Objective:Patient-specific aortic material properties play a critical role in aortic dissection development. In this study, a non-invasive method was employed to assess the in vivo anisotropic mechanical properties of normal and dissected ascending aortas and compare them with their ex vivo material properties. Methods:Biaxial tensile testing was performed on 10 ascending aortic specimens (five patients with type-A aortic dissection and five donors without aortic diseases), with testing data fitted using anisotropic Mooney-Rivlin models. An iterative algorithm was proposed to determine in vivo aortic material properties by matching systolic and diastolic aortic geometries from echocardiography images with those from computed tomography-based computational models. Three settings of initial guesses of material parameters (M01: subject-specific ex vivo parameters; M02: ex vivo parameters of one subject with median stiffness; M03: a 5% variation applied to M02) were investigated in the iterative algorithm for their influence on in vivo property estimation and effective Young's moduli along the circumferential (YMc) and axial (YMa) directions. Results:M01-derived in vivo properties had a maximum relative error of -33.44% in YMc/YMa among 10 subjects compared to ex vivo material properties. The median relative error of YMc was -29.40% for M02. Furthermore, a 5% variation in initial parameters caused less than 1.5% change in the estimated in vivo properties. The anisotropy difference between the initial material guess and real aortic tissue would exert a significant impact on YMa estimation but negligible effects on stress distributions. Conclusion:Overall, in vivo material properties estimated using the proposed method exhibited lower YMc values than the experimental results for normal and dissected ascending aortas.

BACKGROUND: Left ventricular assist devices (LVADs) have undergone significant evolution as a crucial intervention for severe heart failure. This study sought to delineate the developmental trajectory of LVAD research through bibliometric analysis, emphasizing key advancements, principal contributors, and evolutionary trends. METHODS: A comprehensive bibliometric analysis was performed utilizing the Web of Science Core Collection (WoSCC) database, encompassing publications from 1963 to 2024 pertinent to LVADs. This search yielded a total of 9,552 articles published in English. Data visualization and analysis were executed using VOSviewer (version 1.6.20), CiteSpace (version 6.3.R1), and R 4.3.3. RESULTS: The examination of the 9,552 publications revealed notable global collaboration and considerable growth in LVAD research from 1963 to 2024. The United States led contributions, followed by Germany and Japan. Columbia University emerged as the leading institution with strong international collaborative networks. The Journal of Heart and Lung Transplantation and Circulation were identified as the most influential journals. Notable authors like Naka Y and Pagani FD stood out with high citation counts and collaborative networks. Keyword analysis indicated a shift from fundamental device functionality to more intricate themes, such as regenerative medicine and long-term patient management. CONCLUSIONS: This bibliometric analysis of the LVAD domain underscores research progress, emerging hotspots, and major contributors. It serves as a significant reference for future advancements in LVAD technology and its clinical applications, while fostering improvements and innovations in the treatment of heart failure.

Aortic dissection (AD) caused by the intimal tear would progress into the separation of aortic media, leading to devastating sequelae. Quantifying the mechanical and histological changes in aortic intima-media (IM) tissue during the AD development would advance our understanding of the mechanism behind the disease initiation for its prevention and management. Twenty-eight ascending aortic specimens were harvested from 19 patients with type A AD and 9 organ donors to obtain 120 aortic IM tissue samples. Uniaxial tensile experiments were performed on the samples until they failed, and their ultimate stress and stretch data at the time of failure were recorded. Additionally, an extra subsample was cut from each aortic specimen to perform the histological staining to quantify the contents of elastic and collagen fibers. Our statistical results showed that the ultimate stress and stretch of the dissected aortic IM samples were significantly lower than those of normal ones. Furthermore, a positive correlation between the elastic fiber content and ultimate stretch in aortic IM was found. Combining these findings, it suggests that reduced elastic fiber content in aortic IM tissue of the diseased group impairs its ability to withstand high stress and stretch conditions, thereby predisposing to AD.

