Two surgical strategies (early carotid reperfusion vs. Central aortic repair-first) of acute type a aortic dissection complicated with cerebral malperfusion syndrome: a meta-analysis and systematic review.

OBJECTIVE: Cerebral malperfusion (CM) is a common comorbidity in acute type A aortic dissection (ATAAD), which is associated with high mortality and poor neurological prognosis. This meta-analysis investigated the surgical strategy of ATAAD patients with CM, aiming to compare the difference in therapeutic effectiveness between the central repair-first and the early reperfusion-first according to clinical outcomes. METHODS: The meta-analysis and systematic review was conducted based on studies sourced from the PubMed, Embase, and Cochrane literature database, in which cases of ATAAD with CM underwent surgical repair were included. Data for baseline characteristics, mortality, survival were extracted, and risk ratio (RR) values and the pooled mortality were calculated. RESULTS: A total of 17 retrospective studies were analyzed, including 1010 cases of ATAAD with CM underwent surgical repair. The pooled early mortality in early reperfusion group was lower (8.1%; CI, 0.02 to 0.168) than that in the central repair group (16.2%; CI, 0.115 to 0.216). The pooled long-term mortality was 7.9% in the early reperfusion cohort and 17.4% the central repair-first cohort, without a statistically significant heterogeneity (I [2] = 51.271%; p = 0.056). The mean time of symptom-onset-to-the-operation-room in all the reports was 8.87 ± 12.3 h. CONCLUSION: This meta-analysis suggested that early reperfusion-first may achieved better outcomes compared to central repair-first in ATAAD patients complicated with CM to some extent. Early operation and early restoration of cerebral perfusion may reduce the occurrence of some neurological complications. TRIAL REGISTRATION: The meta-analysis was registered in the International Prospective Register of Systematic Reviews database (No. CRD CRD42023475629) on Nov. 8th, 2023.

Valve replacement or repair in native mitral valve infective endocarditis-Which is better? A meta-analysis and systematic review.

BACKGROUND: Native mitral valve infective endocarditis (IE) plagues patients and surgeons alike because of its high mortality and recurrence rates as well as poor prognosis. Mitral valve repair (MVP) and mitral valve replacement (MVR) are two main surgical methods. However, the question of which benefits patients more remains controversial. Thus, we conducted a meta-analysis to systematically review the two approaches, focusing on the early survival rate and long-term outcomes. METHODS: A meta-analysis and systematic review were conducted using studies sourced from the PubMed, Embase, and Cochrane literature databases to compare MVP and MVR, with data extracted for baseline characteristics, mortality, survival, recurrent endocarditis, and valve reoperation. Risk ratio (RR) or hazard ratio (HR) values were calculated, and publication bias was tested. RESULTS: A total of 17 relevant publications with a total population of 3759 patients, with 1180 patients having undergone MVP and 2579 patients having undergone MVR, respectively, were analyzed. Patients who underwent MVP may benefit from a lower risk of early mortality (RR, 0.51; 95% confidence interval [CI], 0.39-0.66; p < .00001), a higher long-term survival rate (HR, 0.69; 95% CI, 0.58-0.81; p < .001; I2 = 0%), and a lower risk of recurrence (RR, 0.66; 95% CI, 0.40-1.09; p = .10; I2 = 0%). However, a similar risk of reoperation was observed for both groups (RR, 1.02; 95% CI, 0.36-2.91; p = .96; I2 = 43%). CONCLUSION: This meta-analysis suggests that MVP may lead to better outcomes compared to MVR. Among patients with mitral valve IE, MVP can reduce in-hospital mortality, improve long-term survival, and has a lower risk of recurrent endocarditis. As a result, MVP may be suitable as a primary treatment choice and should be considered whenever possible in most IE patients.

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.

A Giant Ruptured Noncoronary Sinus of Valsalva Aneurysm: A Case Report.

The occurrence of a giant ruptured aneurysm originating from the noncoronary sinus of Valsalva in the right atrium is extremely rare. Herein, a case is presented of a giant ruptured noncoronary sinus of Valsalva aneurysm (SVA) that was protruding into the right atrium, which was almost completely occupied by an aneurysm. A 61-year-old female was referred to the hospital for exertional palpitation and dyspnea. While a surgical repair was performed by resection of the aneurysm and a sinus remodeling with a patch of fresh bovine pericardium, a very rare case was observed. It was a giant ruptured noncoronary sinus of aneurysm that completely occupied the right atrium, which was difficult to distinguish from the coronary aneurysm. It is also believed that various imaging examinations, such as cardiac computed tomography angiogram (CCTA) and transthoracic echocardiogram (TTE), were useful for the diagnosis.

