Journal of Cardiovascular Medicine最新文献

In Brugada syndrome (BrS), syncope is considered a sign of increased risk for sudden cardiac death (SCD) due to ventricular tachycardia/ventricular fibrillation (VT/VF) episodes. However, arrhythmic syncope in BrS is extremely rare, while nonarrhythmic syncope may occur as in the general active population, mostly from reflex events. Symptomatic patients with BrS show a higher risk profile, requiring a watchful risk stratification. In this scenario, a clinical misjudgment could determine to overlook the risk of SCD as well as to pursue inappropriate therapeutic approaches. Therefore, understanding the correct mechanism of the syncope in BrS is mandatory representing a real sign of increased risk only if linked to VT/VF episodes. This review focuses on the BrS population considering the role of the autonomic nervous system, the issue of a correct syncope classification, the potential link between reflex and arrhythmic syncope, and diagnostic work flow in patients with a concomitant reflex mechanism, with a specific focus on the head-up tilt test and implantable loop recorder roles.

Aims: In patients with significant mitral regurgitation (MR), heart-lung interaction is decisive in defining symptoms and signs of heart failure. Little is known about the direct effects of mitral transcatheter edge-to-edge repair (m-TEER) on pulmonary circulation and changes in lung congestion and function. This study directly evaluates, through the execution of pulmonary function tests, the mid- and long-term impact of m-TEER on lungs.

Methods: Consecutive patients undergoing m-TEER from June 2019 to September 2023 were evaluated at baseline and at 3- and 12-month follow-up. Clinical, laboratory and echocardiographic examinations, quality-of-life questionnaire and walking test were performed, followed by spirometry and diffusing capacity of the lungs for carbon monoxide (DLCO).

Results: Sixty-eight patients (78±6 years, NYHA class III-IV) underwent effective m-TEER. At follow-up they presented improvement in echocardiographic parameters, functional data and quality of life. After TEER, DLCO significantly increased (from 67% ± 17 at baseline to 75% ± 17 and 74% ± 18 at 3- and 12-month respectively, P < 0.001) as well as spirometric indices of forced vital capacity (FVC) (from 84% ± 19 to 96% ± 20 and 91% ± 23, P < 0.001) and forced expiratory volume in the first second (FEV1) (from 90% ± 24 to 99% ± 27 and 97% ± 28, P < 0.001). At 12 months, DLCO was associated with systolic pulmonary artery pressure and right ventricular-to-pulmonary artery coupling, with spirometric measure of FVC with the 6-min walk distance.

Conclusions: This work shows the improvement of spirometric indices and DLCO on patients undergoing m-TEER. These results indicate the retrograde benefit of the procedure resulting in pulmonary decongestion due to the reduction of MR.

Cardiomyopathies are a heterogeneous group of cardiac disorders with significant morbidity and mortality that often manifest as heart failure or sudden cardiac death. Although these conditions can be influenced by environmental factors, genetic causes play a critical role, with both Mendelian and non-Mendelian inheritance patterns contributing to their development. Advances in genetic testing have transformed clinical practice, offering new opportunities for diagnostic and prognostic characterization of cardiomyopathies, and supporting personalized interventions based on genetic profiles. This review explores the diagnostic utility of genetic testing for some specific cardiomyopathies and the complex prognostic insights it provides, especially for assessing arrhythmic risk and guiding implantable cardioverter defibrillator (ICD) implantation in primary prevention. In addition, the review highlights the emerging potential of gene-targeted therapies, which aim to improve outcomes for patients with variants in specific genes. As inherited cardiomyopathies often exhibit familial patterns, genetic testing is also crucial in family screening and management, enabling tailored monitoring and care. Recognizing the challenges posed by phenotypic variability and the interplay of genetic, comorbid, and lifestyle factors, this review emphasizes the need for a deeper understanding of these complexities to optimize precision medicine approaches in the care of inherited cardiomyopathies.