Mitochondrial dysfunction is a key factor in exacerbating pressure overload-induced cardiac hypertrophy and is linked to increased morbidity and mortality. ECSIT, a crucial adaptor for inflammation and mitochondrial function, has been reported to express multiple transcripts in various species and tissues, leading to distinct protein isoforms with diverse subcellular localizations and functions. However, whether an unknown ECSIT isoform exists in cardiac cells and its potential role in regulating mitochondrial function and pathological cardiac hypertrophy has remained unclear. This study identified a 42-kDa ECSIT isoform encoded by the transcript variant Ecsit-X4, which is highly expressed in the mitochondria of adult cardiomyocytes but down-regulated in hypertrophic human heart samples and TAC-treated mouse hearts. AAV9-mediated Ecsit-X4 gene therapy, administered either before or after TAC surgery, significantly attenuated cardiac hypertrophy. Cardiomyocyte-specific Ecsit deficiency worsened TAC-induced cardiac hypertrophy, while Ecsit-X4 compensation independently rescued hypertrophic phenotypes in EcsitcKO mice. Mechanistically, ECSIT-X4 localized to the mitochondria and interacted with STAT3, leading to increased STAT3 levels and enhanced serine 727 phosphorylation in cardiomyocyte mitochondria, thereby promoting strong mitochondrial bioenergetics. This study identified a novel transcript variant of ECSIT localized in the mitochondria of adult cardiomyocytes and highlights its potential as a therapeutic target for heart failure.

Background The regenerative capacity of the adult mammalian hearts is limited. Numerous studies have explored mechanisms of adult cardiomyocyte cell‐cycle withdrawal. This translational study evaluated the effects and underlying mechanism of rhCHK1 (recombinant human checkpoint kinase 1) on the survival and proliferation of cardiomyocyte and myocardial repair after ischemia/reperfusion injury in swine. Methods and Results Intramyocardial injection of rhCHK1 protein (1 mg/kg) encapsulated in hydrogel stimulated cardiomyocyte proliferation and reduced cardiac inflammation response at 3 days after ischemia/reperfusion injury, improved cardiac function and attenuated ventricular remodeling, and reduced the infarct area at 28 days after ischemia/reperfusion injury. Mechanistically, multiomics sequencing analysis demonstrated enrichment of glycolysis and mTOR (mammalian target of rapamycin) pathways after rhCHK1 treatment. Co‐Immunoprecipitation (Co‐IP) experiments and protein docking prediction showed that CHK1 (checkpoint kinase 1) directly bound to and activated the Serine 37 (S37) and Tyrosine 105 (Y105) sites of PKM2 (pyruvate kinase isoform M2) to promote metabolic reprogramming. We further constructed plasmids that knocked out different CHK1 and PKM2 amino acid domains and transfected them into Human Embryonic Kidney 293T (HEK293T) cells for CO‐IP experiments. Results showed that the 1–265 domain of CHK1 directly binds to the 157–400 amino acids of PKM2. Furthermore, hiPSC‐CM (human iPS cell‐derived cardiomyocyte) in vitro and in vivo experiments both demonstrated that CHK1 stimulated cardiomyocytes renewal and cardiac repair by activating PKM2 C‐domain‐mediated cardiac metabolic reprogramming. Conclusions This study demonstrates that the 1–265 amino acid domain of CHK1 binds to the 157–400 domain of PKM2 and activates PKM2‐mediated metabolic reprogramming to promote cardiomyocyte proliferation and myocardial repair after ischemia/reperfusion injury in adult pigs.

