NETs promote pathogenic cardiac fibrosis and participate in ventricular aneurysm formation after ischemia injury through the facilitation of perivascular fibrosis.

Fibrosis has been widely investigated in acute phase of myocardial infarction (MI). However, the mechanism of sustained fibrosis after MI hasn't been elucidated, which eventually gives rise to ventricular aneurysm (VA) formation chronic while lethal. Neutrophil as vital cell facilitating the fibrotic repair after acute MI may not project its effect to chronic phase unless neutrophil extracellular traps (NETs) were secreted and accumulating. The aim of this study was to investigate whether NETs contribute to the sustained fibrosis and VA formation after MI. We identified NETs in ventricular aneurysm of patients. Accordingly, NETs increased in peripheral blood of VA patients. Moreover, in rat VA NETs were also identified. Stimulated by NETs, the migration of fibroblast was enhanced and the differentiation of cardiac myofibroblast was initiated. Smad, MAPK and RhoA signaling pathways were activated by NETs incubation. And additional deposition with DNase I to disrupt NETs and abrogated NETs induced fibrosis both in vivo and vitro. These results collectively demonstrate a novel profibrotic role for NETs in chronic cardiac fibrosis and VA formation.

Postoperative Coronary Artery Spasm After Mitral Valve Replacement and Cox-Maze IV Procedure: A Case Report.

BACKGROUND: Few cases have been reported about coronary artery spasm after a mitral valve replacement and concomitant Cox-Maze IV procedure. We report the case of an adult male who developed right coronary artery (RCA) spasm after a mitral valve replacement with tricuspid valve repair and Cox-Maze IV procedure. CASE REPORT: A 66-year-old male, complaining of progressive exertional shortness of breath, was diagnosed with severe mitral stenosis, moderate tricuspid regurgitation, complete right bundle branch block, and persistent atrial fibrillation (AF) in our clinic. The patient underwent elective mitral valve replacement, tricuspid valve repair, and Cox-Maze IV procedure. Four hours after surgery, a 12-lead electrocardiogram (ECG) showed progressive elevation of ST-segment in the avF and III leads and Troponin-T was over 7000 pg/mL. After one hour, Troponin-T increased to over 10000 pg/mL, and ECG still showed persisted ST-segment elevation in inferior leads. Emergent angiography was performed, and intra-coronary administration of nitroglycerin completely relieved the spasm. CONCLUSION: Potential risks of coronary injury after valvular surgery and Cox-Maze IV procedure need further aggressive investigation and postoperative ischemia should prompt an emergent coronary angiography to identify the cause and apply immediate therapy.

Mitochondrial Dysfunction Secondary to Endoplasmic Reticulum Stress in Acute Myocardial Ischemic Injury in Rats.

BACKGROUND The relationship between endoplasmic reticulum and mitochondria during acute myocardial ischemic injury is still unclear. Our study aimed to define the dynamics of endoplasmic reticulum stress and mitochondrial dysfunction during acute ischemic injury. MATERIAL AND METHODS A rat model of acute myocardial infarction and hypoxic cardiomyocytes were used in this study. Groups were set at 0 hours, 1 hour, 2 hours, 4 hours, and 6 hours after ischemic injury for both in vivo and in vitro studies. ATF6 and GRP-78 were examined to indicate endoplasmic reticulum stress. Cellular ATP and cytosolic levels of mitochondrial DNA and cytochrome c were detected to evaluate mitochondrial dysfunction. Caspase-3 was used for apoptosis analysis. RESULTS Our results showed that both mRNA and protein levels of ATF6 and GRP-78 were elevated from 1 hour after ischemic injury in vivo and in vitro (P<0.05). However, ATP levels were increased at 2 hours after ischemic injury and significantly decreased from 4 hours after ischemic injury in vivo, while ATP level of cultured cardiomyocytes decreased remarkably from 2 hours after ischemic injury (P<0.05). Cytosolic mitochondrial DNA levels began to increase from 2 hours after ischemic injury (P<0.05). Cytosolic levels of cytochrome c increased from 4 hours after ischemic injury. Additionally, both mRNA and protein expressions of caspase-3 started to significantly elevate at 6 hours after ischemic injury (P<0.05). CONCLUSIONS The present study suggested that mitochondrial dysfunction was secondary to endoplasmic reticulum stress, which provides a novel experimental foundation for further exploration of the detailed mechanism after ischemic injury, especially the interaction between endoplasmic reticulum and mitochondria.

