Reviews in cardiovascular medicine最新文献

Background: Clinically useful predictors for risk stratification of long-term survival may assist in selecting patients for endovascular abdominal aortic aneurysm (EVAR) procedures. This study aimed to analyze the prognostic significance of peroperative novel systemic inflammatory markers (SIMs), including the neutrophil-to-lymphocyte ratio (NLR), platelet-to-lymphocyte ratio (PLR), hemoglobin-to-red cell distribution width ratio (HRR), systemic immune-inflammatory index (SIII), and systemic inflammatory response index (SIRI), for long-term mortality in EVAR.

Methods: A retrospective analysis was performed on 147 consecutive patients who underwent their first EVAR procedure at the Department of Vascular Surgery, Beijing Hospital. The patients were divided into the mortality group (n = 37) and the survival group (n = 110). The receiver operating characteristic curves were used to ascertain the threshold value demonstrating the most robust connection with mortality. The Kaplan-Meier survival analysis was performed between each SIM and mortality. The relationship between SIMs and survival was investigated using restricted cubic splines and multivariate Cox regression analysis.

Results: The study included 147 patients, with an average follow-up duration of 34.28 $\pm$ 22.95 months. Deceased patients showed significantly higher NLR (p $<$ 0.001) and reduced HRR (p $<$ 0.001). The Kaplan-Meier estimates of mortality were considerably greater in the higher-NLR group (NLR $>$ 2.77) and lower-HRR group (HRR $<$ 10.64). The hazard ratio (HR) of 0.833 (95% confidence interval (95% CI): 0.71-0.97, p $<$ 0.021) was determined to be statistically significant in predicting death in the multivariable analysis.

Conclusions: Preoperative higher-NLR and lower-HRR have been associated with a lower long-term survival rate in abdominal aortic aneurysm (AAA) patients undergoing elective EVAR. Multivariate Cox regression showed that decreased preoperative HRR is an independent risk factor that increases mortality risk following EVAR. SIMs, such as the NLR and HRR, could be used in future clinical risk prediction methodologies for AAA patients undergoing EVAR. However, additional prospective cohort studies are needed to identify these findings.

Chronic kidney disease (CKD) is affecting more and more individuals over time. The importance of the increased prevalence is enhanced by the close association with the increased risk of poor individual outcomes such as death, fatal and non-fatal cardiovascular (CV) events and progression to end stage kidney disease (ESKD). ESKD requires replacement treatment such as hemodialysis (HD), a particular and complex context that unfortunately has been rarely considered in observational studies in the last few decades. The current perspective of HD as a bridge to kidney transplant requires greater attention from observational and experimental research both in the prevention and treatment of CV events in ESKD patients. We present a narrative review by performing a literature review to extrapolate the most significant articles exploring the CV risk, in particular coronary artery disease (CAD), in ESKD and evaluating possible innovative diagnostic and therapeutic tools in these patients. The risk of CAD increases linearly when the estimated glomerular filtration rate (eGFR) declines and reached the most significant level in ESKD patients. Several diagnostic techniques have been evaluated to predict CAD in ESKD such as laboratory tests (Troponin-T, N-terminal pro b-type natriuretic peptide, alkaline phosphatase), echocardiography and imaging techniques for vascular calcifications evaluation. Similarly, treatment is based on lifestyle changes, medical therapy and invasive techniques such as coronary artery bypass grafting (CABG) and percutaneous coronary intervention (PCI). Unfortunately in the literature there are no clear indications of the usefulness and validity of biomarkers and possible treatments in ESKD patients. Considering the ESKD weight in terms of prevalence and costs it is necessary to implement clinical research in order to develop prognostic reliable biomarkers for CV and CAD risk prediction, in patients with ESKD. It should be highlighted that HD is a peculiar setting that offers the opportunity to implement research and facilitates patient monitoring by favoring the design of clinical trials.

Background: Changes in tricuspid valve (TV) function following transvenous lead extraction (TLE) and their impact on long-term survival have not yet been investigated.

Methods: From 3633 patients undergoing lead extraction between 2006 and 2021, TV function before and after TLE was evaluated in 2693 patients.

Results: After TLE, the TV function remained unchanged in 82.36% of patients, worsened in 9.54%, and improved in 8.10%. Abandoned leads (odds ratio, OR = 1.712; p = 0.044), fibrotic adhesions between leads and TV apparatus (OR = 3.596; p $<$ 0.001), or right ventricular wall (OR = 2.478; p $<$ 0.001) were predisposed to TV worsening. Non-infectious indications for TLE (OR = 1.925; p $<$ 0.001), the severity of tricuspid valve regurgitation (TVR) before TLE (OR = 3.125; p $<$ 0.001), and lead encapsulation (OR = 2.159; p $<$ 0.001) were predictors of improvement in TV function. Although either worsening or improving TV function had no impact on long-term survival in all patients, decreased TVR severity in the subgroup of patients with initial regurgitation grades 3-4 was associated with a better prognosis (hazard ratio, HR = 0.622; p = 0.005).