Purpose: Type A aortic dissection (TAAD) is a life-threatening aortic disease. The tear involves the ascending aorta and progresses into the separation of the layers of the aortic wall and the occurrence of a false lumen. Accurate segmentation of TAAD could provide assistance for disease assessment and guidance for clinical treatment. Methods: This study applied nnU-Net, a state-of-the-art biomedical segmentation network architecture, to segment contrast-enhanced CT images and quantify the morphological features for TAAD. CT datasets were acquired from 24 patients with TAAD. Manual segmentation and annotation of the CT images was used as the ground-truth. Two-dimensional (2D) nnU-Net and three-dimensional (3D) nnU-Net architectures with Dice- and cross entropy-based loss functions were utilized to segment the true lumen (TL), false lumen (FL), and intimal flap on the images. Four-fold cross validation was performed to evaluate the performance of the two nnU-Net architectures. Six metrics, including accuracy, precision, recall, Intersection of Union, Dice similarity coefficient (DSC), and Hausdorff distance, were calculated to evaluate the performance of the 2D and 3D nnU-Net algorithms in TAAD datasets. Aortic morphological features from both 2D and 3D nnU-Net algorithms were quantified based on the segmented results and compared. Results: Overall, 3D nnU-Net architectures had better performance in TAAD CT datasets, with TL and FL segmentation accuracy up to 99.9%. The DSCs of TLs and FLs based on the 3D nnU-Net were 88.42% and 87.10%. For the aortic TL and FL diameters, the FL area calculated from the segmentation results of the 3D nnU-Net architecture had smaller relative errors (3.89–6.80%), compared to the 2D nnU-Net architecture (relative errors: 4.35–9.48%). Conclusions: The nnU-Net architectures may serve as a basis for automatic segmentation and quantification of TAAD, which could aid in rapid diagnosis, surgical planning, and subsequent biomechanical simulation of the aorta.

Myocardial fibrosis is a major pathogenic factor contributing to cardiac remodeling and heart failure. Recent research has indicated that micro RNAs play a crucial role in the progression of cardiac fibrosis. Bone morphogenetic protein and activin membrane-bound inhibitor(BAMBI) have been shown to alleviate myocardial fibrosis by inhibiting the transforming growth factor β1(TGF-β1) signaling pathway. Therefore, the current study aimed to elucidate the post-transcriptional regulation of BAMBI by miR-19a-3p and its role in TGF-β1-induced cardiac fibroblast activation. We found that transverse aortic constriction induced both myocardial interstitial and perivascular collagen deposition. Quantitative reverse transcription-PCR(q RT-PCR) analysis showed that the expression level of miR-19a-3p was increased in the myocardial tissues of cardiac fibrosis, and TGF-β1 induced an upregulation in miR-19a-3p expression in cardiac fibroblasts. The dual-luciferase reporter assay and q RT-PCR verified that miR-19a-3p directly bound to the 3 ′ untranslated regions of BAMBI m RNA, thereby reducing BAMBI expression and diminishing its ability to inhibit the TGF-β1 signaling pathway. Furthermore,overexpression of miR-19a-3p mimic increased the activation of TGF-β1/SMAD2/3 pathway signaling,promoting cardiac fibroblast activation. However, this activation was blocked by BAMBI overexpression. These findings imply that miR-19a-3p enhances the activation of TGF-β1/SMAD2/3 by inhibiting BAMBI, further boosting the activation of cardiac fibroblasts and contributing to myocardial fibrosis.

Mechanical mismatch between native aortas and aortic grafts can induce graft failure. This study aims to compare the mechanical and microstructural properties of different graft materials used in aortic repair surgeries with those of normal and dissected human ascending aortas. Five types of materials including normal aorta (n = 10), dissected aorta (n = 6), human pericardium (n = 8), bovine pericardium (n = 8) and Dacron graft (n = 5) were collected to perform uniaxial tensile testing to determine their material stiffness, and ultimate strength/stretch. The elastin and collagen contents in four tissue groups except for Dacron were quantified by histological examinations, while the material ultrastructure of five material groups was visualized by scanning electron microscope. Statistical results showed that three graft materials including Dacron, human pericardium and bovine pericardium had significantly higher ultimate strength and stiffness than both normal and dissected aortas. Human and bovine pericardia had significantly lower ultimate stretch than native aortas. Histological examinations revealed that normal and diseased aortic tissues had a significantly higher content of elastic fiber than two pericardial tissues, but less collagen fiber content. All four tissue groups exhibited lamellar fiber ultrastructure, with aortic tissues possessing thinner lamella. Dacron was composed of densely coalesced polyethylene terephthalate fibers in thick bundles. Aortic graft materials with denser fiber ultrastructure and/or higher content of collagen fiber than native aortic tissues, exhibited higher ultimate strength and stiffness. This information provides a basis to understand the mechanical failure of aortic grafts, and inspire the design of biomimetic aortic grafts.

