Objective: The pathophysiological mechanism of in-stent restenosis (ISR) is different from atherosclerosis of native coronary arteries. The aim of this study was to evaluate the relationship between ISR and the extent of coronary artery disease (CAD), and to identify other risk factors associated with ISR in ST-segment elevation myocardial infarction (STEMI) patients.
Methods: A total of 372 consecutive patients presenting with first acute STEMI who were successfully treated with primary percutaneous coronary intervention within 12 hours from the onset of symptoms and who had an angiographic follow-up at 3 months were included in the study. The extent of CAD was calculated using the Gensini score.
Results: The incidence of ISR observed in our group of patients was 23.4% (n=87). The mean Gensini score was significantly higher in patients with ISR when compared with group without restenosis (69 [range: 51-90] vs 42 [range: 32-61]; p<0.001). The presence of diabetes mellitus, left ventricular ejection fraction (LVEF), and low-density lipoprotein cholesterol (LDL-C) level differed significantly between the 2 groups (p<0.05 for all). Stent diameter and stent length were found to be significantly different between the ISR group and the no-restenosis group (p<0.05 for both). In multivariate logistic regression analysis, the Gensini score, stent diameter, stent length, LVEF, and LDLC were independently associated with ISR.
Conclusion: Despite the differences in the underlying pathophysiological mechanism of ISR and native coronary atherosclerosis, patients with a greater extent of CAD should be considered candidates for future stent restenosis.
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http://dx.doi.org/10.5543/tkda.2017.72921 | DOI Listing |
PLoS One
January 2025
Center for Inflammation, Immunity, & Infection, Institute for Biomedical Sciences, Georgia State University, Atlanta, Georgia, United States of America.
Microbiota-induced production of IL-22 by type 3 innate lymphoid cells (ILC3) plays an important role in maintaining intestinal health. Such IL-22 production is driven, in part, by IL-23 produced by gut myeloid cells that have sensed select microbial-derived mediators. The extent to which ILC3 can directly respond to microbial metabolites via IL-22 production is less clear, in part due to the difficulty of isolating and maintaining sufficient numbers of viable ILC3 ex vivo.
View Article and Find Full Text PDFJACC Asia
December 2024
Department of Regenerative Medicine, Research Institute for Radiation Biology and Medicine, Hiroshima University, Hiroshima, Japan.
Vascular function is impaired by conditions such as hypertension, dyslipidemia, and diabetes as well as coronary risk factors including age, smoking, obesity, menopause and physical inactivity. Measurement of vascular function is useful not only for assessment of atherosclerosis itself but also in many other aspects such as understanding the pathophysiology, assessing treatment efficacy, and predicting prognosis of cardiovascular events. It is therefore important to accurately assess the extent of vascular function.
View Article and Find Full Text PDFPhysiol Rep
January 2025
Department of Biological Sciences in Sport, Faculty of Sport Sciences and Health, Shahid Beheshti University, Tehran, Iran.
Given the growing concern over the impact of brain health in individuals with overweight, understanding how mental exertion (ME) during exercise affects substrate oxidation and cardiorespiratory outcomes is crucial. This study examines how ME impacts these outcomes during an incremental exercise test in adults with overweight. Seventeen adults who were overweight completed an incremental exercise test on a cycle ergometer two times, with and without the Stroop task.
View Article and Find Full Text PDFJ Indian Soc Pedod Prev Dent
October 2024
Department of Pedodontics and Preventive Dentistry, Sardar Patel Post Graduate Institute of Dental and Medical Sciences, Lucknow, Uttar Pradesh, India.
J Clin Med
December 2024
Department of Cardiology, Esbjerg Hospital-University Hospital of Southern Denmark, Finsensgade 35, DK-6700 Esbjerg, Denmark.
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