Conclusions: 1. Changes in TV function after TLE were observed in 17.64% of patients. 2. Various factors can predispose to lead-related TV changes, although the common denominator in these events is an extensive buildup of scar tissue. 3. Worsening TV function had no impact on survival after TLE. In patients with severe TV dysfunction, reduction in TVR following TLE was associated with a 40% reduction in mortality during a mean follow-up of 1673 days.

Background: The objective of this study is to estimate the causal relationship between plasma proteins and myocardial infarction (MI) through Mendelian randomization (MR), predict potential target-mediated side effects associated with protein interventions, and ensure a comprehensive assessment of clinical safety.

Methods: From 3 proteome genome-wide association studies (GWASs) involving 9775 European participants, 331 unique blood proteins were screened and chosed. The summary data related to MI were derived from a GWAS meta-analysis, incorporating approximately 61,000 cases and 577,000 controls. The assessment of associations between blood proteins and MI was conducted through MR analyses. A phenome-wide MR (Phe-MR) analysis was subsequently employed to determine the potential on-target side effects of protein interventions.

Results: Causal mediators for MI were identified, encompassing cardiotrophin-1 (CT-1) (odds ratio [OR] per SD increase: 1.16; 95% confidence interval [CI]: 1.13-1.18; p = 1.29 $\times$ ${\mathrm{10}}^{-31}$ ), Selenoprotein S (SELENOS) (OR: 1.16; 95% CI: 1.13-1.20; p = 4.73 $\times$ ${\mathrm{10}}^{-24}$ ), killer cell immunoglobulin-like receptor 2DS2 (KIR2DS2) (OR: 0.93; 95% CI: 0.90-0.96; p = 1.08 $\times$ ${\mathrm{10}}^{-5}$ ), vacuolar protein sorting-associated protein 29 (VPS29) (OR: 0.92; 95% CI: 0.90-0.94; p = 8.05 $\times$ ${\mathrm{10}}^{-13}$ ), and histo-blood group ABO system transferase (NAGAT) (OR: 1.05; 95% CI: 1.03-1.07; p = 1.41 $\times$ ${\mathrm{10}}^{-5}$ ). In the Phe-MR analysis, memory loss risk was mediated by CT-1, VPS29 exhibited favorable effects on the risk of 5 diseases, and KIR2DS2 showed no predicted detrimental side effects.

Conclusions: Elevated genetic predictions of KIR2DS2 and VPS29 appear to be linked to a reduced risk of MI, whereas an increased risk is associated with CT-1, SELENOS, and NAGAT. The characterization of side effect profiles aids in the prioritization of drug targets. Notably, KIR2DS2 emerges as a potentially promising target for preventing and treating MI, devoid of predicted detrimental side effects.

Background: Patients with coronary artery disease (CAD) often experience pulmonary ventilation dysfunction following their initial event. However, there is insufficient research exploring the relationship between this dysfunction and CAD prognosis.

Methods: To address this gap, a retrospective observational study was conducted involving 3800 CAD patients without prior pulmonary ventilation disease who underwent cardiopulmonary exercise testing (CPET) during hospitalization between November 2015 and September 2021. The primary endpoint was a composite of major adverse cardiovascular events (MACE), such as death, myocardial infarction (MI), repeat revascularization, and stroke. Propensity score matching (PSM) was used to minimize selection bias between the two groups, with a subgroup analysis stratified by smoking status.

Results: The results showed that patients were divided into normal (n = 2159) and abnormal (n = 1641) groups based on their pulmonary ventilation function detected by CPET, with 1469 smokers and 2331 non-smokers. The median follow-up duration was 1237 (25-75% interquartile range 695-1596) days. The primary endpoint occurred in 390 patients (10.26%). 1472 patients in each of the two groups were enrolled in the current analysis after PSM, respectively. However, pulmonary function was not associated with MACE before (hazard ratio (HR) 1.20, 95% confidence interval (95% CI) 0.99-1.47; Log-rank p = 0.069) or after PSM (HR 1.07, 95% CI 0.86-1.34; Log-rank p = 0.545) among the entire population. Nonetheless, pulmonary ventilation dysfunction was significantly associated with an increased risk of MACE in smoking patients (HR 1.65, 95% CI 1.25-2.18; p $<$ 0.001) but not in non-smoking patients (HR 0.81, 95% CI 0.60-1.09; p = 0.159). In addition, there was a significant interaction between current smoking status and pulmonary ventilation dysfunction on MACE (p for interaction $<$ 0.001).