Recent studies have attempted to characterize the layer-specific mechanical and microstructural properties of the aortic tissues in either normal or pathological state to understand its structural-mechanical property relationships. However, layer-specific tissue mechanics and compositions of normal and dissected ascending aortas have not been thoroughly compared with a statistical conclusion obtained. Eighteen ascending aortic specimens were harvested from 13 patients with type A aortic dissection and 5 donors without aortic diseases, with each specimen further excised to obtain three tissue samples including an intact wall, an intima-media layer and an adventitia layer. For each tissue sample, biaxial tensile testing was performed to obtain the experimental stress-stretch ratio data, which were further fed into the Fung-type model to quantify the tissue stiffness, and Elastin Van Gieson stain and Masson's trichrome stain were employed to quantify the elastic and collagen fiber densities. Statistical analyses were performed to determine whether any significant differences exist in mechanical properties and compositions between diseased and normal aortic tissues. The tissue stiffness of intima-media samples was significant higher in diseased group than that of normal group in longitudinal direction at the stretch ratio 1.30 (p = 0.0068), while no significant differences were found in the other direction or other tissue types. Even though there was no significant difference in elastic or collagen fiber densities between two groups, the diseased group generally had lower elastic fiber density, but higher collagen fiber density for all three tissue layers. Compared to normal aortic tissues, the elastic fiber density of the intima-media layer in the dissected aortic tissue was lower, while its tissue stiffness was significantly higher, indicating the tissue stiffness of the intima-media layer could be a potential indicator for aortic dissection.

Background The study aimed to assess the correlation between the monitoring frequency of PT-INR and the long-term prognosis in patients with mechanical heart valve (MHV) replacement after discharge. Methods This single-center, observational study enrolled patients who underwent MHV replacement and discharged from June 2015 to May 2018. Patients or their corresponding family members were followed with a telephone questionnaire survey in July-October 2020. Based on monitoring intervals, patients were divided into frequent monitoring (FM) group (≤ 1 month) and less frequent monitoring (LFM) group (> 1 month). The primary endpoint was the composite of thromboembolic event, major bleeding or all-cause death. The secondary endpoints were thromboembolic event, major bleeding or all-cause death, respectively. Results A total of 188 patients were included in the final analysis. The median follow-up duration was 3.6 years (Interquartile range: 2.6 to 4.4 years). 104 (55.3%) patients and 84 (44.7%) patients were classified into the FM group and the LFM group, respectively. The FM group had a significantly lower incidence of the primary endpoint than the LFM group (3.74 vs. 1.16 per 100 patient-years, adjusted HR: 3.31 [95% CI 1.05–10.42, P = 0.041]). Secondary analysis revealed that the risk of thromboembolic events and all-cause death were also reduced in the FM group. Conclusions The management of warfarin treatment in patients after MHV replacement remains challenging. Patients with less frequent monitoring of PT-INR might have worse clinical prognosis than those with frequent PT-INR monitoring.

