Cardiol Discovery最新文献

{"title":"Rationale, Criteria, and Impact of Identifying Extreme Risk in Patients with Atherosclerotic Cardiovascular Disease","authors":"Yuhong Zeng, Dong Zhao","doi":"10.1097/CD9.0000000000000053","DOIUrl":"https://doi.org/10.1097/CD9.0000000000000053","url":null,"abstract":"Abstract Assessment of the overall risk of atherosclerotic cardiovascular disease (ASCVD) is the first step in managing dyslipidemia and is an important reference for the target and intensity of treatment. Recently, different guidelines and consensuses on the management of this condition have successively recommended further risk stratification among patients with ASCVD, and a new “extreme risk” category has been proposed to identify patients who may obtain greater benefit from more intensive lipid-lowering therapy. The definition and terminology of extreme risk varies among different guidelines and consensuses; however, they all recommended an aggressive lipid-lowering therapeutic approach and/or a more stringent low-density lipoprotein cholesterol target for patients at extreme risk. Regardless of the definitions, this general approach may have a remarkable effect on the treatment of this condition in clinical practice. To help clinicians and patients to better understand the new strategy for the secondary prevention of ASCVD, this review provides a summary highlighting the necessity of further risk stratification among ASCVD patients, how patients at extreme risk can be identified, and the potential impact of applying the new “extreme risk” category in clinical practice.","PeriodicalId":359492,"journal":{"name":"Cardiol Discovery","volume":"98 1","pages":"0"},"PeriodicalIF":0.0,"publicationDate":"2022-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"127099072","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Relationship of Microchannels and Plaque Erosion in Patients with ST-Segment Elevation Myocardial Infarction: An Optical Coherence Tomography Study","authors":"Senqing Jiang, Junchen Guo, Yanwei Yin, C. Fang, Jifei Wang, Yidan Wang, F. Lei, Sibo Sun, Xueying Pei, R. Jia, Shaotao Zhang, Lulu Li, Yini Wang, Lei Xing, Huai Yu, Hui-min Liu, Maoen Xu, X. Ren, Lijia Ma, G. Wei, J. Hou, J. Dai, B. Yu","doi":"10.1097/CD9.0000000000000054","DOIUrl":"https://doi.org/10.1097/CD9.0000000000000054","url":null,"abstract":"Abstract Objective: Microchannels are associated with the progression of atherosclerotic vulnerable plaques. However, in patients with culprit optical coherence tomography (OCT)-defined plaque erosion, the knowledge of microchannels and culprit lesion vulnerability is limited. The aim of this study was to investigate culprit lesion characteristics in patients with ST-segment elevated myocardial infarction (STEMI) caused by plaque erosion with and without microchannels using OCT. Methods: In all, 348 STEMI patients with plaque erosion who underwent OCT of the culprit lesion at the 2nd Affiliated Hospital of Harbin Medical University (Harbin, China) from August 2014 to December 2017 were included and divided into the microchannel group (n = 116, 33.3%) and no-microchannel group (n = 232, 66.7%). The clinical characteristics and OCT-derived plaque features were compared between both groups. Results: Among the 348 STEMI patients with plaque erosion, culprit lesions with microchannels had higher incidence of lipid plaque (59.5% vs. 45.3%, P = 0.012); calcification (41.4% vs. 24.6%, P = 0.002); spotty calcification (30.2% vs. 18.1%, P = 0.014); macrophages accumulation (72.4% vs. 45.7%, P < 0.001); and cholesterol crystals (32.8% vs. 14.2%, P < 0.001) than those without microchannels. In addition, minimal lumen area was smaller ((1.9 ± 0.9) mm2vs. (2.8 ± 2.3) mm2, P < 0.001) and lumen area stenosis was greater ((71.3% ± 13.4%) vs. (65.3% ± 19.3%), P = 0.001) in the microchannel group than in the no-microchannel group. Conclusion: In patients with STEMI caused by plaque erosion, one-third manifested typical microchannel characteristics, and those with microchannels were associated with more severe luminal stenosis and more vulnerable plaque features than those without microchannels.","PeriodicalId":359492,"journal":{"name":"Cardiol Discovery","volume":"1 1","pages":"0"},"PeriodicalIF":0.0,"publicationDate":"2022-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"127414503","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Cardioprotective Effect of Growth Differentiation Factor 15 Against Isoproterenol-Induced Cardiomyocyte Apoptosis via Regulation of the Mitochondrial Fusion","authors":"Yan Zhang, Zhu Mei, X. Jia, Hai-xu Song, Jing Liu, X. Tian","doi":"10.1097/CD9.0000000000000051","DOIUrl":"https://doi.org/10.1097/CD9.0000000000000051","url":null,"abstract":"Abstract Objective: Pressure overload-induced myocardial apoptosis is a critical pathologically initiated process leading to heart failure (HF). Growth differentiation factor 15 (GDF15) dramatically increases during cardiac hypertrophy and dysfunction, but its functions and mechanisms are barely known. This study aims to elucidate the role and mechanism of GDF15 in HF. Methods: Between January 2017 and August 2018, 57 patients diagnosed with chronic HF (aged >18  years, with left ventricular ejection fraction (LVEF) ≤35%) and 57 non-HF patients (aged >18  years, LVEF >35%) were prospectively enrolled in this study based on the balance of the baseline characteristics. Other acute or chronic diseases and pregnant/lactating women were excluded. The serum concentrations of GDF15 were detected. Isoproterenol (ISO)-induced HF mouse model was established by pumping with ISO (30 mg/(kg·day)) for 4  weeks, and the GDF15 expression in serum and heart tissue was evaluated in vivo. Primary cardiomyocytes were cultured and treated with ISO to induce cardiomyocytes damage. The apoptosis of cardiomyocytes and the effect of GDF15 on ISO-induced cardiomyocytes injury was evaluated in vitro. Results: After adjusting the baseline characteristic, serum levels of GDF15 were significantly higher in HF subjects than in non-HF patients. Similarly, in the ISO-induced HF mouse model, the significant increase in GDF15 was associated with the process of HF in vivo. Moreover, the elevation of GDF15 occurred prior to heart remodeling in the ISO-induced HF mouse model. Furthermore, using primary cardiomyocytes, we demonstrated that the GDF15 was remarkably enhanced in serum from pathological HF patients and cardiac tissue from the ISO-induced mouse model. Reducing GDF15 exaggerated the ISO-induced cell apoptosis by blocking mitochondrial fusion and increasing oxidative stress. In contrast, the silence of GDF15 aggravated the ISO-induced cardiomyocytes damage. Conclusions: GDF15 acts as a protective factor against cardiomyocyte apoptosis by improving mitochondria fusion during HF. These findings indicate that GDF15 may be a potential therapeutic target for HF.","PeriodicalId":359492,"journal":{"name":"Cardiol Discovery","volume":"64 1","pages":"0"},"PeriodicalIF":0.0,"publicationDate":"2022-02-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"131892045","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}