The morbidity of coronary heart disease (CHD) is high, and the prognosis is unfavorable. Fibrinogen is both coagulation and inflammation factor, which has important influence on the occurrence and development of CHD. Previous studies reported that fibrinogen had relevance with traditional risk factors of CHD such as hypertension, diabetes and subclinical diseases such as left ventricular hypertrophy. The incidence of CHD increases with the fibrinogen level increasing. The fibrinogen level is higher in patients with CHD than that in healthy people. The coronary stenosis degree is heavier and the lesion is wider in patients with hyperfibrinogenemia. But the effects of fibrinogen on the secondary prevention of CHD is controversial. This paper summarized research progress based on the new understanding to fibrinogen on CHD recently.
Mitral valve regurgitation is one of the most common heart valve diseases, of which secondary mitral valve regurgitation (sMR) has large proportion and poor prognosis. For patients who still have symptoms after the guideline-directed management and therapy, the effects of surgery are controversial, and transcatheter therapy provides a new option. Transcatheter edge-to-edge repair has become one of the recommended therapies by the guidelines, meanwhile transcatheter mitral valve annuloplasty and transcatheter mitral valve replacement are developing. However, the etiological mechanism of sMR is complex and diverse. There is an interaction between cardiac function and structure and sMR in dynamic change. It brings challenges to the selection of indicators and evaluation timing. The complex anatomical structure also makes it more difficult to design instruments and select surgical methods. This paper reviews the challenges and progress of transcatheter therapy for sMR.
Objective To search and review the best clinical evidence to compare the clinical therapeutic effects and safety between TAVR and SAVR, thereby guiding its clinical use and providing references of treatments for such patients. Methods EMbase (1974～2016), MEDLINE (1996～2016) and The Cochrane Library (Issue 5, 2016) were systematically retrieved to collect randomized control trials, case-control studies and meta-analyses. Then, we assessed the quality of all the evidences to develop treatments based on those evidences and the situations of such patients. Results We identified 21 articles, including 2 articles of meta-analysis. With regard to the mortality and incidence of cardiovascular events, TAVR was not worse than SAVR. In addition, TAVR was more dominant than SAVR for patients who combined more basic diseases. Conclusion TAVR is one of the effective treatments for most patients with severe AS after sufficient assessment.
Aortic valve calcification (AVC) is one of the major causes of aortic stenosis (AS), and its pathogenesis is related to inflammation infiltration, lipid deposition, endothelial damage, calcification osteogenesis and angiogenesis. Previous studies have shown that AVC is associated with the severity of AS, the incidence of cardiovascular events, mortality, and surgical outcomes. The quantitative analysis of AVC using imaging methods not only has diagnostic value for AS, but also has guiding significance for the selection of surgical timing, assessment of surgical risk, and prognosis prediction. This article comprehensively elaborates on the methods and values of evaluating AVC using echocardiography, CT, and positron emission tomography.
According to new clinical evidence, the European Society of Cardiology (ESC) and European Association for Cardio-Thoracic Surgery (EACTS) updated and published 2021 ESC/EACTS guidelines for the management of valvular heart disease. This new guideline gives recommendation for clinical assessment, internal treatment and intervention for patients with valvular heart disease with/without comorbidities, which is a globally approbatory reference for clinical practice. This article summarized the updated contents of the new guideline in terms of transcatheter therapy for valvular heart disease.
At present, transeatheter aortic valve replacement is an effective treatment for elderly patients with severe aortic valve stenosis. Cardiac rehabilitation after transeatheter aortic valve replacement can effectively improve cardiopulmonary endurance and exercise capacity, and improve the quality of life. In order to better carry out cardiac rehabilitation for patients undergoing transeatheter aortic valve replacement, the Structural Heart Disease Professional Committee of Chinese College of Cardiovascular Physicians has drawn up Expert Consensus on Motor Rehabilitation after Transeatheter Aortic Valve Replacement. This consensus mainly elaborates the specific implementation process and methods of cardiac rehabilitation from three time periods of perioperative rehabilitation, outpatient rehabilitation and home rehabilitation. This article will interpret the main content of the consensus.
Mitral regurgitation is the most prevalent valvular heart disease, with a poor prognosis that brings a heavy burden to population health and socio-economics. Transcatheter repair is a relatively mature technique for mitral regurgitation, but is strict in anatomical screening and the reduction of regurgitation is limited. With the advance in techniques and technology, transcatheter replacement has become an attractive treatment modality for mitral regurgitation in succession to transcatheter repair. At present, several replacement devices have initiated clinical trials to establish feasibility. Early data has shown that transcatheter replacement for mitral regurgitation is safe and effective, which needs to be confirmed with larger population and longer follow-up. Besides, some technical challenges remain to be addressed, in order to increase accessibility of this innovative technology.
Objective To investigate the role and mechanism of peroxisome proliferator-activated receptor gamma coactivator 1α (PGC-1α) in the activation of aortic valve interstitial cells (AVICs) in aortic stenosis. Methods Isolating primary AVICs and stimulating their activation with transforming growth factor β1 (TGF-β1, 30 ng/mL), the expression of PGC-1α was detected. The activation of AVICs induced by TGF-β1 was observed after overexpression of PGC-1α by adenovirus or inhibition of PGC-1α function by GW9662. The possible downstream molecular mechanism of PGC-1α in AVICs activation was screened. Finally, the phenotype was further verified in primary human AVICs. Results The expression of PGC-1α decreased after the activation of AVICs induced by TGF-β1 (control group: 1.00±0.18; 24 h: 0.31±0.10; 48 h: 0.32±0.06; 72 h: 0.20±0.07; P<0.05). Specific overexpression of PGC-1α by adenovirus inhibited the activation of AVICs induced by TGF-β1 stimulation (periostin: 3.17±0.64 vs. 1.45±0.54, P<0.05; α-smooth muscle actin: 0.77±0.11 vs. 0.28±0.06, P<0.05). On the contrary, inhibition of PGC-1α function by GW9662 promoted the activation of AVICs (periostin: 2.20±0.68 vs. 7.99±2.50, P<0.05). Subsequently, it was found that PGC-1α might inhibit the activation of AVICs through downregulating the expression of calcium/calmodulin-dependent protein kinase (CAMK1δ) (0.97±0.04 vs. 0.74±0.11, P<0.05), and downregulating the expression of CAMK1δ alleviated the activation of AVICs (periostin: 1.76±0.11 vs. 0.99±0.20, P<0.05). The possible mechanism was that the activation of mammalian target of rapamycin (mTOR) signaling pathway was inhibited by reducing the accumulation of reactive oxygen species (ROS) (778.3±139.4 vs. 159.3±43.2, P<0.05). Finally, the protective effect of PGC-1α overexpression was verified in the activated phenotype of human AVICs (periostin: 2.73±0.53 vs. 1.63±0.14, P<0.05; connective tissue growth factor: 1.27±0.04 vs. 0.48±0.09, P<0.05). Conclusions The expression of PGC-1α significantly decreases during the activation of AVICs induced by TGF-β1. The overexpression of PGC-1α significantly inhibites the activation of AVICs, suggesting that PGC-1α plays a protective role in the activation of AVICs. The possible mechanism is that PGC-1α can inhibit the activation of CAMK1δ-ROS-mTOR pathway. In conclusion, interventions based on PGC-1α expression levels are new potential therapeutic targets for aortic stenosis.