[Endoplasmic Reticulum Stress and Mitochondrial Damage in Rat Cardiomyocytes after Acute Myocardial Infarction].

OBJECTIVE: To study the alterations of endoplasmic reticulum (ER) stress and mitochondrial damage after acute myocardial infarction (AMI). METHODS: A total of 40 SD rats were used in this study and 32 of them were subjected to AMI by ligation of left anterior descending artery. The rats were sacrificed and the heart tissues were collected after 1 h, 2 h, 4 h and 6 h of AMI ( n=8 per group). The mRNA levels of activating transcription factor 6 alpha ( ATF6) and immunoglobulin heavy chain binding potein ( BiP), as well as the expression of mitochondrial DNA (mtDNA) in cytoplasm were detected by RT-PCR. The ATP levels in the cardiomyocytes were detected by a commercial ATP assay kit. RESULTS: The mRNA levels of ATF6 and BiP were significantly increased after 1 h of AMI, which were maintained at high level from 2 h of AMI to the end of the experiment ( P<0.05). The ATP concentrations in the cardiomyocytes were significantly elevated after 1 h of AMI but remarkably decreased after 4 h and 6 h of AMI ( P<0.05). The release of mtDNA in cytoplasm was significantly increased after 2 h of AMI, followed by further elevations at 4 h and 6 h after AMI ( P<0.05). CONCLUSION: Mitochondrial damage is secondary to ER stress in AMI.

Giant right atrial aneurysm with atrial fibrillation.

Congenital right atrial aneurysm is a rare condition. Here we reported a 16-year-old male with giant right atrial aneurysm, atrial fibrillation, and atrial septal defect. Surgical resection of extensive right atrium, ASD repair, and maze procedure were performed. In the present case, we found extensive enlargement of right atrium protruding to the apex on the surface of the right ventricle. With the exist of atrial fibrillation, thrombus formation was always a lethal threat. Surgical treatment can provide excellent clinical results and further avoided life-threatening complications.

The diosgenin prodrug nanoparticles with pH-responsive as a drug delivery system uniquely prevents thrombosis without increased bleeding risk.

Thrombosis is the leading cause of death in patients with cardiovascular disease in the world. Current antithrombotic agent aspirin has serious side effects such as higher bleeding risk and serious gastrointestinal ulcers. Diosgenin reported in clinical research could prevent thrombosis without side effects. However, poor bioavailability and low knowledge on its molecular targets limit its clinical application. A novel prodrug with antithrombotic effect was prepared based on conjugating diosgenin derivatives to PEG with Schiff-base bond. The prodrug with long blood circulation time and satisfying safety could self-assemble into micelles in water. The prodrug micelles with pH-responsibility could targetedly release diosgenin in position of thrombus in vivo. The results indicate that the prodrug micelles without bleeding risk and histological damages prevent thrombosis by inhibiting platelet activation and apoptosis. Our studies demonstrate that the prodrug micelles could obviously enhance the efficacy in the prevention of arterial thrombus and venous thrombus than aspirin.

Comparison between balanced and unbalanced precoding technique in high-order QAM vector mm-wave signal generation based on intensity modulator with photonic frequency doubling.

We experimentally investigate high-order quadrature-amplitude-modulation (QAM) vector millimeter-wave (mm-wave) signal generation based on intensity modulator (IM) with photonic frequcney doubling and precoding in this paper. In order to obtain an ordinary QAM modulated radio-frequency (RF) signal after the square-law detection of the photodiode, amplitude and phase precoding technique should be employed. In this paper, we experimentally investigate the generation of 1~4 Gbaud vector mm-wave signal with the modulation formats of 8QAM and 16QAM at the carrier frequency of 40 GHz, and study the bit-error-rate (BER) performance of both balanced precoding scheme and unbalanced precoding scheme adopting high-order QAM modulation.

North American ginseng inhibits myocardial NOX2-ERK1/2 signaling and tumor necrosis factor-α expression in endotoxemia.