BACKGROUND:Heart failure, characterized by cardiac remodeling, is associated with abnormal epigenetic processes and aberrant gene expression. Here, we aimed to elucidate the effects and mechanisms of NAT10 (N-acetyltransferase 10)-mediated N4-acetylcytidine (ac4C) acetylation during cardiac remodeling.METHODS:NAT10 and ac4C expression were detected in both human and mouse subjects with cardiac remodeling through multiple assays. Subsequently, acetylated RNA immunoprecipitation and sequencing, thiol-linked alkylation for the metabolic sequencing of RNA (SLAM-seq), and ribosome sequencing (Ribo-seq) were employed to elucidate the role of ac4C-modified posttranscriptional regulation in cardiac remodeling. Additionally, functional experiments involving the overexpression or knockdown of NAT10 were conducted in mice models challenged with Ang II (angiotensin II) and transverse aortic constriction.RESULTS:NAT10 expression and RNA ac4C levels were increased in in vitro and in vivo cardiac remodeling models, as well as in patients with cardiac hypertrophy. Silencing and inhibiting NAT10 attenuated Ang II-induced cardiomyocyte hypertrophy and cardiofibroblast activation. Next-generation sequencing revealed ac4C changes in both mice and humans with cardiac hypertrophy were associated with changes in global mRNA abundance, stability, and translation efficiency. Mechanistically, NAT10 could enhance the stability and translation efficiency of CD47 and ROCK2 transcripts by upregulating their mRNA ac4C modification, thereby resulting in an increase in their protein expression during cardiac remodeling. Furthermore, the administration of Remodelin, a NAT10 inhibitor, has been shown to prevent cardiac functional impairments in mice subjected to transverse aortic constriction by suppressing cardiac fibrosis, hypertrophy, and inflammatory responses, while also regulating the expression levels of CD47 and ROCK2 (Rho associated coiled-coil containing protein kinase 2).CONCLUSIONS:Therefore, our data suggest that modulating epitranscriptomic processes, such as ac4C acetylation through NAT10, may be a promising therapeutic target against cardiac remodeling.

To investigate the feasibility and effectiveness of establishing porcine ischemia-reperfusion models by ligating the left anterior descending (LAD) coronary artery, we first randomly divided 16 male Bama pigs into a sham group and a model group. After anesthesia, we separated the arteries and veins. Subsequently, we rapidly located the LAD coronary artery at the beginning of its first diagonal branch through a mid-chest incision. Then, we loosened and released the ligation line after five minutes of pre-occlusion. Finally, we ligated the LAD coronary artery in situ two minutes later and loosened the ligature 60 min after ischemia. Compared with the sham group, electrocardiogram showed multiple continuous lead ST-segment elevations, and ultrasound cardiogram showed significantly lower ejection fraction and left ventricular fractional shortening at one hour and seven days post-operation in the model group. Twenty-four hours after the operation, cardiac troponin T and creatine kinase-MB isoenzyme levels significantly increased in the model group, compared with the sham group. Hematoxylin and eosin staining showed the presence of many inflammatory cells infiltrating the interstitium of the myocardium in the model group but not in the sham group. Masson staining revealed a significant increase in infarct size in the ischemia/reperfusion group. All eight pigs in the model group recovered with normal sinus heart rates, and the survival rate was 100%. In conclusion, the method can provide an accurate and stable large animal model for preclinical research on ischemia/reperfusion with a high success rate and homogeneity of the myocardial infarction area.

Background: Aortic dissection and atherosclerosis are two common pathological conditions affecting the aorta. Aortic biomechanics are believed to be closely associated with the pathological development of these diseases. However, the biomechanical environment that predisposes the aortic wall to these pathological conditions remains unclear. Methods: Sixteen ascending aortic specimens were harvested from 16 human subjects and further categorized into three groups according to their disease states: aortic dissection group, aortic dissection with accompanied atherosclerosis group and healthy group. Experimental stress-strain data from biaxial tensile testing were used to fit the anisotropic Mooney-Rivlin model to determine material parameters. Computed tomography images or transesophageal echocardiography images were collected to construct computational models to simulate the stress/strain distributions in aortas at the pre-dissection state. Statistical analyses were performed to identify the biomechanical factors to distinguish three groups of aortic tissues. Results: Material parameters of anisotropic Mooney-Rivlin model were fitted with average R2 value 0.9749. The aortic diameter showed no significant difference among three groups. Changes of maximum and average stress values from minimum pressure to maximum pressure (oMaxStress and oAveStress) had significantly difference between dissection group and dissection with accompanied atherosclerosis group (p = 0.0201 and 0.0102). Changes of maximum and average strain values from minimum pressure to maximum pressure (oMaxStrain and oAveStrain) from dissection group were significant different from healthy group (p = 0.0171 and 0.0281). Conclusion: Changes of stress and strain values during the cardiac cycle are good biomechanical factors for predicting potential aortic dissection and aortic dissection accompanied with atherosclerosis.

