Minerva cardiology and angiology最新文献

Background: Heart failure with preserved ejection fraction (HFpEF) is a significant public health concern with high morbidity. This study evaluates the prognostic significance of Prognostic Nutritional Index (PNI) and Pan-Immune-Inflammation Value (PIV) in HFpEF, aiming to enhance understanding of its inflammatory and nutritional aspects and identify markers for better diagnosis and risk stratification.

Methods: This retrospective cohort study included 71 patients diagnosed with HFpEF using the HFA-PEFF algorithm and 81 control subjects without heart failure. The PIV, and PNI indices were calculated. A 6-month follow-up of the HFpEF group was conducted to assess rehospitalization rates.

Results: The study found that patients with HFpEF had significantly higher PIV and PNI rates than the control group (P=0.016, P<0.001). A negative correlation (r=-0.328, P<0.001) was observed between the PNI and HFA-PEFF scores. The ROC analysis demonstrated that PIV (AUC: 0.92) had the strongest predictive ability for rehospitalization, followed by Systemic Immune-Inflammatory Index (SII, AUC: 0.87) and PNI (AUC: 0.78), while BMI showed the weakest performance (AUC: 0.59). The multivariate logistic regression analysis demonstrated that both PNI (OR: 0.783, 95% CI: 0.627-0.977, P=0.031) and PIV (OR: 1.012, 95% CI: 1.003-1.021, P=0.008) were significant predictors of rehospitalization in HFpEF patients.

Conclusions: PIV and PNI are important parameters that play a predictive role in diagnosing HFpEF and independently predicting rehospitalization. In the multivariate analyses for rehospitalization, that PIV stands out more than SII, and PNI stands out more than BMI, was current and valuable information.

Atrial cardiomyopathy (ACM) is increasingly recognized as a key contributor to the development and perpetuation of atrial fibrillation (AF), a prevalent cardiac arrhythmia with significant clinical implications. ACM involves complex structural, electrical, and functional remodeling of the atrial myocardium, driven by various pathological conditions such as hypertension, heart failure, and obesity. Key mechanisms include atrial fibrosis, inflammation, and oxidative stress, which collectively contribute to the pro-arrhythmic and pro-thrombotic state associated with AF. Recent studies highlight the role of epicardial adipose tissue in promoting atrial fibrosis and the importance of genetic predispositions in ACM development. Advanced imaging techniques, including left atrial strain and cardiac magnetic resonance, are emerging as valuable tools for assessing atrial remodeling and guiding therapeutic decisions. Understanding the intricate relationship between ACM and AF may enable earlier identification and targeted interventions, potentially improving outcomes in affected patients. Despite advances, gaps remain in identifying early markers of ACM and developing specific therapeutic strategies. This review focuses on the analysis of ACM as a contributor to AF and its pathophysiological and clinical implications. Future research should focus on refining diagnostic criteria and exploring novel treatment approaches to manage ACM and its associated risks more effectively.

Introduction: Fabry disease (FD) is a rare X-linked lysosomal disorder caused by deficient α-galactosidase A (α-Gal A) activity. This scoping review synthesizes evidence on screening, diagnostic, and follow-up methods for FD.

Evidence acquisition: We searched six databases for English and Spanish articles published from 2017 until April 2023. Eligible studies included human research on clinical manifestations and methods for screening, diagnosing, and monitoring FD, such as experimental and quasi-experimental studies, observational research, reviews, and guidelines. We followed PRISMA-ScR guidelines for screening and data extraction. We analyzed data with descriptive statistics and qualitative synthesis.

Evidence synthesis: We included 383 studies, with cross-sectional designs being the most common (N:=155, 41%). Most studies were from high-income countries, and 199 (52%) did not report patients' phenotypes. Screening methods often combined clinical presentation, laboratory results, and imaging findings. Specifically, 14 studies (4%) focused on newborn screening. Clinical symptoms were described in 315 studies (82%) and were instrumental in diagnostic investigation. While hallmark manifestations were prevalent, less-recognized symptoms like tinnitus, early stroke, cerebrovascular dolichoectasia, conduction disorders, aortic root dilatation, and parapelvic cysts, were highlighted as important in clinical suspicion. Laboratory, particularly α-Gal A measurement (N.=183, 48%), and genetic sequencing were fundamental to diagnosis confirmation. Follow-up assessments concentrated on cardiovascular, genitourinary, and nervous systems, employing imaging and electrophysiological studies, along with various scales and questionnaires.

Conclusions: This review provides a comprehensive overview of screening, diagnostic, and monitoring strategies for FD, offering evidence-based insights to improve the clinical management of FD patients.