Sepsis is a systemic inflammatory response to infection with a high mortality but has no specific treatment despite decades of research. North American (NA) ginseng (Panax quinquefolius) is a popular natural health product with anti-oxidant and anti-inflammatory properties. The aim of the present study was to investigate the effects of NA ginseng on pro-inflammatory cytokine expression and cardiac function in endotoxemia, a model of sepsis. Mice were challenged with lipopolysaccharide (LPS) to induce endotoxemia. Myocardial expression of tumor necrosis factor-alpha (TNF-α), a major pro-inflammatory cytokine that causes cardiac dysfunction, was upregulated in mice with endotoxemia, which was accompanied by increases in NOX2 expression, superoxide generation and ERK1/2 phosphorylation. Notably, pretreatment with NA ginseng aqueous extract (50mg/kg/day, oral gavage) for 5days significantly inhibited NOX2 expression, superoxide generation, ERK1/2 phosphorylation and TNF-α expression in the heart during endotoxemia. Importantly, cardiac function and survival in endotoxemic mice were significantly improved. Additionally, pretreatment with ginseng extract inhibited superoxide generation, ERK1/2 phosphorylation and TNF-α expression induced by LPS in cultured cardiomyocytes. We conclude that NA ginseng inhibits myocardial NOX2-ERK1/2-TNF-α signaling pathway and improves cardiac function in endotoxemia, suggesting that NA ginseng may have the potential in the prevention of clinical sepsis.

Potential Mechanism of Post-Acute Aortic Dissection Inflammatory Responses: The Role of mtDNA from Activated Platelets.

BACKGROUND: Acute aortic dissection (AD) is a lethal cardiovascular disease with severe inflammatory complications. Considering the proinflammatory properties of plasma mitochondrial DNA (mtDNA), we postulate that plasma mtDNA from activated platelets may be responsible for post-acute AD inflammatory responses. METHODS: We consecutively enrolled 68 patients with acute AD as well as matched hypertensive and healthy participants. Blood samples were collected on admission for blood routine tests, mtDNA assay, and inflammatory cytokine analysis. A computed tomography scan was used to evaluate the extent of dissections. RESULTS: Our results demonstrate that plasma mtDNA, platelet activation, and inflammatory levels were remarkably higher in acute AD patients than in hypertensive or healthy participants. These parameters were also higher in the Stanford A group than in the Stanford B group (p < 0.05). Bivariate correlation analysis demonstrated positive associations between mtDNA and inflammatory levels (tumor necrosis factor-α: r = 0.577; interleukin-6: r = 0.632), mtDNA and platelet activation (r = 0.642), and platelet activation and the extent of dissection (r = 0.635). CONCLUSION: Our study suggests that acute AD-induced tunica media exposure causes platelet activation, which leads to the initiation of inflammatory responses via the release of mtDNA into the circulation. Our study provides a novel fundamental basis and a potential therapeutic target for the prevention and treatment of post-AD inflammatory responses.

[Epigallocatechin-3-gallate Attenuates Myocardial Reperfusion Injury in Rats Through Activation of PI3K/Akt Signaling Pathway].

OBJECTIVE: This study was designed to investigate whether epigallocatechin-3-gallate (EGCG) postconditioning protects the heart against ischemic-reperfusion injury (IRI), and to explore its potential mechanisms in a rat model. METHODS: Male Wistar rats were subjected to myocardial ischemia (30 min) and reperfusion (up to 2 h) and the rats were divided into sham group (SO) group, ischemia-reperfusion (I/R) model group and EGCG group. EGCG group were treated with EGCG (10 mg/kg) via intravenous infusion 5 min before reperfusion. Electrocardiogram were applied to record ventricular arrhythmia frequency. The severity of myocardial injury [serum level of lactate dehydrogenase (LDH) and creatine kinase (CK), hematoxylineosin (HE) staining] and ventricular arrhythmia, and the serum levels of inflammatory cytokines [tumor necrosis factor-α (TNF-α), interleukins-6 (IL-6) and IL-8] were assessed with ELISA, electrocardiogram and Western blot respectively. RESULTS: EGCG given before reperfusion could effectively reduce the serum level of LDH and CK and the incidence of ventricular arrhythmia (P < 0.05, respectively), improved the pathological damage. Meanwhile, EGCG could down-regulate the expression levels of TNF-α, IL-6, IL-8 in the myocardial tissue after IRI (P < 0.05, repectively). The expression levels of p-p85 and p-Akt in the EGCG group were significantly up-regulated compared to those in I/R group (P < 0.05, repectively). CONCLUSION: EGCG-related anti-inflammatory action could attenuate rat myocardial IRI and this cardioprotective effect might be activated through the PI3K/Akt pathway.

[Mechanisms for reversal of pulmonary hypertension by rapamycin in rats].

