Clinical outcomes of patients with hepatic insufficiency undergoing transcatheter aortic valve implantation: a systematic review and meta-analysis.

BACKGROUND: Transcatheter aortic valve implantation (TAVI) is currently a common treatment in high-risk aortic stenosis patients, but the impact of hepatic insufficiency on prognosis after TAVI is debatable and whether TAVI is superior to surgical aortic valve replacement (SAVR) in patients with hepatic insufficiency is uncertain. OBJECTIVE: To investigate the effect of abnormal liver function on the outcome and safety after TAVI and whether TAVI is superior to SAVR in patients with hepatic insufficiency. METHODS: PubMed, Embase, the Cochrane Library and Web of Science were systematically searched from inception up to 26 November 2021. Studies were eligible if mortality and complications after TAVI in patients with and without hepatic insufficiency, or mortality and complications for TAVI versus SAVR in patients with hepatic insufficiency were reported. The Newcastle-Ottawa scale (NOS) was used to evaluate the quality of each study. This meta-analysis was registered with PROSPERO (CRD42021253423) and was carried out by using RevMan 5.3 and Stata 14.0. RESULTS: This meta-analysis of 21 studies assessed a total of 222,694 patients. Hepatic insufficiency was associated with higher short-term (in-hospital or 30-day) mortality [OR = 1.62, 95% CI (1.18 to 2.21), P = 0.003] and 1-2 years mortality [HR = 1.64, 95% CI (1.42 to 1.89), P < 0.00001] after TAVI. Between TAVI and SAVR in patients with hepatic insufficiency, there was a statistically significant difference in in-hospital mortality [OR = 0.46, 95% CI (0.27 to 0.81), P = 0.007], the occurrence rate of blood transfusions [OR = 0.29, 95% CI (0.22 to 0.38), P < 0.00001] and the occurrence rate of acute kidney injury [OR = 0.55, 95% CI (0.33 to 0.91), P = 0.02]. CONCLUSIONS: TAVI patients with hepatic insufficiency may have negative impact both on short-term (in-hospital or 30-day) and 1-2-years mortality. For patients with hepatic insufficiency, TAVI could be a better option than SAVR.

Predictors for the risk of permanent pacemaker implantation after transcatheter aortic valve replacement: A systematic review and meta-analysis.

BACKGROUND: Transcatheter aortic valve replacement (TAVR) is a less invasive treatment than surgery for severe aortic stenosis. However, its use is restricted by the fact that many patients eventually require permanent pacemaker implantation (PPMI). This meta-analysis was performed to identify predictors of post-TAVR PPMI. METHODS: The PubMed, Embase, Web of Science, and Cochrane Library databases were systematically searched. Relevant studies that met the inclusion criteria were included in the pooling analysis after quality assessment. RESULTS: After pooling 67 studies on post-TAVR PPMI risk in 97,294 patients, balloon-expandable valve use was negatively correlated with PPMI risk compared with self-expandable valve (SEV) use (odds ratio [OR]: 0.44, 95% confidence interval [CI]: 0.37-0.53). Meta-regression analysis revealed that history of coronary artery bypass grafting and higher Society of Thoracic Surgeons (STS) risk score increased the risk of PPMI with SEV utilization. Patients with pre-existing cardiac conduction abnormalities in 28 pooled studies also had a higher risk of PPMI (OR: 2.33, 95% CI: 1.90-2.86). Right bundle branch block (OR: 5.2, 95% CI: 4.37-6.18) and first-degree atrioventricular block (OR: 1.97, 95% CI: 1.38-2.79) also increased PPMI risk. Although the trans-femoral approach was positively correlated with PPMI risk, the trans-apical pathway showed no statistical difference to the trans-femoral pathway. The approach did not increase PPMI risk in patients with STS scores >8. Patient-prosthesis mismatch did not influence post-TAVR PPMI risk (OR: 0.88, 95% CI: 0.67-1.16). We also analyzed implantation depth and found no difference between patients with PPMI after TAVR and those without. CONCLUSIONS: SEV selection, pre-existing cardiac conduction abnormality, and trans-femoral pathway selection are positively correlated with PPMI after TAVR. Pre-existing left bundle branch block, patient-prosthesis mismatch, and implantation depth did not affect the risk of PPMI after TAVR.

Tricuspid Valve Replacement: Mechanical or Biological Prostheses? A Systematic Review and Meta-Analysis.

