ISSN 1671-5411 CN 11-5329/R
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One-year survival in recipients older than 50 bridged to heart transplant with Impella 5.5 via axillary approach
Smit Paghdar, Smruti Desai, Ji-Min Jang, Jose Ruiz, Sharan Malkani, Parag Patel, Daniel S Yip, Juan C Leoni, Jose Nativi, Basar Sareyyupoglu, Kevin Landolfo, Si Pham, Rohan M Goswami
2023, 20(5): 319-329.   doi: 10.26599/1671-5411.2023.05.002
Abstract(118) FullText HTML(58) PDF (13)
Predictive validation of existing bleeding and thromboembolic scores in elderly patients with comorbid atrial fibrillation and acute coronary syndrome
Hong-Hong ZHANG, Qi LIU, Hai-Jing ZHAO, Ya-Ni YU, Liu-Yang TIAN, Ying-Yue ZHANG, Zi-Hao FU, Li ZHENG, Yue ZHU, Yu-Han MA, Shuang LI, Yang-Yang MA, Yu-Qi LIU
2023, 20(5): 330-340.   doi: 10.26599/1671-5411.2023.05.001
Abstract(55) FullText HTML(27) PDF (8)
Identification of an LDLR variant in a Chinese familial hypercholesterolemia and its relation to ROS/NLRP3-Mediated pyroptosis in hepatic cells
Wen-Zhuo CHENG, Wei-Hua WANG, Ai-Ping DENG, Xiao DANG, Chao LIU, Xian-Can WANG, Ju-Yi LI, Si JIN
2023, 20(5): 341-349.   doi: 10.26599/1671-5411.2023.05.003
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A circRNA–miRNA–mRNA network analysis underlying pathogenesis of human heart failure
Ran XU, Jian WU, Chun-Jie YANG, Le KANG, Yu-Yao JI, Chang LI, Zhi-Wen DING, Yun-Zeng ZOU
2023, 20(5): 350-360.   doi: 10.26599/1671-5411.2023.05.004
Abstract(19) FullText HTML(9) PDF (0)
Cardiac amyloidosis: state-of-the-art review
Syed Bukhari
2023, 20(5): 361-375.   doi: 10.26599/1671-5411.2023.05.006
Abstract(30) FullText HTML(14) PDF (42)
Ultrasound-guided stellate ganglion blockade: an appealing tactic for cardiac electrical storm
Zi-Hao LAI, Li-Hui ZHENG, Yan YAO
2023, 20(5): 376-382.   doi: 10.26599/1671-5411.2023.05.009
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A faraway complex bifurcation hidden behind an occluded left main in an elderly patient
Gianluca Rigatelli, Giulio Rodino, Giuseppe Marchese, Marco Zuin
2023, 20(5): 383-385.   doi: 10.26599/1671-5411.2023.05.007
Abstract(17) FullText HTML(7) PDF (1)
Risk analysis of gastrointestinal bleeding in hospital patients with acute myocardial infarction undergoing primary PCI
Yan-Yan JIN, Ming YE, Hai GAO
2023, 20(5): 386-390.   doi: 10.26599/1671-5411.2023.05.005
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From post-COVID-19-associated myocarditis to hemopericardium: a dangerous domino effect
Francesco Bellanti, Ripalta Amato, Antonio Centola, Valeria Ercolano, Lucia Barbera, Annamaria Tesse, Grazia Divittorio, Cristiano Capurso, Aurelio Lo Buglio, Gianluigi Vendemiale
2023, 20(5): 391-396.   doi: 10.26599/1671-5411.2023.05.008
Abstract(6) FullText HTML(2) PDF (0)
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Jing YU, Wen-Zhao YAN, Xin-Hua ZHANG, Bin ZHENG, Wen-Sen PAN, Zhan YANG, Hong ZHANG, Zi-Yuan NIE, Ying MA, Yang BAI, Long ZHANG, Dan-Dan FENG, Jin-Kun WEN
 doi: 10.26599/1671-5411.2023.06.002
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 BACKGROUND  Abnormal type I collagen (COL1) expression is associated with the development of many cardiovascular diseases. The TGF-beta/Smad signaling pathway and circRNAs have been shown to regulate COL1 gene expression, but the underlying molecular mechanisms are still not fully understood.  METHODS  Gain- and loss-of-function experiments were prformed to study the effect of circZBTB46 on the expression of alpha 2 chain of type I collagen (COL1A2). Co-immunoprecipitation assay was performed to observe the interaction between two proteins. RNA immunoprecipitation assay and biotin pull-down assay were performed to observe the interaction of circZBTB46 with PDLIM5.  RESULTS  In this study, we investigated the role of circZBTB46 in regulating COL1A2 expression in human vascular smooth muscle cells (VSMCs). We found that circZBTB46 is expressed in VSMCs and that TGF-beta inhibits circZBTB46 formation by downregulating KLF4 expression through activation of the Smad signaling pathway. CircZBTB46 inhibits the expression of COL1A2 induced by TGF-beta. Mechanistically, circZBTB46 mediates the interaction between Smad2 and PDLIM5, resulting in the inhibition of Smad signaling and the subsequent downregulation of COL1A2 expression. Furthermore, we found that the expression of TGF-beta and COL1A2 is decreased, while circZBTB46 expression is increased in human abdominal aortic aneurysm tissues, indicating that circZBTB46-mediated regulation of TGF-beta/Smad signaling and COL1A2 synthesis in VSMCs plays a crucial role in vascular homeostasis and aneurysm development.  CONCLUSIONS  CircZBTB46 was identified as a novel inhibitor of COL1 synthesis in VSMCs, highlighting the importance of circZBTB46 and PDLIM5 in regulating TGF-beta/Smad signaling and COL1A2 expression.