OBJECTIVE: To investigate the effects of rapamycin (RAP) on pulmonary hypertension (PH) in rats, and to provide new insights into medication selection for the clinical treatment of PH. METHODS: Fifty male Sprague-Dawley rats were randomly divided into blank control, PH model, solvent control, RAP 1, and RAP 2 groups. A rat model of PH was induced by left pneumonectomy (PE) and monocrotaline (MCT). At 5 days after PH model establishment, the solvent control group and the RAP 1 group received an intramuscular injection of solvent and RAP, respectively. At 35 days after PH model establishment, the RAP 2 group received an intramuscular injection of RAP. The mean pulmonary artery pressure (mPAP) and the right ventricle/left ventricle plus septum weight ratio (RV/LV+S) were measured in each group. Histopathological changes in the right lung were evaluated by hematoxylin-eosin (HE) staining. The relative expression of alpha-smooth muscle actin (α-SMA) and smooth muscle protein 22-alpha (SM22α) in each group was determined using real-time PCR. RESULTS: At 35 days after surgery, the PH model and the solvent control groups had significantly higher mPAP and RV/LV+S than the blank control group, while the RAP 1 and the RAP 2 groups had significantly lower mPAP than the solvent control group (P<0.05). The RV/LV+S in the RAP 1 group was significantly lower than that in the solvent control group (P<0.05); however, there was no significant difference in RV/LV+S between the RAP 2 and the solvent control groups (P>0.05). HE staining in the right lung showed the substantially thickened pulmonary artery wall and narrowed arterial lumen in the PH model and the solvent control groups compared with the blank control group. Different degrees of reversal of the pulmonary artery wall thickening were observed after RAP administration. The results of real-time PCR revealed that the relative expression of α-SMA and SM22α in the PH model and the solvent control groups was significantly lower than in the blank control group, while the relative expression of α-SMA and SM22α in the RAP 1 and the RAP 2 groups was significantly higher than in the solvent control group (P<0.05). CONCLUSIONS: RAP can reverse the increase in pulmonary artery pressure and the right ventricular hypertrophy probably by regulation of the phenotypic conversion of vascular smooth muscle cells.

Maternal medication use, fetal 3435 C>T polymorphism of the ABCB1 gene, and risk of isolated septal defects in a Han Chinese population.

The fundamental etiology of the majority of nonsyndromic congenital heart defects is commonly believed to involve the interaction of multiple environmental and genetic factors. This study aimed to explore the joint effects of fetal 3435 C>T polymorphism in the ABCB1 gene and maternal medication use on the risk of septal defects in a Han Chinese population. An age- and gender-matched case-control study involving 265 pairs was conducted from March 2012 to September 2013. Information on maternal periconceptional medication use was obtained through questionnaires. The genotyping of 3435 C>T polymorphism was performed by sequencing. Logistic regression analysis was performed to assess the joint effects of ABCB1 gene 3435 C>T polymorphism and maternal medication use on the risk of septal defects. Use of maternal medication periconceptionally was significantly associated with an increased risk of septal defects [adjusted odds ratio (OR) 2.133; 95 % confidence interval (CI) 1.361-3.444; P = 0.001)]. The genotype distributions of 3435 C>T polymorphism differed significantly between cases and control subjects (P < 0.001). Meanwhile, more patients were carriers of the ABCB1 CC/CT genotypes, which were significantly associated with an increased risk of septal defects (OR 2.414; 95 % CI 1.418-4.110; P = 0.001). Children who carry the CC/CT genotype and have been exposed periconceptionally to medication have an almost fourfold increased risk of having septal defects than nonexposed children with the TT genotype (adjusted OR 3.932; 95 % CI 1.708-9.051), particularly perimembranous ventricular septal defects (VSD) (adjusted OR 4.070; 95 % CI 1.570-10.552). In conclusion, fetal 3435 C>T polymorphism in the ABCB1 gene increases the risk for isolated septal defects in the presence of maternal medication use periconceptionally, particularly for perimembranous VSD.

Unique Approach for Isolating Rat Bone Marrow Neutrophils with Comparable Capacity.

The primary aim of this research was to develop a reliable and efficient approach for isolating neutrophil extracellular traps (NETs) from rat bone marrow. This effort arose due to limitations associated with the traditional method of extracting NETs from peripheral blood, mainly due to the scarcity of available neutrophils for isolation. The study revealed two distinct methodologies for obtaining rat neutrophils from bone marrow: a streamlined one-step procedure that yielded satisfactory purification levels, and a more time-intensive two-step process that exhibited enhanced purification efficiency. Importantly, both techniques yielded a substantial quantity of viable neutrophils, ranging between 50 to 100 million per rat. This efficiency mirrored the results obtained from isolating neutrophils from both human and murine sources. Significantly, neutrophils derived from rat bone marrow exhibited comparable abilities to secrete NETs when compared with neutrophils obtained from peripheral blood. However, the bone marrow-based method consistently produced notably larger quantities of both neutrophils and NETs. This approach demonstrated the potential to obtain significantly greater amounts of these cellular components for further downstream applications. Notably, these isolated NETs and neutrophils hold promise for a range of applications, spanning the realms of inflammation, infection, and autoimmune diseases.