BACKGROUND: Tricuspid valve replacement (TVR) is seldom performed in cardiac valve surgery, and there currently are no clinical guidelines as to which type of prostheses is better in tricuspid valve position. This meta-analysis was performed to compare the results of mechanical and biological prostheses for TVR. METHODS: We searched the Pubmed, Cochrane, and Embase clinical trial databases to collect all related studies published from January 1, 2000 to July 31, 2020. A random-effects model was used to evaluate the odds ratios (OR) and its 95% confidence intervals (CI) of time-to-event related effects of the surgical procedures; every study's quality was evaluated by the Newcastle-Ottawa Scale (NOS). RESULTS: A total of 13 retrospective studies, including 1453 patients were analyzed. There were no statistically differences between mechanical and biological prostheses with respect to prosthetic valve failure [OR = 0.84, 95% CI(0.54, 1.28), P = .41], bleeding [OR = 0.84, 95% CI(0.54,1.28), P = .41], reoperation [OR = 1.02, 95% CI(0.58,1.78), P = .95], early mortality [OR = 1.35, 95% CI(0.82,2.25), P = .24] and long-time survival [OR = 1.09, 95% CI(0.70, 1.69), P = .70], but a significant difference can be seen in mechanical prostheses with a higher risk of thrombosis [OR = 0.17, 95% CI(0.05, 0.60), P = .006, I2 = 0%]. CONCLUSIONS: In tricuspid valve position, mechanical valve prostheses have a higher risk of thrombosis than biological prostheses, but no statistical differences between mechanical and biological prostheses with respect to prosthetic valve failure, bleeding, reoperation, early mortality, and long-term survival. The valve disease and patient's age and risk factors are the most important considerations in the decision-making process. The more specific conclusion needs to be further proved by large-sample, multi-center, randomized, double-blind and control trials.

Typical Retrograde Type A Dissection After Previous Type B Dissection.

BACKGROUND: Stanford type B aortic dissection (TBAD) retrograde tears to Stanford type A AD (RTAAD) have been reported only rarely, but are often fatal. Early diagnosis and timely surgery are essential. We present a typical case of RTAAD after the tip of the stent directly damaged the ascending aorta wall. CASE: A 71-year-old woman was admitted to our department for chest pain and back pain for 10 hours. She had undergone coated stent graft implantation surgery a month previously for TBAD. On first impression, we suspected the AD may have progressed or torn retrogradely. RTAAD was confirmed by computed tomography angiography, and we successfully performed open surgery. CONCLUSION: RTAAD should be suspected in patients with chest and back pain after endovascular stent repair. Prompt recognition is essential, and early surgical treatment is strongly recommended.

The Potential Causes of Paraplegia after Coronary Artery Bypass Grafting: A Literature Review.

Paraplegia is an unpredictable neurologic complication after coronary artery bypass grafting (CABG) surgery. It is rare but fatal, and the mechanism still is unclear. We aimed to make a summary of the possible causes of paraplegia after CABG. Pubmed database was searched from January 1, 1978 to December 31, 2019, and 14 studies were finally included. Paraplegia after CABG is a multifactorial consequence, but spinal cord ischemia is the key pathological factor to postoperative paraplegia.

Letter to the Editor: Admission Values of Plasma Biomarkers Predict the Short-Term Outcomes in Acute Aortic Dissection.

Not applicable.

Peripheral Artery Disease on The Prognosis Value of Patients with Stable Coronary Artery Disease Undergoing Percutaneous Coronary Intervention: A Retrospective, Single-Center Cohort Study.

OBJECTIVE: The purpose of this investigation aimed to clarify the impact of peripheral artery disease (PAD) on the prognosis value of patients with stable coronary artery disease (CAD) who underwent percutaneous coronary intervention (PCI). METHODS: The SPSS 16 software was used for secondary analysis of DRYAD database data. A total of 204 patients were enrolled from Shinonoi General Hospital for newly diagnosed stable CAD and received PCI performance between October 2014 and October 2017. Patients with old myocardial infarction (MI) were excluded. We divided patients into two groups with PAD and without PAD. The primary endpoints were major adverse cardiac events (MACE, defined as all-cause death, non-fatal MI, and non-fatal stroke) and cardiovascular events (defined as cardiovascular death, non-fatal MI, and non-fatal stroke). The secondary outcomes were the individual components of the composite primary outcomes. The median follow-up time was 783 days. RESULTS: No statistical difference was found between PAD and non-PAD patients of lesional characteristics. Spearman's rank correlations indicate diabetes mellitus (DM) (P = 0.019) and HbA1c (P = 0.009) are positively correlated with PAD. In Kaplan-Meier analysis, patients with PAD predicted poor prognosis in MACE (P < 0.05) and cardiovascular events (P < 0.05). In Multivariable Cox proportional hazards analysis, patients with PAD independently predicted MACE and cardiovascular events. CONCLUSIONS: PAD is a significant mediator for the prognosis of patients with stable CAD who underwent PCI treatment.

