Observational studyThe international journal of cardiovascular imaging2014
ST elevation acute myocardial infarction accelerates non-culprit coronary lesion atherosclerosis.
Observational study in The international journal of cardiovascular imaging, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.
What it found
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The trial behind it
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Who cites it
24 citing papers in PubMed.
- Trial
- Bone Marrow Niche in Cardiometabolic Disease: Mechanisms and Therapeutic Potential.Circulation research · 2025Review
- Clinical Predictors of the Rapid Progression and Revascularization of Coronary Non-Target Lesions: A Serial Angiographic Study.Reviews in cardiovascular medicine · 2024Article
- 'Training' of innate immunity following myocardial infarction exacerbates atherosclerosis.European heart journal · 2024Article
- miR-186-5p Dysregulation in Serum Exosomes from Patients with AMI Aggravates Atherosclerosis via Targeting LOX-1.International journal of nanomedicine · 2022Article
- Article
- Eosinophil percentage as a new prognostic marker in patients with ST-segment elevation myocardial infarction undergoing primary percutaneous coronary intervention.Interventional medicine & applied science · 2020Article
- Pravastatin attenuates atherosclerosis after myocardial infarction by inhibiting inflammatory Ly6CThe Journal of international medical research · 2020Article
- Hematopoiesis and Cardiovascular Disease.Circulation research · 2020Review
- Inflammation in atherosclerotic cardiovascular disease.F1000Research · 2019Review
- Epicardial adipose tissue is associated with high-risk plaque feature progression in non-culprit lesions.The international journal of cardiovascular imaging · 2017Article
- Inflammation - Cause or Consequence of Heart Failure or Both?Current heart failure reports · 2017Review
- Prolonged Fever After ST-Segment Elevation Myocardial Infarction and Long-Term Cardiac Outcomes.Journal of the American Heart Association · 2017Observational
- E-Selectin Inhibition Mitigates Splenic HSC Activation and Myelopoiesis in Hypercholesterolemic Mice With Myocardial Infarction.Arteriosclerosis, thrombosis, and vascular biology · 2016Article
- Homocysteine is associated with the progression of non-culprit coronary lesions in elderly acute coronary syndrome patients after percutaneous coronary intervention.Journal of geriatric cardiology : JGC · 2016Article
- Innate immune cells in ischaemic heart disease: does myocardial infarction beget myocardial infarction?European heart journal · 2016Review
- Systemic Atherosclerotic Inflammation Following Acute Myocardial Infarction: Myocardial Infarction Begets Myocardial Infarction.Journal of the American Heart Association · 2015Article
- Non-culprit coronary lesions in young patients have higher rates of atherosclerotic progression.The international journal of cardiovascular imaging · 2015Observational
- Monocytes in myocardial infarction.Arteriosclerosis, thrombosis, and vascular biology · 2015Review
- Inhibiting macrophage proliferation suppresses atherosclerotic plaque inflammation.Science advances · 2015Article
Corrections and comments
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Authors and funding
9 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The previously study found, using a mouse model, that acute myocardial infarction accelerated atherosclerosis. This study assessed whether ST elevation myocardial infarction (STEMI) accelerates the progression of non-culprit coronary lesion (NCCL) in patients who underwent percutaneous coronary interventions (PCI). Four hundred and forty-nine patients who underwent successful PCI with stents and follow-up coronary angiography in a single center were enrolled. The NCCL progression was assessed using three-dimensional quantitative coronary angiography and was defined as ≥10 % diameter reduction of a preexisting stenosis ≥50, ≥30 % diameter reduction of a stenosis <50 %, development of a new stenosis ≥30 % in a previously normal segment, or progression to total occlusion. The patients were classified into two groups according to whether the progression existed or not. The median age of patients was 58.4 years. The mean angiographic follow-up period was 12.3 months, 134 (29.8 %) patients had NCCL progression. Multivariate Cox regression analysis (step-wise) showed that STEMI was the only independent determinant of NCCL progression. Compared to the other coronary artery disease group, the crude hazard ratio (HR) of NCCL progression for the STEMI group was 3.20 (95 % CI 2.27-4.50; p < 0.001), and the association remained significantly after adjustment for age, sex, BMI, SBP, DBP, serum lipids, fasting blood glucose, peak monocyte count, smoking, drinking, hypertension, diabetes mellitus and lesion characteristics of NCCL (adjusted HR 3.56, 95 % CI 2.41-5.27; p < 0.001). The ST elevation acute myocardial infarction accelerates non-culprit coronary lesion atherosclerosis.
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Registered trials
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