Frontiers in Cardiovascular Medicine最新文献

Background: Several studies have demonstrated an association between tricuspid regurgitation (TR) and organ dysfunction including hepatic and renal insufficiency. Improvement of liver function following transcatheter edge-to-edge repair (T-TEER) has already been linked to reduction of venous congestion due to TR reduction. This study analyzes whether TR-reduction using T-TEER is also associated with improved renal function.

Methods and results: The TRIC-ULM registry includes 92 selected patients undergoing T-TEER between March 2017 and May 2023. Estimated glomerular filtration rate (eGFR) improvement was evident in 53 patients (57%) at 3-months follow-up (FU) and defined by FU eGFR > baseline eGFR. Median age was 80 [interquartile range 75-83] years, pre- and postinterventional TR grades were 4 [3-5] and 1 [1-2], baseline eGFR was 36 [30-53] ml/min and New Yeark Heart Association (NYHA) IV was evident in 15% of patients. Multiple logistic regression analysis revealed TR vena contracta reduction (Odds ratio (OR) 1.35 [95% CI: 1.12-1.64] per mm, p = 0.002) and reduced preinterventional tricuspid annular plane systolic excursion (TAPSE) [OR 0.89 (95% CI: 0.79-0.99) per mm, p = 0.033] to independently predict renal improvement at FU. An eGFR improvement threshold of >9 ml/min was associated with reduced 1-year heart failure hospitalization rates [adjusted hazard ratio 0.22 (95% CI: 0.07-0.62) p = 0.005].

Conclusion: Effective tricuspid edge-to-edge repair is associated with improved renal function and reduced heart failure hospitalization. In patients without renal improvement at 3-months follow-up, residual tricuspid regurgitation should be reevaluated for reintervention.

Introduction: There is no consensus on the optimal concentration of lipoprotein(a) (Lp(a)) for the risk of atherosclerotic cardiovascular diseases (ASCVD) and aortic valve stenosis. In various clinical guidelines and agreed documents, the threshold level of Lp (a) is 30 mg/dl or 50 mg/dl. We estimated the cut-off value of Lp (a) associated with the risk of developing various localizations of atherosclerosis for the Central Asia, including Kazakhstani population.

Methods: This study was conducted at National Research Cardiac Surgery Center, Kazakhstan. 487 patients were included, of which 61.3% were men. The mean age of all participants was 57.3 ± 12.6 years. Bivariate and multivariable logistic regression analysis was used to study the relationship between risk factors and plasma lipoprotein (a) levels. The threshold value of lipoprotein (a) was predicted using the Youden index.

Results: For Kazakhstani population the lipoprotein (a) cut offs for the risk of developing atherosclerotic CVD and aortic valve calcification was 21.1 mg/dl (p < 0.05). There was no relationship with the level of lipoprotein (a) and low-density lipoprotein cholesterol (LDL-C), which suggests that lipoprotein (a) is an independent risk factor for the development of ASCVD.

Discussion: This study offers new insights into the threshold value of lipoprotein (a) in Kazakhstan, highlighting its role as a risk factor for atherosclerotic cardiovascular diseases and aortic valve calcification. The findings suggest that the internationally recommended Lp(a) cutoffs may not be suitable for Central Asian populations, as the threshold in our study is significantly lower at 21.2 mg/dL. These results emphasize the need for further research with larger sample sizes to establish more region-specific cutoffs.

Background: Electrocardiographic markers differentiating between death caused by ventricular arrhythmias and non-arrhythmic death could improve the selection of patients for implantable cardioverter-defibrillator (ICD) implantation. QRS fragmentation (fQRS) is a parameter of interest, but subject to debate. We investigated the association of an automatically quantified probability of fragmentation with the outcome in ICD patients.

Methods: From a single-center retrospective registry, all patients implanted with an ICD between January 1996 and December 2018 were eligible for inclusion. Patients with active pacing were excluded. From the electronical medical record, clinical characteristics at implantation were collected and a 12-lead ECG was exported and analyzed by a previously validated machine-learning algorithm to quantify the probability of fQRS. To compare fQRS(+) and fQRS(-) patients, dichotomization was performed using the Youden index. Patients with a high probability of fragmentation in any region (anterior, inferior or lateral), were labeled fQRS(+). The impact of this fQRS probability on outcomes was investigated using Cox regression.

Results: A total of 1,242 patients with a mean age of 62.6 ± 11.5 years and a reduced left ventricular ejection fraction of 31 ± 12% were included of which 227 (18.3%) were female. The vast majority suffered from ischemic heart disease (64.3%) and were implanted in primary prevention (63.8%). 538 (43.3%) had a high probability of fragmentation in any region. Patients with a high probability of fragmentation had more frequently dilated cardiomyopathy (39.4% vs. 33.0%, p = 0.019), left bundle branch block (40.8% vs. 32.5%, p = 0.006) and a higher use of cardiac resynchronization therapy with defibrillator (CRT-D) devices (33.9% vs. 26.3%, p = 0.004). After adjustment in a multivariable Cox model, there was no significant association between the probability of global or regional fQRS and appropriate ICD therapy, inappropriate shock and short- or long-term mortality.