[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.

Cation-Induced Self-Assembly of α-MnO2 Nanowires into High-Purity Self-Standing Three-Dimensional Network Aerogels for Catalytic Decomposition of Carcinogenic Formaldehyde at Ambient Temperature.

Formaldehyde (HCHO), a ubiquitous gaseous pollutant in indoor environments, threatens human health under long-term exposure, necessitating its effective elimination. Due to its advantages in enhancing mass transfer and effectively exposing active sites, aerogels with a three-dimensional (3D) interconnected network structure are expected to achieve efficient and stable decomposition of HCHO at ambient temperature. However, how to realize the self-assembly of transition metal oxides to construct high-purity 3D network aerogels is still a huge challenge. Herein, the cation-induced self-assembly strategy was developed to construct high-purity self-standing 3D network manganese dioxide aerogels. The interaction between cations and the surface groups of nanowires is crucial for successful self-assembly, which leads to the cross-winding of nanowires with each other, forming a 3D-structured network. The K+-induced 3D-MnO2 exhibited excellent catalytic performance for HCHO, which could continuously and steadily decompose HCHO into CO2 and H2O at ambient temperature. Thanks to the 3D interconnected network structure, on the one hand, it provides a large specific surface area and porosity, reducing mass transfer resistance and promoting the adsorption of HCHO and O2 molecules. On the other hand, it is more important to fully expose the active sites, which can generate more surface active oxygen species and achieve effective recycling and regeneration. Importantly, 3D-MnO2 has a strong ability to capture and activate water molecules in the atmosphere, which could be further involved in the replenishment of the consumed hydroxyl groups. This study proposes a strategy for self-assembly of transition metal oxides through cation-induction, which provides a new catalyst design approach for the room temperature decomposition of VOCs.

Mechanism of heart failure after myocardial infarction.

Despite the widespread use of early revascularization and drugs to regulate the neuroendocrine system, the impact of such measures on alleviating the development of heart failure (HF) after myocardial infarction (MI) remains limited. Therefore, it is important to discuss the development of new therapeutic strategies to prevent or reverse HF after MI. This requires a better understanding of the potential mechanisms involved. HF after MI is the result of complex pathophysiological processes, with adverse ventricular remodeling playing a major role. Adverse ventricular remodeling refers to the heart's adaptation in terms of changes in ventricular size, shape, and function under the influence of various regulatory factors, including the mechanical, neurohormonal, and cardiac inflammatory immune environments; ischemia/reperfusion injury; energy metabolism; and genetic correlation factors. Additionally, unique right ventricular dysfunction can occur secondary to ischemic shock in the surviving myocardium. HF after MI may also be influenced by other factors. This review summarizes the main pathophysiological mechanisms of HF after MI and highlights sex-related differences in the prognosis of patients with acute MI. These findings provide new insights for guiding the development of targeted treatments to delay the progression of HF after MI and offering incremental benefits to existing therapies.

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.

N6-methyladenosine (m6A) RNA modification in the pathophysiology of heart failure: a narrative review.