目的 评价超声刀不接触获取大隐静脉在非体外循环冠状动脉旁路移植术(OPCABG)中的应用效果.方法 回顾性分析2020年1月至8月南京医科大学第一附属医院80例三支冠状动脉病变采用大隐静脉移植行OPCABG患者的临床资料,获取大隐静脉的方法分别为超声刀不接触技术(NT组,n=26)或常规方法(常规组,n=54).对比两组手术时间、静脉桥吻合口数、需钛夹/结扎/缝合处理的大隐静脉侧支数、二次开胸止血情况、术后机械通气时间、术后ICU停留时间、术后住院时间及术后下肢切口并发症等指标的差异.结果 两组术后无再发急性心肌梗死,无死亡,均痊愈出院.两组手术时间、静脉桥吻合口数、术后机械通气时间、术后ICU停留时间、术后住院时间差异无统计学意义(P＞0.05).NT组需钛夹/结扎/缝合处理的大隐静脉侧支数以[M(P25,P75)]统计为4(3,5)个,显著少于常规组的9(8,11)个(P＜0.01).NT组1例、常规组5例发生术后下肢切口愈合不良,两组比较差异无统计学意义(P＞0.05);术后二次开胸止血常规组发生1例、NT组无发生.结论 超声刀不接触技术获取的大隐静脉在OPCABG术中应用安全有效,不增加手术时间和下肢切口并发症.

目的:总结孤立性房颤外科微创消融术同期行肺部占位切除术的方法与经验.方法:回顾性分析南京医科大学第一附属医院心脏大血管外科行微创孤立性房颤消融术同期行肺部占位切除术的6例患者的临床资料及手术过程,加以总结分析.其中双侧肺占位者2例,单侧肺占位者4例.结果:6例患者均手术顺利,无围手术期二次开胸、恶性心律失常及死亡.单纯行肺组织楔形切除术者3例,肺叶切除术者1例,肺癌根治术者2例.病理结果分别为:慢性肉芽肿4例,浸润性腺癌2例.出院前动态心电图示窦性心律5例,房扑心律1例.结论:通过合理的手术方案和手术路径,腔镜下同期处理孤立性房颤及肺部占位不但能减少患者的疾病痛苦也能减少社会的医疗经济负担,此手术方法是安全有效的.

目的:比较内窥镜辅助下大隐静脉采集术(endoscopicopic vein harvesting,EVH)与常规切开法(open vein harvesting,OVH)获取大隐静脉术中及术后并发症的发生率,探讨EVH在冠状动脉旁路移植术(coronary artery bypass grafting,CABG)中应用的可行性及安全性.方法:回顾性分析2020年7月-2021年7月80例行CABG的冠状动脉粥样硬化性心脏病患者,根据大隐静脉获取方式,将患者分为EVH组40例与OVH组40例,观察术前、术中及术后指标.结果:EVH组与OVH组术中及术后观察资料相比,手术时间(P=0.370)、搭桥总数(P=0.819)、大隐静脉修补次数(P=0.474)、术后机械通气时间(P=0.080)术后住院时间(P=0.994)、二次开胸止血率(P=1.000)、围术期死亡率(P=1.000)、住院总费用(P=0.078)及不良事件发生率(P=1.000)差异均无统计学意义.与OVH组相比较,EVH组下肢切口长度(P＜ 0.001)明显缩短,术后下肢切口疼痛(P＜ 0.001)、麻木(P=0.025)及脂肪液化(P=0.005)发生率明显下降,差异有统计学意义.结论:EVH可显著降低冠状动脉粥样硬化性心脏病患者CABG术后的下肢并发症,术后下肢的疼痛、麻木感及切口愈合不良的发生率大大降低,患者早日下地活动,有利于患者康复.