Conclusion: There was no association between the automatically quantified probability of the presence of fQRS and outcome. This lack of predictive value might be due to the algorithm used, which identifies only the presence but not the severity of fragmentation.

Background: Observational studies have found that vascular endothelial growth factor (VEGF) levels are associated with the risk of cardiovascular disease. However, it remains unclear whether VEGF levels have a causal effect on the risk of atrial fibrillation.

Methods: A two-sample Mendelian randomization (MR) study was conducted to explore the causal relationship between VEGF levels and the risk of atrial fibrillation. Genetic variants associated with VEGF [VEGF-A, VEGF-C, VEGF-D, VEGF receptor-2 (VEGFR-2), VEGFR-3] and atrial fibrillation (atrial fibrillation, atrial fibrillation and flutter) were used as instrumental variables. Data on genetic variants were obtained from published genome-wide association studies (GWAS) or the IEU Open GWAS project. Inverse-variance weighted (IVW) analysis was used as the primary basis for the results, and sensitivity analyses were used to reduce bias. Causal relationships were expressed as odds ratio (OR) with 95% confidence interval (CI), and a P-value of <0.1 corrected for False Discovery Rate (FDR) (P_FDR  < 0.1) was considered to have a significant causal relationship.

Results: Genetically predicted high levels of VEGF-A [OR = 1.025 (95%CI: 1.004-1.047), P_FDR  = 0.060] and VEGF-D [OR = 1.080 (95%CI: 1.039-1.123), P_FDR  = 0.001]] were associated with an increased risk of atrial fibrillation, while no causal relationship was observed between VEGF-C (P_FDR  = 0.419), VEGFR-2 (P_FDR  = 0.784), and VEGFR-3 (P_FDR  = 0.899) and atrial fibrillation risk. Moreover, only genetically predicted high levels of VEGF-D [OR = 1.071 (95%CI: 1.014-1.132), P_FDR  = 0.087] increased the risk of atrial fibrillation and flutter. Sensitivity analysis demonstrated that the relationship between VEGF-D levels and the risk of atrial fibrillation was robust.

Conclusion: This study supports a causal association between high VEGF-D levels and increased risk of atrial fibrillation.

[This corrects the article DOI: 10.3389/fcvm.2024.1447487.].

Background: Since 2000, we have been grafting the right coronary artery system (RCAs) using the proximal portion of the right internal thoracic artery (RITA) as the inflow of the saphenous vein graft (SVG) to increase the number of patients undergoing beating heart complete myocardial revascularization.

Methods: From 2000 to 2022, 928 consecutive patients underwent SVG on the RCAs. In 546 patients (58.8%), the inflow was the RITA (I-graft group), and in 382 patients (41.2%), the inflow was the aorta (Ao-graft group). The inclusion criteria were age ≤75 years, ejection fraction >35%, only one SVG per patient, bilateral internal thoracic arteries as a Y-graft on the left system (three-vessel disease, n = 817, 88.0%) or left internal thoracic artery on the left anterior descending artery and RITA + SVG on the RCAs (two-vessel disease, n = 111, 12.0%). Propensity matching identified 306 patients per group. After a median follow-up of 8 (5-10) years, graft patency was assessed by coronary computed tomographic angiography in 132 patients (64 in the I-graft group and 68 in the Ao-graft group).

Results: Early results were similar in both groups. The I-graft group had higher 10-year survival and freedom from main adverse cardiac events (90.0 ± 2.0 vs. 80.6 ± 3.8, p = 0.0162, and 81.3 ± 2.7 vs. 64.7 ± 5.6, p = 0.0206, respectively). When RITA was the inflow, SVG had a higher estimated 10-year patency rate (82.8% ± 6.5 vs. 58.8% ± 7.4, p = 0.0026) and a smaller inner lumen diameter (2.7 ± 0.4 vs. 3.4 ± 0.6 mm, p < 0.0001).

Conclusion: When the inflow is the RITA, SVG grafted to the RCAs (I-graft) may result in a higher patency rate and better outcome than when the inflow is the ascending aorta (Ao-graft). The continuous supply of nitric oxide by RITA may be the cause of the higher patency rate of the I-graft, which can behave like an arterial conduit.

Introduction: It has been found that programmed cell death protein-1 (PD-1) or its ligand PD-L1 may play an important role in the onset and progression of coronary heart disease (CHD). Thus, we conducted this mendelian randomization analysis (MR) to estimate the causal relationship between PD-1/PD-L1 and 5 specific CHDs (chronic ischemic heart disease, acute myocardial infarction, angina pectoris, coronary atherosclerosis, and unstable angina pectoris), complemented by gene set enrichment analysis (GSEA) for further validation.