Background and Objective: Heart failure is the end-stage of various cardiovascular diseases. Recent progress in molecular biology has facilitated the understanding of the mechanisms of heart failure development at the molecular level. N6-adenosine methylation (m6A) is a post-transcriptional modification of RNA. Recent research work reported that m6A regulates gene expression and subsequently affects the activation of cell signaling pathways related to heart failure. Moreover, m6A regulators like methyltransferase-like 3 (METTL3) were reported to participate in myocardium hypertrophy. However, the current research work related to the role of m6A participating in the occurrence of heart failure is rare in some aspects like immune cell infiltration and diabetic heart diseases. Thus, it is reasonable to review the current achievements and provide further study orientation. Methods: We searched related literature using the keywords: m6A AND heart failure in PubMed, Web of Science and Medline. The language was confined to English. The published year of searched literature ranged from 2012 to 2022. The searched results were put into Endnote software for management. Two authors investigated the searching terms and reviewed the full text of selected terms. Key Content and Findings: m6A and its regulators are involved in the metabolism of various types of RNAs. m6A modification can regulate various types of cell signaling pathways related to the heart failure via interaction with m6A regulators. m6A and its regulators broadly participate in the myocardium fibrosis, myocardium hypertrophy, myocardial cell apoptosis, and ischemic reperfusion injury. Specifically, m6A participates in the cell apoptosis via regulation of autophagy flux. However, the current research work does not have enough evidence to prove that m6A regulator played its specific effect on the target transcript via regulating the m6A level. Conclusions: m6A and its regulators participates in the progression of heart failure via modifying the RNA level. Future investigation of m6A should focus on the interaction between the m6A regulators and targeted transcript. Besides, the regulation role of m6A in immune cell infiltration and diabetic heart diseases should also be focused.

Comparison of the Efficacy and Safety Endpoints of Five Therapies for Atrial Fibrillation: A Network Meta-Analysis.

Introduction: Atrial fibrillation (AF) is a prevalent arrhythmia that occurs in 2-4% of adults and poses a threat to human health. Thus, comparison of the efficacy and safety of therapies for AF is warranted. Here, we used network analysis to compare efficacy (arrhythmia recurrence and re-hospitalization) and safety (ischemic cerebral vascular events, all-cause mortality, and cardiovascular mortality) endpoints among five major therapies for AF. Methods: The PubMed, Cochrane, and Embase databases were searched, and relevant literature was retrieved. Only studies that made comparisons among the therapies of interest and involved patients with AF were included. Pairwise comparisons and frequentist method (SUCRA plot) analyses were conducted. Results: In total, 62 studies were included in the pooled analysis. In pairwise comparisons, atrioventricular nodal ablation plus permanent pacemaker (AVN + PPM) was associated with a significantly higher risk of atrial arrhythmia recurrence than surgical ablation [odds ratio (OR): 23.82, 95% confidence interval (CI): 1.97-287.59, fixed-effect model; 3.82, 95% CI: 1.01-559.74, random-effects model]. Furthermore, radiofrequency ablation was associated with a significantly lower risk of cardiovascular mortality than medication in pairwise comparison (OR: 0.49, 95% CI: 0.29-0.83, fixed-effect model; OR: 0.49, 95% CI: 0.27-0.9, random-effects model). Frequentist analysis indicated that AVN + PPM had the best performance in reducing the risk of safety and efficacy endpoints. Conclusion: Non-pharmaceutical therapies showed superior performance to traditional drug therapy in lowering the risk of safety and efficiency endpoint events. AVN + PPM performed best in reducing the risk of safety and efficacy endpoints.

Five-year follow-up report: Box lesion radiofrequency ablation procedure for atrial fibrillation under video-assisted thoracoscope.

We report the initial 5-year follow-up of a novel mini-invasive procedure for epicardial ablation for the treatment of atrial fibrillation. The initial 5-year survival rate is acceptable and comparable with that of hybrid ablation. And this shared procedure has the advantages of shorter operation time and less surgical trauma.

Improvement of Clinical Outcomes of Total Aortic Arch Replacement and Frozen Elephant Trunk Surgery With Aortic Balloon Occlusion.

Background: Total aortic arch replacement (TAR) with frozen elephant trunk (FET) surgery provides improved long-term results, but the surgery itself is associated with higher risks compared with isolated proximal reconstructions. We applied an aortic balloon occlusion (ABO) technique to reduce the circulatory arrest (CA) time and improve other clinical outcomes. Methods: All patients who underwent TAR with FET surgery (130 with ABO technique, 230 with the conventional approach) in Fuwai Hospital from August 2017 to February 2019 were reviewed in this retrospective observational cohort study. Intra- and early-postoperative results and clinical characteristics were analyzed. Results: After 1:1 propensity score matching (130 cases in each group), the 30-day mortality of the ABO group and the conventional group were 4.6% and 10.8% (p = 0.063), respectively. Although the reduction in complications was not statistically significant, the complication rate in the ABO group was relatively low, having fewer cases of postoperative renal (23.1 vs. 38.5%, p = 0.007) and hepatic (12.3 vs. 30.0%, p < 0.001) injury, lower postoperative wake-up time (15.2 ± 23.6 h vs. 20.1 ± 26.5 h, respectively, p < 0.001), reduced chest tube output (176.03 ± 143.73 ml vs. 213.29 ± 130.12 ml, respectively, p = 0.003), lower red blood cell transfusion volume (4.98 ± 6.53 u vs. 7.28 ± 10.41 u, respectively, p = 0.008), and no fatal events. Conclusions: The ABO technique is a simple method that can reduce the CA time and improve the recovery stage following TAR with FET surgery. The technique represents a practical strategy to treat patients with high operative risks due to its lower complication rate compared with the conventional approach.