Prosthetic valve detachment complicated with intervalvular fibrous body destruction in Behcet's disease: a case report.

BACKGROUND: Prosthetic valve detachment is not rare after aortic valve replacement in Behcet's disease. However, destruction of the intervalvular fibrous body (IFB) due to Behcet's disease was rarely reported. CASE PRESENTATION: We report a case of 30 year-old woman, with valve detachment and IFB separation. The patient received aortic valve replacement three months ago. Her medical history included recurrent oral ulcers and cutaneous lesions. Finally, reoperation was performed and peri-operative steroid therapy was carried out. CONCLUSIONS: The case presented a rare complication of valve detachment in Behcet's disease.

Developmental endothelial locus 1: the present and future of an endogenous factor in vessels.

Developmental Endothelial Locus-1 (DEL-1), also known as EGF-like repeat and discoidin I-like domain-3 (EDIL3), is increasingly recognized for its multifaceted roles in immunoregulation and vascular biology. DEL-1 is a protein that is mainly produced by endothelial cells. It interacts with various integrins to regulate the behavior of immune cells, such as preventing unnecessary recruitment and inflammation. DEL-1 also helps in resolving inflammation by promoting efferocytosis, which is the process of clearing apoptotic cells. Its potential as a therapeutic target in immune-mediated blood disorders, cardiovascular diseases, and cancer metastasis has been spotlighted due to its wide-ranging implications in vascular integrity and pathology. However, there are still unanswered questions about DEL-1's precise functions and mechanisms. This review provides a comprehensive examination of DEL-1's activity across different vascular contexts and explores its potential clinical applications. It underscores the need for further research to resolve existing controversies and establish the therapeutic viability of DEL-1 modulation.

A modified adventitial inversion with graft insertion technique in acute Type A aortic dissection.

Acute type A aortic dissection may originate from a primary intimal tear located in the ascending aorta and often extends retrogradely into the aortic root. How to prevent bleeding in the aortic root and eliminate false lumen is very important in aortic dissection. We have developed a modified anastomotic technique that involves inverting adventitial and graft into aorta and reinforcing with a felt strip on the external border of the aortic wall. Since 2020, 45 consecutive patients with type A aortic coarctation have undergone this aortic root reconstruction procedure, to date, none have been reopened for bleeding or remnant dissection.

Uncovering Druggable Targets in Aortic Dissection: An Association Study Integrating Mendelian Randomization, pQTL, and Protein-Protein Interaction Network.

Aortic dissection (AD) is a life-threatening acute aortic syndrome. There are limitations and challenges in the discovery and application of biomarkers and drug targets for AD. Mendelian randomization (MR) analysis is a reliable analytical method to identify effective therapeutic targets. We aimed to identify novel therapeutic targets for AD and investigate their potential side-effects based on MR analysis. Data from protein quantitative trait loci (pQTLs) were used for MR analyses to identify potential therapeutic targets. We probed druggable proteins involved in the pathogenesis of aortic dissection from deCODE. In this study, a two-sample MR analysis was conducted, with druggable proteins as the exposure factor and data on genome-wide association studies (GWAS) of AD as the outcome. After conducting a two-sample MR, summary data-based Mendelian randomization (SMR) analysis and colocalization analysis were performed. A protein-protein interaction (PPI) network was also constructed to delve into the interactions between identified proteins. After MR analysis and the Steiger test, we identified five proteins as potential therapeutic targets for AD. SMR analysis and colocalization analysis also confirmed our findings. Finally, we identified ASPN (OR = 1.36, 95% CI: 1.20, 1.54, p = 4.22 × 10-5) and SPOCK2 (OR = 0.57, 95% CI: 0.41, 0.78, p = 4.52 × 10-4) as the core therapeutic targets. Through PPI network analysis, we identified six druggable targets, enabling the subsequent identification of six promising drugs from DrugBank for treating AD. This discovery of specific proteins as novel therapeutic targets represents a significant advancement in AD treatment. These findings provide more effective treatment options for AD.

Colchicine in atrial fibrillation: are old trees in bloom?