Peripheral artery disease (PAD) is a global health burden due to its high prevalence, morbidity, and mortality. It affects more than 200 million people worldwide. PAD is a manifestation of systemic atherosclerosis that is often associated with coronary and cerebrovascular disease, underscoring its crucial role as an indicator of advanced vascular pathology. Despite its strong association with cardiovascular morbidity, PAD remains underdiagnosed and undertreated compared with coronary artery disease (CAD), highlighting a significant gap in care. Patients with PAD are at increased risk of myocardial infarction (MI), stroke, and limb amputation, so a multidisciplinary approach is required to reduce adverse outcomes. Identifying at-risk patients through early screening and implementing evidence-based therapeutic strategies is crucial in treating PAD. Modern lipid-lowering agents, dual antithrombotic therapies, and aggressive risk factor control are essential treatment components. Recent advances, including PCSK9 inhibitors and novel antiplatelet agents, have shown promise for improving cardiovascular and limb-related outcomes, although further validation is needed. Given the systemic nature of atherosclerosis, managing PAD should be a cornerstone of cardiovascular care, requiring individualised treatment plans. Increasing awareness and understanding of PAD is critical to bridging gaps in diagnosis and treatment to improve the overall prognosis and quality of life of patients with this debilitating disease. This work aims to enhance practical approaches to PAD by providing comprehensive insights into its management and offering a foundation for exploring innovative future treatment options.

Aims: Inflammation is a main pathophysiological driver in atherosclerotic cardiovascular diseases (ASCVD). Low-dose long-term colchicine for secondary prevention in patients with established ASCVD has been studied in multiple randomized trials in the last decade.This meta-analysis aimed to evaluate the efficacy and safety of long-term low-dose colchicine for secondary prevention in patients with established ASCVD.

Methods: We conducted a systematic review and meta-analysis following PRISMA guidelines to evaluate studies reporting long-term outcomes in patients with ASCVD. We systematically searched PubMed, EMBASE and Scopus databases for relevant studies up to 1 December 2024. The primary outcome was the occurrence of major adverse cardiovascular events (MACE), a composite of cardiovascular death (CVD), myocardial infarction (MI) and stroke. Random-effects models were used to calculate pooled risk ratios (RRs).

Results: Ten randomized clinical trials enrolling 22 532 patients were identified. Addition of colchicine to standard medical treatment in patients with established ASCVD reduced the risk for MACE by 27% [RR 0.73, 95% confidence interval (CI) 0.57-0.95], with a number needed to treat of 52. Colchicine was found to significantly reduce the risk of MI (RR 0.83, 95% CI 0.72-0.96) and coronary revascularization (RR 0.79, 95% CI 0.65-0.94). There were no significant differences between the two groups concerning cardiovascular and noncardiovascular mortality, risk of serious gastrointestinal events, infections requiring hospitalization and cancer.

Conclusions: These findings support the use of long-term low-dose colchicine for secondary prevention of MACE in clinical practice.

Aims: The implications of obesity on phenotype presentation and outcomes in acute decompensated heart failure (ADHF) are relatively unexplored. The aim of this study was to investigate the characteristics and prognostic implications related to obesity in ADHF, according to left ventricular and right ventricular function.

Methods: Consecutive patients hospitalized for ADHF were retrospectively enrolled. Obesity was defined as BMI at least 30 kg/m2. Patients were classified according to the range of left ventricular ejection fraction (LVEF) and to the presence of right ventricular dysfunction (RVD). The primary outcome was 1-year all-cause mortality or rehospitalization for ADHF (HFH).

Results: Two thousand and ninety-eight patients were enrolled; 27% had BMI at least 30 kg/m2. Obese patients were younger, more frequently men and diabetic, with higher blood pressure and lower natriuretic peptides; they had smaller left ventricular volumes, lower pulmonary arterial systolic pressure, and lower prevalence of mitral or tricuspid regurgitation. In heart failure with reduced LVEF, obese patients were treated with higher dosages of antineurohormonal drugs and diuretics. At multivariable logistic regression analysis, obesity was an independent predictor of heart failure with preserved ejection fraction (HFpEF) phenotype [odds ratio (OR) = 2.046, P = 0.012] and of RVD (OR = 1.711, P = 0.034). At adjusted analysis, obesity was independently associated with a lower risk of 1-year mortality/HFH (hazard ratio = 0.608, P = 0.003), consistently across LVEF subgroups and presence/absence of RVD. RVD was associated with a higher risk of 1-year mortality/HFH in nonobese but not in obese patients.

Conclusion: Obesity was highly prevalent (27%) in ADHF and associated with a lower risk of 1-year mortality or HFH. Obesity was an independent predictor of HFpEF phenotype and of RVD, but RVD was associated with higher mortality/morbidity risk only in nonobese patients.