Hypertrophic Cardiomyopathy: From Phenotype and Pathogenesis to Treatment.

Hypertrophic cardiomyopathy (HCM) is a very common inherited cardiovascular disease (CAD) and the incidence is about 1/500 of the common population. It is caused by more than 1,400 mutations in 11 or more genes encoding the proteins of the cardiac sarcomere. HCM presents a heterogeneous clinical profile and complex pathophysiology and HCM is the most important cause of sudden cardiac death (SCD) in young people. HCM also contributes to functional disability from heart failure and stroke (caused by atrial fibrillation). Current treatments for HCM (medication, myectomy, and alcohol septal ablation) are geared toward slowing down the disease progression and symptom relief and implanted cardiac defibrillator (ICD) to prevent SCD. HCM is, however, entering a period of tight translational research that holds promise for the major advances in disease-specific therapy. Main insights into the genetic landscape of HCM have improved our understanding of molecular pathogenesis and pointed the potential targets for the development of therapeutic agents. We reviewed the critical discoveries about the treatments, mechanism of HCM, and their implications for future research.

Behcet's disease involved the root of aorta in the treatment with modified Bentall procedure: a case report.

BACKGROUND: Behcet's disease (BD) is a multisystemic vasculitis of unknown etiology, the incidence of cardiovascular system involvement is rare, about1-5% (Sakane et al., N Engl J Med 341:1284-91, 1999). BD combined with aortic pseudoaneurysm and aortic valve regurgitation is usually need surgical treatment, but there is controversy about which surgical method to choose. CASE PRESENTATION: We report a case of BD combined with severe aortic valve regurgitation and two giant pseudoaneurysms of the aortic sinus. The patient underwent modified Bentall procedure (MBP) and use oral immunosuppressive as well as corticosteroid strictly, after 8 months follow-up, the patient recovered well. CONCLUSION: For patient with aortic valve regurgitation and ascend aortic pseudoaneurysm caused by BD, we recommend modified Bentall procedure when rheumatism in a stable period. Corticosteroids and immunosuppressive drugs should be used before and after surgery.

Transcatheter aortic valve implantation versus surgical aortic valve replacement for treatment of severe aortic stenosis: comparison of results from randomized controlled trials and real-world data.

OBJECTIVE: Results from randomized controlled trials (RCTs) and real-world study (RWS) appear to be discordant. We aimed to investigate whether data derived from RCTs and RWS evaluating long-term all-cause mortality of transcatheter aortic valve implantation (TAVI) versus surgical aortic valve replacement (SAVR) in patients with severe aortic stenosis (AS) were in agreement. METHODS: RCTs or RWS comparing TAVI and SAVR, reporting longterm (≥2-year follow-up) all-cause mortality, were identified. We also carried out subgroup analyses to access the effect in different subgroups. A pre-designated data extraction form including 5 domains and 26 items was used to explore the relationship between RCTs and RWS. Mortality and effect in different subgroups were evaluated using random-effects meta-analyses. RESULTS: Five RCTs (5421 participants, TAVI: 2759, SAVR: 2662) and 33 RWS (20839 participants; TAVI: 6585, SAVR: 14254) were identified. Pooled RCT analysis showed no difference in all-cause mortality between TAVI and SAVR (HR=0.97, 95% CI: 0.88-1.07; P=0.55). In RWS, TAVI was associated with an increased risk of allcause mortality (HR=1.46, 95% CI: 1.26-1.69; P<0.001) compared to SAVR. CONCLUSION: These results highlight the inconsistencies between RCTs and RWS in assessing long-term all-cause mortality in the treatment of AS using TAVI or SAVR, which may be caused by interactions of clinical characteristics or study design. RCTs as well as RWS are both developing and improving; the advantages of one kind of design, measurement and evaluation can and should be thoughtfully referred to the other.