Colchicine is a widely used drug that was originally used to treat gout and rheumatic diseases. In recent years, colchicine has shown high potential in the cardiovascular field. Atrial fibrillation (AF) is a cardiovascular disease with a high incidence. One of the most frequent complications following cardiovascular surgery is postoperative atrial fibrillation (POAF), which affects patient health and disease burden. This article reviews the research status of colchicine in AF and summarizes the relevant progress.

The emerging role of ferroptosis in myocardial fibrosis of atrial fibrillation.

Introduction: The aim of this study was to investigate the relationship between ferroptosis and myocardial fibrosis in atrial fibrillation (AF). Methods: The patient's left atrial appendage tissue was obtained in cardiac surgery. Sirius red staining, Prussian blue and Western blot were used to detect staining to assess histological fibrosis and ferroptosis changes. Results: There is a certain correlation between the degree of tissue fibrosis and ferroptosis in AF (r = 0.7763, p = 0.0004). The key proteins related to the regulation of ferroptosis were significantly abnormal in the AF group. Conclusions: Ferroptosis is involved in myocardial fibrosis of AF and is a potential target for the diagnosis, prevention and treatment of AF.

Interaction between neutrophil extracellular traps and cardiomyocytes contributes to atrial fibrillation progression.

Atrial fibrillation (AF) is a frequent arrhythmia associated with cardiovascular morbidity and mortality. Neutrophil extracellular traps (NETs) are DNA fragments with cytoplasm proteins released from neutrophils, which are involved in various cardiovascular diseases. To elucidate the role of NETs in AF, we investigated the effect of NETs on AF progression and the secretion of NETs in AF. Results showed that: NETs induced the autophagic apoptosis of cardiomyocytes, and NETs also led to mitochondrial injury by promoting mitochondrial depolarization and ROS production. Ongoing tachy-pacing led to the structural loss of cardiomyocytes and provided potent stimuli to induce NETs secretion from neutrophils. In the meanwhile, increased Ang II in AF facilitated NETs formation through the upregulation of AKT phosphorylation, while it could not directly initiate NETosis as the autophagy was not induced. In vivo, DNase I was administrated to abrogate NETs formation, and AF-related fibrosis was ameliorated as expected. Correspondingly, the duration of the induced AF was reduced. Our study addresses the formation mechanism of NETs in AF and demonstrates the lethal effects of NETs on cardiomyocytes through the induction of mitochondrial injury and autophagic cell death, which comprehensively describes the positive feedback comprised of NETs and stimuli secreted by cardiomyocytes that sustains the progression of AF and AF related fibrosis.

Effects of COVID-19 on Arrhythmia.

The World Health Organization announced that COVID-19, with SARS-CoV-2 as its pathogen, had become a pandemic on 11 March 2020. Today, the global epidemic situation is still serious. With the development of research, cardiovascular injury in patients with COVID-19, such as arrhythmia, myocardial injury, and heart failure, is the second major symptom in addition to respiratory symptoms, and cardiovascular injury is related to the prognosis and mortality of patients. The incidence of arrhythmia in COVID-19 patients ranges from 10% to 20%. The potential mechanisms include viral infection-induced angiotensin-converting enzyme 2 expression change, myocarditis, cytokine storm, cardiac injury, electrophysiological effects, hypoxemia, myocardial strain, electrolyte abnormalities, intravascular volume imbalance, drug toxicities and interactions, and stress response caused by virus infection. COVID-19 complicated with arrhythmia needs to be accounted for and integrated in management. This article reviews the incidence, potential mechanisms, and related management measures of arrhythmia in COVID-19 patients.

Colchicine: Emerging therapeutic effects on atrial fibrillation by alleviating myocardial fibrosis in a rat model.

Although many research have found that colchicine has general therapeutic effect in cardiovascular disease, the therapeutic mechanism in atrial fibrillation has not been clearly studied. To explore whether colchicine plays a role in the treatment of AF by reducing myocardial fibrosis, we performed a series of studies. Rat models of AF were induced by Ach-CaCl2 to assess the therapeutic effect of colchicine at doses of 0.8 mg/kg on the duration of AF rhythm, degree of myocardial fibrosis, and secretion of inflammatory factors in the serum. RNA-Seq was also performed to elucidate the possible mechanisms by which colchicine might reduce the alleviation of myocardial fibrosis associated with AF. These studies showed that colchicine reduced the duration of AF and the degree of fibrosis in the left atrium and that it significantly reduced the secretion of TGFß1, activin A, collagen I, and collagen III. These results suggest that colchicine may reduce myocardial fibrosis by (1) inhibiting the TGFß1/ALK5 and activin A/ALK4 fibrosis pathways; (2) inhibiting the activation, phenotypic transformation, and apoptosis resistance of myocardial fibroblasts; and (3) reducing the synthesis of inflammatory factors and collagen.