Conclusions: Pulmonary ventilation dysfunction identified through CPET was independently associated with long-term poor prognosis in smoking patients with CAD but not in the overall population.

Background: Intravascular ultrasound (IVUS) has been utilized to determine acute stent mal-apposition (ASM) after percutaneous coronary intervention (PCI) in the left main coronary artery (LMCA). However, the clinical consequences of this finding remain uncertain. This research aimed to evaluate the clinical implications of ASM in the LMCA using IVUS.

Methods: In this study, 408 patients who underwent successful drug-eluting stent (DES) implantation in the LMCA were evaluated. We analyzed the prevalence and characteristics of ASM and its correlation with clinical outcomes. ASM is characterized by stent struts that are not in immediate proximity to the intimal surface of the vessel wall after initial stent deployment.

Results: The observed incidence of LMCA-ASM post-successful PCI was 26.2%, both per patient and per lesion. Lesions with LMCA-ASM had a longer stent diameter, larger stent areas, and larger lumen areas compared to those without LMCA-ASM (4.0 $\pm$ 0.5 vs. 3.7 $\pm$ 0.4 mm, p $<$ 0.001; 9.8 $\pm$ 2.0 vs. 9.0 $\pm$ 1.6 ${\mathrm{mm}}^2$ , p $<$ 0.001; 12.3 $\pm$ 1.9 vs. 10.1 $\pm$ 2.1 ${\mathrm{mm}}^2$ , p $<$ 0.001, respectively). The mean external elastic membrane (EEM) area (odds ratio (OR): 1.418 [95% confidence interval (CI): 1.295-1.556]; p $<$ 0.001) emerged as an independent predictor of LMCA-ASM. During the observation period, LMCA-ASM did not display any association with device-oriented clinical endpoints (DoCE), which included cardiac death, target vessel-induced myocardial infarction (MI), stent thrombosis, and target lesion revascularization (TLR). Moreover, the DoCE incidence exhibited no significant disparity between patients with or without ASM (13.1 vs. 6.0%, p = 0.103).

Conclusions: While LMCA-ASM was a not uncommon finding post-PCI, it did not correlate with adverse cardiac events in the present study.

Background: Atrioventricular block (AVB) is thought to be a rare cardiovascular complication of the coronavirus disease 2019 (COVID-19), though limited data are available beyond case reports. We aim to describe the baseline characteristics, proteomics profile, and outcomes for patients with COVID-19-related AVB.

Methods: We prospectively recruited patients diagnosed with COVID-19-related AVB between November 2022 and March, 2023. Inclusion criteria were hospitalization for COVID-19 with the diagnosis of AVB. A total of 24 patients diagnosed with COVID-19 without AVB were recruited for control. We analyzed patient characteristics and outcomes and performed a comparative proteomics analysis on plasma samples of those patients and controls.

Results: A total of 17 patients diagnosed with COVID-19-related AVB and 24 individuals diagnosed with COVID-19 infection without AVB were included. Among patients with COVID-19-related AVB, the proportion of concurrent pneumonia was significantly higher than controls (7/17 versus 2/24, p $<$ 0.05). All 17 AVB patients (9 of permanent AVB, 8 of paroxysmal AVB) received permanent pacemaker implantation. No procedural-related complication occurred. In laboratory tests, the level of biomarkers indicating myocardial damage were substantially higher than controls, including high-sensitivity cardiac troponin-I (median 0.005 versus 0.002 ng/mL, p $<$ 0.05), myoglobulin (median 39.0 versus 27.6 ng/mL, p $<$ 0.05), and MB isoenzyme of creatine kinase (median 1.2 versus 0.8 U/L, p $<$ 0.05). The level of N-terminal pro-b-type natriuretic peptide (median 241.0 versus 33.5 pg/mL, p $<$ 0.05), C-reactive protein (median 4.8 versus 2.0 mg/L, p $<$ 0.05), D-dimer (median 1.2 versus 0.2 µg/mL, p $<$ 0.05), left ventricular end-diastolic diameter (median 49.3 versus 45.7 mm, p $<$ 0.05) in patients with COVID-19-related AVB were significantly higher than controls. The level of albumin (median 41.9 versus 44.5 g/L, p $<$ 0.05) was significantly lower than controls. In comparative proteomics analysis, we identified 397 human proteins. Several significantly altered plasma proteins related to inflammatory response (Serum amyloid A protein, C-reactive protein, Protein Adenosine 5'-monophosphate-activated protein kinase (AMPK), Alpha-2-macroglobulin), complement and coagulation cascades (Tetranectin, haptoglobin), and immune response (Neutrophil defensin 3, Fibrinogen beta chain) may contribute to the pathogenesis of COVID-19-related AVB.