Aortic stenosis (AS) and cardiac amyloidosis (CA) often coexist in elderly patients, complicating diagnosis and treatment. AS is characterized by the narrowing of the aortic valve, leading to left ventricular outflow obstruction, primarily due to age-related calcification and congenital defects. CA, the most common cause of restrictive cardiomyopathy, results from amyloid protein deposits in the myocardium, causing diastolic dysfunction. Accurate diagnosis of CA in AS patients is challenging due to overlapping symptoms and the need for advanced imaging and biomarkers. Aortic valve replacement (AVR), through surgical aortic valve replacement (SAVR) or transcatheter aortic valve replacement (TAVR) methods, is the primary treatment for severe AS. However, the presence of CA significantly impacts perioperative risk and long-term outcomes, with increased rates of heart failure, pacemaker placement, and mortality. Despite conflicting study results, CA in AS patients is associated with poorer long-term survival and more complications. Future research should enhance AI-based diagnostics, explore novel biomarkers, and clarify AS-CA interactions. Gene-silencing therapies and optimizing perioperative management and enhancing patient education are also crucial. Addressing these challenges will improve the prognosis and quality of life for patients with concurrent AS and CA, facilitating better clinical management of this complex dual pathology.

Background: Ankle-Brachial Index (ABI) has been validated for the diagnosis and risk stratification of vascular disease in the healthy population. The prognostic role and predictors of ABI in patients with established coronary artery disease still remain debated, and especially among patients with acute myocardial infarction (AMI) and represented therefore the aim of the present study.

Methods: We included patients undergoing coronary angiography and PCI for AMI in a single center from May 2022 to November 2024 and with no established history of peripheral arterial disease. ABI was measured before discharge in a phase of hemodynamic stability. Peripheral Arterial Disease (PAD) was defined for ABI ≤0.90.

Results: Overall, 130 patients with AMI were included, of whom 28 (21.5%) had impaired ABI values. No clinical or demographic difference was observed according to ABI, but for lower platelet count (216.7±52.9 vs. 264.8±86.9, P=0.006), that emerged as the only independent predictor of impaired ABI (OR=0.989 [95% CI: 0.982-0.997], P=0.007). Patients with higher platelet count (III tertile, >267.6×10³/µL, N.=44) displayed significantly higher white blood cells count (P<0.001) and lower use of acetylsalicylic acid (P=0.06). At multivariable regression analysis, we confirmed the independent association between higher platelet tertiles values and impaired ABI (adjusted OR=0.147 [95% CI: 0.037-0.576], P=0.006).

Conclusions: Among patients with acute myocardial infarction, abnormal values of ABI are common, although similarly distributed across major established cardiovascular risk factors. In fact, platelet count emerged as the only independent predictor of impaired ABI and the inverse association between higher platelet count and ABI values was confirmed in different higher-risk subsets of patients. Future dedicated large-scale studies could provide the prognostic implications and more insightful understanding of our findings.

Introduction: New-onset postoperative atrial fibrillation (POAF) is a common complication following cardiac surgeries. N-acetylcysteine (NAC) showed a significant reduction in the incidence of POAF. This review aimed to systematically summarize and Meta-analyze data from previously published Randomized Controlled Trials (RCTs).

Evidence acquisition: Electronic databases: PubMed, Cochrane, Embase, Scopus, and Web of Science were searched. Data was extracted and the quality of the included studies was assessed. A random-effects DerSimonian Laird model was employed for meta-analysis.

Evidence synthesis: Fifteen RCTs were included in this study (NAC, N.=940; control, N.=935). In the NAC group, 16.38% developed POAF compared with 23.53% in the control group. NAC supplementation was associated with a decreased incidence of POAF in patients undergoing cardiothoracic surgery (RR 0.69; 95% CI 0.52, 0.91; P=0.008). Meta-regression of randomized trial data showed that the incidence of POAF was not related to the NAC dose (P=0.439). A subgroup analysis in terms of the time of NAC administration revealed that preoperative and postoperative NAC administration was the only subgroup that demonstrated a statistically significant difference (RR 0.48, 95% CI 0.32, 0.71; P=0.0003) compared with placebo and showed no heterogeneity.

Conclusions: Atrial fibrillation is a significant postoperative complication, particularly in cardiothoracic surgery. This study highlights the need for further research on optimal NAC dosing and timing, with evidence suggesting that preoperative and postoperative NAC administration may significantly decrease postoperative atrial fibrillation in cardiothoracic surgery patients, although limitations and variability in study designs need to be considered.

Background: To investigate the protective effect of carvedilol against atherosclerosis by inhibiting the NLRP3 inflammasome.