Curcumin, novel application in reversing myocardial fibrosis in the treatment for atrial fibrillation from the perspective of transcriptomics in rat model.

In order to explore the possible mechanism of curcumin in the treatment of AF, we focused on the myocardial fibrosis in the pathogenesis of atrial fibrillation to explore whether curcumin could play a role in the treatment of AF by reducing myocardial fibrosis.Rats were given daily gavage of saline (control and AF groups) or curcumin (4 mL/kg, concentration: 50 mg/mL, curcumin groups) during days 4-28. The rat model of AF was induced by Ach - CaCl2, and evaluate the therapeutic effect of curcumin on the duration of AF rhythm, the degree of myocardial fibrosis and the secretion of inflammatory factors in serum. RNA-seq to explore the possible mechanism of curcumin alleviating myocardial fibrosis of AF. curcumin significantly inhibits the duration of AF and reduces the degree of left atrial fibrosis. ELISA results showed curcumin could significantly reduce the secretion of IL-17A, IL-1ß, IL -6 and TGF-ß1. Bioinformatics analyses revealed that the IL-17 signaling pathway are involved in the therapeutic mechanism of curcumin. Furthermore, The genes encoding Col1a1, Fasn, Pck1, Bmp10, IL33 and Figf were pivotal and possible key genes for the therapeutic mechanisms of curcumin.Curcumin can reduce the degree of left atrial fibrosis of AF and the secretion of inflammatory factors. The therapeutic effect of curcumin on AF was attributed to its effect on the IL-17 signaling pathway. Besides, COL1A1, FASN, PCK1, BMP10, IL33 and FIGF were the pivotal genes associated with mechanisms of action of curcumin on AF.

Long-term single-lead electrocardiogram monitoring to detect new-onset postoperative atrial fibrillation in patients after cardiac surgery.

Background: Postoperative atrial fibrillation (POAF) is often associated with serious complications. In this study, we collected long-term single-lead electrocardiograms (ECGs) of patients with preoperative sinus rhythm to build statistical models and machine learning models to predict POAF. Methods: All patients with preoperative sinus rhythm who underwent cardiac surgery were enrolled and we collected long-term ECG data 24 h before surgery and 7 days after surgery by single-lead ECG. The patients were divided into a POAF group a no-POAF group. A clinical model and a clinical + ECG model were constructed. The ECG parameters were designed and support vector machine (SVM) was selected to build a machine learning model and evaluate its prediction efficiency. Results: A total of 100 patients were included. The detection rate of POAF in long-term ECG monitoring was 31% and that in conventional monitoring was 19%. We calculated 7 P-wave parameters, Pmax (167 ± 31 ms vs. 184 ± 37 ms, P = 0.018), Pstd (15 ± 7 vs. 19 ± 11, P = 0.031), and PWd (62 ± 28 ms vs. 80 ± 35 ms, P = 0.008) were significantly different. The AUC of the clinical model (sex, age, LA diameter, GFR, mechanical ventilation time) was 0.86. Clinical + ECG model (sex, age, LA diameter, GFR, mechanical ventilation time, Pmax, Pstd, PWd), AUC was 0.89. In the machine learning model, the accuracy (Ac) of the train set and test set was above 80 and 60%, respectively. Conclusion: Long-term ECG monitoring could significantly improve the detection rate of POAF. The clinical + ECG model and the machine learning model based on P-wave parameters can predict POAF.

Case Report: Hematoma Formation After Spontaneous Coronary Artery Rupture.

We report a case of hematoma formation in the right coronary artery after spontaneous rupture. A 48-year-old female patient was admitted with a suspected right cardiac mass. Despite diagnostic work-up, the dignity of the mass could not be determined. Due to acute clinical symptoms, explorative surgery was decided and performed. Hereby, the mass was partially incised, and thrombus-like tissue was detected without active bleeding. We described the challenges during the diagnostic process, and the diagnosis was finally made according to a multimodality approach. For further assessment, we reviewed related literature and highlighted the importance of coronary angiography in the preoperative evaluation of such patients. The therapy may vary according to the location and size of such lesions.