Outcomes of valve-sparing aortic root replacement in patients with bicuspid aortic valve and tricuspid aortic valve: a systematic review and meta-analysis.

BACKGROUND: Valve-sparing aortic root replacement (VSARR) is a safe and effective surgical procedure to treat aortic root aneurysm. This meta-analysis aimed to investigate how this procedure might differ in patients with bicuspid aortic valve (BAV) and tricuspid aortic valve (TAV). DESIGN: Meta-analysis with meta-regression and systematic review. SETTING: Systematic search in the following databases: PubMed, Cochrane Central Register of Controlled Trials, and Embase. INTERVENTIONS: All observational studies of VSARR in patients with BAV or TAV were included in our study. Studies were included without any restrictions on language or publication date. A trial sequential analysis and a post-hoc meta-regression was performed on the main outcomes. RESULT: Eleven articles met the inclusion criteria. A total of 1138 patients in BAV group, and 2125 patients in TAV group. No significant differences in gender and age were observed between BAV and TAV patients. BAV and TAV patients showed no differences in in-hospital mortality rate [0.00% vs. 1.93%; RR (95% CI) 0.33 (0.09, 1.26), I2 = 0%, P = 0.11] and the rate of in-hospital reoperation [5.64% vs. 5.99%; RR (95% CI) 1.01(0.59, 1.73), I2 = 33%, P = 0.98]. The overall long-term mortality rate of BAV patients was better than that of TAV patients [1.63% vs. 8.15%; RR (95% CI) 0.34 (0.13, 0.86), I2 = 0%, P = 0.02]. During the follow-up observation period, patients in TAV group showed small but no statistic advantage in 3-year, 5-year, and over 10-year incidences of reintervention. Regarding the secondary endpoints, the two groups showed similar aortic cross-clamping time and total cardiopulmonary bypass time. CONCLUSION: The VSARR techniques yielded similar clinical outcomes in both BAV and TAV patients. Although patients with BAV might have a higher incidence of reinterventions after initial VSARR, it is still a safe and effective approach to treat aortic root dilation with or without aortic valve insufficiency. TAV patients showed small but no statistic advantage in long-term (over 10 years) reintervention rate, which means, patients with BAV may face a higher risk of reintervention in the clinic.

Bio-Bentall and hybrid arch frozen elephant trunk repair for acute type A aortic dissection with malperfusion.

The extent of repair in patients with acute type A aortic dissection is often determined by factors such as entry tear location, aortic anatomy, malperfusion and team expertise. The hybrid arch frozen elephant trunk, which has become an established technique to extend the distal acute type A aortic dissection repair, is particularly useful in malperfusion; however, it remains technically challenging and is associated with increased duration of circulatory arrest and risks of spinal cord ischaemia. Proximal dissection flap extension often determines repairability versus replacement of the aortic root. We present a case report highlighting the proximal and distal extent of repair in a patient with a known ascending aortic aneurysm presenting with an acute type A aortic dissection, with malperfusion, undergoing a successful bio-Bentall procedure and hybrid arch frozen elephant trunk repair.

A Metabolomics-Based Study on NMDAR-Mediated Mitochondrial Damage through Calcium Overload and ROS Accumulation in Myocardial Infarction.

