NCA.
Conclusions:
CAE was closely related to inflammation, whereas CAA was closely related to atherosclerosis. Platelet activation was present in both diseases; therefore, antiplatelet therapy is recommended.
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