Conclusions: Patients with COVID-19-related AVB are more prone to have myocardial damage and concurrent pneumonia. Through laboratory tests and comparative proteomics analysis

Background: Clinical and experimental data on the cardiac effects of acute hypernatremia are scarce and inconsistent. We aimed to determine and understand the effects of different levels of acute hypernatremia on the human ventricular action potential.

Methods: We performed computer simulations using two different, very comprehensive models of the electrical activity of a single human ventricular cardiomyocyte, i.e., the Tomek-Rodriguez model following the O'Hara-Rudy dynamic (ORd) model and the Bartolucci-Passini-Severi model as published in 2020 (known as the ToR-ORd and BPS2020 models, respectively). Mild to extreme levels of hypernatremia were introduced into each model based on experimental data on the effects of hypernatremia on cell volume and individual ion currents.

Results: In both models, we observed an increase in the intracellular sodium and potassium concentrations, an increase in the peak amplitude of the intracellular calcium concentration, a hyperpolarization of the resting membrane potential, a prolongation of the action potential, an increase in the maximum upstroke velocity, and an increase in the threshold stimulus current at all levels of hypernatremia and all stimulus rates tested. The magnitude of all of these effects was relatively small in the case of mild to severe hypernatremia but substantial in the case of extreme hypernatremia. The effects on the action potential were related to an increase in the sodium-potassium pump current, an increase in the sodium-calcium exchange current, a decrease in the rapid and slow delayed rectifier potassium currents, and an increase in the fast and late sodium currents.

Conclusions: The effects of mild to severe hypernatremia on the electrical activity of human ventricular cardiomyocytes are relatively small. In the case of extreme hypernatremia, the effects are more pronounced, especially regarding the increase in threshold stimulus current.

Researchers have investigated ways to develop optimal imaging techniques to increase the safety and effectiveness of electrophysiological (EP) procedures. Intracardiac echocardiography (ICE) is an advanced imaging tool that can directly visualize cardiac anatomical structures in high resolution, assess tissue heterogeneity and arrhythmogenic substrates, locate intracardiac catheters, monitor catheter-tissue contact and ablation injury in real-time, excluding intracardiac thrombi, and quickly detect procedural complications. Additionally, real-time imaging via ICE can be integrated with a three-dimensional (3D) electroanatomical mapping (EAM) system to reconstruct cardiac anatomy. This technique also promotes the development of zero-radiation EP procedures. Many EP studies and procedures have implemented ICE because it has several advantages over fluoroscopy and transesophageal echocardiography (TEE). ICE-guided EP procedures can be performed under conscious sedation; esophageal intubation and additional anesthesiologists are not required. Atrial fibrillation (AF) and supraventricular tachycardias (SVT) are the most common tachyarrhythmias in clinical settings. A comprehensive understanding of critical anatomical structures, such as the atrial septum, fossa ovalis (FO), and great heart vessels, is needed for the successful catheter ablation of these arrhythmias.

Background: The impact of dominant ventricular morphology on Fontan patient outcomes remain controversial. This study evaluates long-term results of right ventricle (RV) dominance versus left ventricle (LV) dominance in Fontan circulation without hypoplastic left heart syndrome (HLHS).

Methods: We retrospectively examined 323 Fontan operations from our center. To minimize pre- and intra-Fontan heterogeneity, 42 dominant RV patients were matched with 42 dominant LV patients using propensity score matching, allowing for a comparative analysis of outcomes between groups.

Results: The mean follow-up was 8.0 $\pm$ 4.6 years for matched RV dominant and 6.5 $\pm$ 4.7 years for matched LV dominant group (p $>$ 0.05), showing no significant difference. The cumulative incidence of moderate or greater atrioventricular valve regurgitation was also comparable between the two groups (p $>$ 0.05). Similarly, 10-year freedom from death or transplantation following the Fontan operation was 84% $\pm$ 7% in the matched dominant RV group, similar to 81% $\pm$ 7% in the matched dominant LV group (p $>$ 0.05). The 10-year freedom from Fontan failure was 78% $\pm$ 8% in the matched dominant RV group, also similar to 75% $\pm$ 8% in the matched dominant LV group (p $>$ 0.05). Multivariate analysis did not identify RV dominance as a risk factor for Fontan failure (p $>$ 0.05).

Conclusions: In the pre- and intra-Fontan context, RV dominance demonstrated similar and comparable long-term outcomes compared to LV dominance in non-HLHS Fontan circulation.