Methods: In-vitro experiments, human umbilical vein endothelial cells (HUVEC) were divided into the control group, ox-LDL group, carvedilol 5 μM group, carvedilol 10 μM group, and carvedilol 20 μM group. The optimal concentration of carvedilol was determined using the CCK-8 method to assess cell proliferation levels and oil red O staining to observe intracellular lipid droplet formation. Subsequently, the cells were further divided into the control group, ox-LDL group, carvedilol 5 μM (optimal concentration) group, and MCC950 (inhibitor of NLRP3 Inflammasome) group. The expression levels of intracellular proteins NLRP3, pro-Caspase-1, Caspase1, pro-IL-1β, IL-1β, p65, GSDMD, and N-GSDMD were detected by ELISA, or Western Blotting.

Results: Compared to the control group, the ox-LDL group exhibited a significant reduction in cell proliferation level (P<0.05), accompanied by an increase in lipid droplet formation upon induction. In contrast, pretreatment with carvedilol at concentrations of 5 μM, 10 μM, and 20 μM effectively promoted cell proliferation (P<0.05) and inhibited intracellular lipid droplet formation. Notably, the most pronounced effect was observed with carvedilol pretreatment at a concentration of 5μM. Furthermore, compared to the control group, HUVEC cells in the ox-LDL group demonstrated substantial upregulation of NLRP3, pro-Caspase-1, Caspase1, pro-IL-1β, IL-1β, p65 GSDMD and N-GSDMD; however, these markers were downregulated following treatment with carvedilol and MCC950 administration-particularly evident in the carvedilol group.

Conclusions: Carvedilol effectively inhibits the progression of atherosclerosis by targeting the NLRP3 inflammasome, thereby providing valuable mechanistic insights into its beneficial effects on atherosclerotic cardiovascular disease.

Obesity is a major risk factor for chronic non-communicable diseases (NCDs) and it has increased to epidemic proportions. Unhealthy diet represents a modifiable risk factor for both obesity and NCDs, however, there is no universal dietary intervention to improve obesity-related NCDs and particularly to reduce the risk for major adverse cardiovascular events. Energy restriction (ER) and diet quality changes, with and without ER, have been widely investigated in preclinical and clinical studies, however, the potential underlying mechanisms driving the benefits of those dietary interventions remain largely unclear. ER affects multiple metabolic, physiological, genetic, and cellular adaptation pathways associated with prolonged lifespan, particularly in preclinical models, while these benefits remain to be established in humans. Moreover, the sustainability of ER and its implementation across the different diseases remains challenging. On the other hand, diet quality with improvements, with or without ER, has been associated with more favorable long-term metabolic and cardiovascular outcomes. This narrative review will describe the role of ER and/or diet quality improvements on the risk for NCDs. It will also discuss the potential mechanisms of action underlying the potential beneficial effects of those dietary approaches.

Coronary physiological assessment has garnered extensive application in managing patients with coronary artery disease, encompassing both acute and chronic scenarios. Beyond the historical purpose as tool to define the hemodynamic significance of a given artery lesion, coronary artery physiology allows for a complete investigation of epicardial and microvascular circulation. The longitudinal assessment of the distribution pattern of coronary disease based on pressure wire technology provides crucial information to define the best management and procedural planning. Moreover, post-percutaneous coronary intervention physiology reassessment showed a strong association with clinical outcomes and, more importantly, it can spot residual pressure gradients potentially amenable to further intervention and optimization. Growing evidence about the non-invasive angiography-based indices helps to overcome the limitations of the use of intracoronary physiology. This review aims to provide an overview of different utilizations of coronary physiology offering a historical perspective with a particular focus on current challenges and future potential applications.

Residual shunt (RS) after percutaneous patent foramen ovale (PFO) closure has classically been a question of debate for controversial results about its association with increased risk of recurrent ischemic events. Different underlying processes of neural tissue injury have to be taken into account evaluating clinical impact of residual shunt after PFO closure: clotting mechanisms and non-clotting, vasoactive or oxidative mechanisms. Some biochemical studies demonstrated the importance of effective PFO closure aimed to obtain significant reduction of several molecules involved in PFO related strokes. Blood levels of serotonin and homocysteine seem to significantly decrease after percutaneous procedures. A recent study on a pro-thrombotic phenotype of migraineurs with aura and PFO demonstrated that PFO closure reduce activated platelets and thrombin at the value of healthy subjects, underlining the importance of the correct sealing of the defect. The aim of this review is to examine currently available literature studies. Different and discordant results have been obtained due to heterogeneity of study population, instrumental assessment of RS and follow-up methods and length. In the 2021 American Guidelines for the prevention of stroke, RS was definitely considered a predictor of recurrence of ischemic events. Management of this subset of patients is still an unresolved issue and more studies are encouraged.