Qiong-Yu ZHANG, Yan GUO, Xiao-Liang JIANG, Xing LIU, Shu-Guang ZHAO, Xian-Liang ZHOU, Zhi-Wei YANG
 doi: 10.26599/1671-5411.2023.07.001
Abstract(23) FullText HTML(11) PDF (2)
 OBJECTIVES  To investigate the value of CCKBRfl/fl villin-Cre mice as a mouse model of salt-sensitive hypertension (SSH).  METHODS  In the first part, 2-month-old CCKBRfl/fl villin-Cre mice (CKO) and control CCKBRfl/fl mice (WT) were fed with normal diet (0.4% NaCl) or high salt diet (4% NaCl), separately for 6 weeks. In the rescue study, one week of hydrochlorothiazide or saline injection were treated with the CKO mice fed high salt diet. The blood pressure, biochemical indexes, and the expression of small intestinal sodium transporters (NHE3, NKCC1, eNaC) was detected. The organ injury markers (MMP2/MMP9) and the histopathological changes of kidneys were observed, whereas the changes of duodenal sodium absorption were detected by small intestinal perfusion in vivo.  RESULTS The CCKBRfl/fl villin-Cre mice with high salt intake exhibited high blood pressure, increased duodenal sodium absorption and urinary sodium excretion, and with renal injury. The protein expression of NHE3, NKCC1 and eNaC were also significant increase in the intestine of CKO-HS mice. Treatment with hydrochlorothiazide remarkably attenuated the elevated blood pressure by high salt absorption in the CCKBRfl/fl villin-Cre mice, but no significant histopathological changes were observed.  CONCLUSIONS  These results support a crucial role of intestinal Cckbr deficiency on SSH development and the diuretic antihypertension effect in CCKBRfl/fl villin-Cre mice. The CCKBRfl/fl villin-Cre mice with the high salt intake may serve as a stable model of salt-sensitive hypertensive induced by sodium overloading.
Yang LIU, Xi-Yao ZHU, Zi-Liang SONG, Mu QIN, Chang-Hao XU, Xu LIU
 doi: 10.11909/j.issn.1671-5411.2022.12.011
Abstract(128) FullText HTML(43) PDF (15)
 OBJECTIVES To investigate proarrhythmic substrates of atrial fibrillation (AF) in a canine model of dehydromonophylline (DMCT)-induced pulmonary arterial hypertension (PAH). METHODS All cannines (n = 12) underwent baseline echocardiographic and hemodynamic examinations, 7 of which were injected with DMCT (3.0 mg/kg) to induce PAH via jugular vein cannulation. The control beagles (n = 5) were given the same dose of normal saline. Then, both groups were monitored by insertable cardiac monitors. Hemodynamic, echocardiographic, electrophysiological and histological examinations were performed 8 weeks later. RESULTS In PAH group, two died after the injection (mortality 28.6%). Thus, 10 beagles (PAH group: 5, control group: 5) underwent all the examinations. The pulmonary artery pressure increased significantly while the right atrium (RA) and right ventricle expanded slightly. Spontaneous AF episodes were recorded in all PAH canines 1 week after the injection. The AF burden increased rapidly from 1 week (7.6% ± 1.8%) and remained high after 2-3 weeks (32.0% ± 4.9% at 8 weeks). Compared with the control group, the PAH group had abbreviated effective refractory periods (ERPs), increased atrial ERP dispersion, and slower conduction velocities. Notably, AF susceptibility and atrial remodeling in RA was more significant those in LA, such as increased WOV (39.0 ± 6.5 vs. 28.0 ± 5.7 ms, P = 0.022), enlarged low voltage regions (7.66% ± 0.46% vs. 4.40% ± 0.55%, P < 0.0001) and fibrosis (8.22% ± 0.61% vs. 4.93% ± 0.60%, P < 0.0001). CONCLUSIONS  DMCT-induced canine PAH model increased the incidence of spontaneous and induced AF. The electrophysiological and structural remodeling of the RA facilitated the AF genesis.
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We would delightedly report that the 2020 SCI impact factor of Journal of Geriatric Cardiology(JGC,ISSN 1671-5411/ CN 11-5329/R) has increased from 2.491 to 3.327, according to the 2020 Journal Citation Reports (InCites, Clarivate Analytics), ranking 33/53 and 65/142 in the fields of Geriatrics & Gerontology and Cardiac & Cardiovascular Systems, respectively. Show more
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