Methods: Publicly available summary-level data were attained from the UK Biobank with genetic instruments obtained from the largest available, nonoverlapping genome-wide association studies (GWAS). Our analysis involved various approaches including inverse variance-weighted meta-analysis, alternative techniques like weighted median, MR-Egger, MR-multipotency residuals and outliers detection (PRESSO), along with multiple sensitivity assessments such as MR-Egger intercept test, Cochran's Q test, and leave-one-out sensitivity analysis to evaluate and exclude any anomalies.

Results: Gene expression profile (GSE71226) was obtained from Gene Expression Omnibus (GEO) database for GSEA. IVW analysis showed a causal association between PD-1 and chronic ischemic heart disease (OR, 0.997; 95%CI, 0.995-0.999; P, 0.009), chronic ischemic heart disease and PD-1 (beta, -3.1; 95%CI, -6.017 to -0.183; P, 0.037), chronic ischemic heart disease and PD-L1 (beta, -3.269; 95%CI, -6.197 to -0.341; P, 0.029). No significant causal relationship was found between PD-1/PD-L1 and other 4 CHDs. The accuracy and robustness of these findings were confirmed by sensitivity tests. GSEA found that the KEGG pathway and related core genes of "PD-L1 expression and PD-1 checkpoint pathway in cancer" pathway were downregulated in CHD.

Discussion: This study provided evidence of a bidirectional causal relationship between PD-1 and chronic ischemic heart disease and a protective association between chronic ischemic heart disease and PD-L1.

Sea buckthorn (Hippophae rhamnoides L.) contains a variety of biologically active compounds, including flavonoids, terpenoids, polysaccharides, organic acids, volatile oils, and vitamins. It has been demonstrated to be effective in the treatment of cardiovascular disorders. In this paper, we evaluated the pharmacological effects of sea buckthorn in cardiovascular diseases through preclinical studies, and revealed the mechanism of action of the active components in sea buckthorn in cardiovascular diseases, including anti-inflammatory, lipid oxidation regulation, antioxidant, vascular function modulation, anti-platelet aggregation, autophagy, intestinal microorganism regulation, and cell apoptosis reduction. In clinical trials, sea buckthorn was proven to be effective in managing lipid metabolism, blood pressure, and blood glucose levels in patients. We also extensively reviewed the safety of sea buckthorn medicine and its toxicity to numerous organs. To summarize, sea buckthorn has a beneficial effect on cardiovascular disease and may give a novel strategy for clinical intervention and therapy. This paper summarizes the phytochemistry, pharmacology, clinical applications, safety, and toxicity of sea buckthorn in order to better understand the mechanism of action of the various bioactive components in sea buckthorn, investigate its medicinal potential, and provide more options for the treatment of cardiovascular diseases.

Objectives: Mitral annulus calcification (MAC) has been linked to cardiovascular disease severity, but its relationship with the SYNTAX score (SS) in acute coronary syndrome (ACS) patients remains unclear. This study aimed to investigate the association between MAC and SS in ACS patients to explore the role of MAC in predicting cardiovascular disease severity.

Methods: We conducted a cross-sectional study of 233 ACS patients at Tehran Heart Center, Tehran, Iran, from December 2021 to August 2022. Patients with prior coronary artery disease (CAD) were excluded. Demographic data, risk factors, and medical history were extracted from clinical files. SS was determined using coronary angiography, and MAC was assessed via two-dimensional transthoracic echocardiography.

Results: The study population had a mean age of 58.79 years, with 74.7% male. MAC was present in 24.9% of participants, and 57% of those with MAC had an SS above 23. Univariate analysis revealed a significant association between MAC and higher SSs (odds ratio: 1.84, 95% CI: 1.02-3.39; P = 0.046). However, multivariable analysis showed that only left ventricular ejection fraction (LVEF) was independently associated with SS (odds ratio: 0.94, 95% CI: 0.89-0.99; P = 0.015).

Conclusion: While MAC was initially associated with higher SSs in ACS patients, only LVEF emerged as an independent predictor in the multivariable analysis. Although MAC may not be independently associated with SS, it may serve as a useful echocardiographic indicator of more severe CAD in ACS.

Even with significant advancements in the treatment modalities for patients with heart failure (HF), the rates of morbidity and mortality associated with HF are still high. Various therapeutic interventions, including cardiac resynchronization therapy, Implantable Cardiovascular-Defibrillators, and left ventricular assist devices, are used for HF management. Currently, more research and developments are required to identify different treatment modalities to reduce hospitalization rates and improve the quality of life of patients with HF. In relation to this, various non-valvular catheter-based therapies have been recently developed for managing chronic HF. These devices target the pathophysiological processes involved in HF development including neurohumoral activation, congestion, and left ventricular remodeling. The present review article aimed to discuss the major transcatheter devices used in managing chronic HF. The rationale and current clinical developmental stages of these interventions will also be addressed in this review.