BACKGROUND: Coronary artery disease is a leading public health problem. However, the mechanisms underlying mitochondrial damage remain unclear. The present study verified and explored the novel mechanisms underlying ischemic injury based on a metabolomic analysis. METHODS: Mouse models of acute myocardial infarction were established, and serum samples were collected for targeted liquid chromatography with tandem mass spectrometry analysis. Based on metabolomic analyses, the N-methyl-d-aspartic acid receptor (NMDAR)-related calcium transporting signaling pathway was selected. Primary cardiomyocyte cultures were used, and N-methyl-d-aspartic acid (NMDA) was used as an agonist to confirm the role of NMDAR in ischemic injury. In addition, Bax, Bcl-2, mitochondrial calcium, potential, and mitochondrial reactive oxygen species accumulation were used to explore the role of NMDAR in mitochondrial damage-induced apoptosis. RESULTS: Glutamate-related metabolism was significantly altered following in acute myocardial infarction. NMDA induces apoptosis under hypoxic conditions NMDAR was translocated to the mitochondrial-related membrane after activation, and its mitochondrial expression was significantly increased (p < 0.05). Mitochondrial damage-induced apoptosis was significantly inhibited by a selective NDMAR antagonist (p < 0.05), while Bax expression was remarkably decreased and Bcl-2 expression was increased (p < 0.05). To further explore the mechanism of NMDAR, mitochondrial calcium, membrane potential, and reactive oxygen species were detected. With NMDAR inhibition under hypoxic conditions, mitochondrial morphology and function were preserved (p < 0.05). CONCLUSIONS: Our metabolomic study identified NMDAR as a promising target. In conclusion, our study provides solid data for further studies of the role of NMDAR in cardiovascular diseases and a promising target to interfere with apoptosis in acute myocardial infarction.

The effect of postoperative anticoagulation on acute aortic dissection: a systematic review and meta-analysis.

Background and aim: The evolution of the false lumen after the repair of acute aortic dissection has been linked to numerous adverse clinical outcomes, including increased late mortality and a higher risk of reoperation. Despite the widespread use of chronic anticoagulation in patients who have undergone repair for acute aortic dissection, the effects of this therapy on false lumen evolution and its subsequent consequences are yet to be fully understood. This meta-analysis aimed to investigate the impact of postoperative anticoagulation on patients with acute aortic dissection. Methods: In PubMed, Cochrane Libraries, Embase, and Web of Science, we performed a systematic review of nonrandomized studies, comparing outcomes with postoperative anticoagulation vs. non-anticoagulation on aortic dissection. We investigated the status of false lumen (FL), aorta-related death, aortic reintervention, and perioperative stroke in aortic dissection patients with anticoagulation and non-anticoagulation. Results: After screening 527 articles, seven non-randomized studies were selected, including a total of 2,122 patients with aortic dissection. Out of these patients, 496 received postoperative anticoagulation while 1,626 served as controls. Meta-analyses of 7 studies revealed significantly higher FL patency in Stanford type A aortic dissection (TAAD) postoperative anticoagulation with an OR of 1.82 (95% CI: 1.22 to 2.71; Z = 2.95; I²=0%; P = 0.93). Moreover, there was no statistically significant difference between the two groups in aorta-related death, aortic reintervention, and perioperative stroke with an OR of 1.31 (95% CI: 0.56 to 3.04; Z = 0.62; I² = 0%; P = 0.40), 0.98 (95% CI: 0.66 to 1.47; Z = 0.09; I² = 23%; P = 0.26), 1.73 (95% CI: 0.48 to 6.31; Z = 0.83; I² = 8%; P = 0.35), respectively. Conclusions: Postoperative anticoagulation was associated with higher FL patency in Stanford type A aortic dissection patients. However, there was no significant difference between the anticoagulation and non-anticoagulation groups in terms of aorta-related death, aortic reintervention, and perioperative stroke.

Adherence, belief, and knowledge about oral anticoagulants in patients with bioprosthetic heart valve replacement: a cross-sectional study.

Aims: To investigate adherence to oral anticoagulants among patients after mechanical heart valve (BHV) replacement and further examine the mediating role of medication belief in the relationship between knowledge and medication adherence. Background: The number of patients who undergo BHV replacement has increased in recent years. Short-term anticoagulant therapy is recommended for patients after BHV replacement. However, little is known about adherence to oral anticoagulant therapy and the underlying mechanisms among patients with BHV replacement. Methods: A cross-sectional study was conducted between September 2022 and November 2022. A convenience sample of 323 patients who underwent BHV replacement was recruited from a tertiary public hospital in Southwest China. Data were collected by using the 8-item Morisky Medication Adherence Scale, Beliefs about Medicines Questionnaire-specific, and the Knowledge of Anticoagulation Questionnaire. The mediation model was tested by Hayes's PROCESS macro. The STROBE checklist was used. Results: Approximately 17.3% of participants had low adherence, 47.1% had medium adherence, and only 35.6% reported high adherence to oral anticoagulants. Knowledge and necessity beliefs were positively related to medication adherence, while concern beliefs were negatively correlated with medication adherence. Medication belief mediated the relationship between knowledge and adherence to oral anticoagulants. Conclusion: Patients with BHV replacement demonstrated relatively low adherence to oral anticoagulant therapy. Efforts to enhance medication adherence should consider improving patients' knowledge and medication beliefs.