BACKGROUND:A combination of endocardial and epicardial approaches has improved the overall success rate of ventricular tachycardia (VT) ablation in patients with cardiomyopathy. However, the origins of some VTs are truly intramural or close to coronary arteries, which makes this combined strategy either prone to failure or too risky.OBJECTIVES:This observational study aimed to explore the feasibility and efficacy of direct epicardial ablation combined with intramural ethanol injection via surgical approach for inaccessible intramural VTs or VTs too close to coronary arteries.METHODS:In four canines ventricular lesions produced by direct epicardial injection of ethanol were assessed. Six consecutive patients with recurrent VT refractory to catheter endocardial and epicardial RF ablation and that remained inducible after surgical epicardial mapping and RF ablation were included. Ethanol was injected by needle at the epicardial RF ablation sites. The primary outcome was freedom of sustained VT determined by device interrogation and periodical 24-h holter recordings subsequently.RESULTS:In an animal study, the lesions were homogenous and increased in size with the volume of ethanol injected. In all six patients, ethanol injection at the target sites in the anterior or lateral left ventricle abolished inducible VT. Over a median follow-up of 22 months (range, 6-65), all patients remained free of sustained VT. One patient died of pulmonary infection one year after the procedure.CONCLUSIONS:A hybrid strategy of surgical ablation combined with intramural ethanol injection is feasible and effective in patients with multiple failed percutaneous ablation attempts.

Background Pregnancy-associated acute myeloid leukemia (PA-AML) is rare. Cardiac surgery in the context of AML poses challenges that are seldom encountered.Case Description The subject is a 31-year-old woman at 38 weeks' gestational age diagnosed with AML and partial atrioventricular septal defect. After multidisciplinary consulting, an urgent cesarean section was performed, then chemotherapy was initiated, followed by minimally invasive cardiac surgery with an uneventful recovery.Conclusion Efficient multidisciplinary approach is essential in the management of PA-AML and cardiac disease. Minimally invasive cardiac surgery may be safe and useful in patients with AML.

OBJECTIVE This study aimed to investigate the functions of mRNA, long non-coding RNA (lncRNA), and circular RNA (circRNA) in paroxysmal and persistent atrial fibrillation (AF) patients. METHODS A total of 9 left atrial appendage (LAA) tissues were collected from patients with AF (ParoAF patients = 3 and PersAF patients = 3) and donors (n=3). Genes and circRNAs were identified by per kilobase per million reads (RPKM) and number of circular reads/number of mapped reads/read length (SRPBM), respectively. Differentially expressed mRNAs (DE mRNAs), lncRNAs (DE lncRNAs), and circRNAs (DE circRNAs) were identified by | log2 (Fold Change) | ≥ 2 and p-value < 0.05. Gene Ontology (GO) and the Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway enrichment analyses were performed. Protein-protein, mRNA-lncRNA, and circRNA-miRNA interaction networks were constructed. In addition, logistic analysis was conducted among AF and circRNAs. RESULTS A total of 285 (116 up-regulated and 169 down-regulated) and 275 (110 up-regulated and 165 down-regulated) DE mRNAs, 575 (276 up-regulated and 299 down-regulated) and 583 (330 up-regulated and 253 down-regulated) DE lncRNAs, and 83 (48 up-regulated and 35 down-regulated) and 99 (58 up-regulated and 41 down-regulated) circRNAs were detected in ParoAF and PersAF, respectively, as compared with control. MAPK signal pathway as well as voltage-dependent, L type, and alpha 1C subunit calcium channel (CACNA1C) might participate in AF occurrence by preventing atrial parasympathetic remodeling. Collagen type I alpha 1 (COL1A1) and COL1A2 mostly participated in the enriched GO and KEGG terms and connected with most of the DE mRNAs. The expression of chr10: 69902697|69948883 was a protective factor against PersAF after adjusting for age (p=0.022, 95% CI: 0.003-0.634). CONCLUSION We found that some mRNAs, lncRNAs, circRNAs, and pathways play essential roles in AF pathogenesis and development. Moreover, one protective factor against PersAF was detected.