The post-percutaneous coronary intervention (post-PCI) fractional flow reserve (FFR) can detect suboptimal PCI or residual ischemia and potentially lead to fewer adverse clinical outcomes. We sought to investigate the predictive value of the angiography-derived FFR for adverse cardiovascular events in patients after PCI. We conducted a comprehensive search of electronic databases, MEDLINE, EMBASE, and the Cochrane Library, for studies published until March 2023 that investigated the prognostic role of angiography-derived fractional flow reserve values after PCI. We investigated the best predictive ability of the post-PCI angiography-derived FFR and relative risk (RR) estimates with 95% confidence intervals (CIs) between post-PCI angiography-derived FFR values and adverse events. Thirteen cohort studies involving 6961 patients (9719 vascular lesions; mean follow-up: 2.2 years) were included in this meta-analysis. The pooled HR of the studies using specific cut-off points for post-PCI angiography-derived FFR was 4.13 (95% CI, 2.92–5.82) for total cardiovascular events, while the pooled HRs for target vessel revascularization, cardiac death, target vessel myocardial infarction, and target lesion revascularization were 6.87 (95% CI, 4.93–9.56), 6.17 (95% CI, 3.52–10.80), 3.98 (95% CI, 2.37–6.66) and 6.27 (95% CI, 3.08–12.79), respectively. In a sensitivity analysis of three studies with 1789 patients assessing the predictive role of the post-PCI angiography-derived FFR as a continuous variable, we found a 58% risk reduction for future adverse events per 0.1 increase in the post-PCI angiography-derived FFR value. In conclusion, post-PCI angiography-derived FFR is an effective tool for predicting adverse cardiovascular events and could be potentially used in decision making, both during PCI and in the long-term follow-up.

Background/Objectives: The quantitative flow ratio (QFR)-based functional Synergy Between Percutaneous Coronary Intervention with Taxus and Cardiac Surgery (SYNTAX) score (FSSQFR) combines coronary arteries’ anatomy and physiology. Methods: We performed an offline FSSQFR calculation in all-comers undergoing coronary angiography in a single center. Based on the tertiles of SYNTAX Score (SS), patients were divided into low-, intermediate-, and high-risk groups with the following cut-offs: SS/FSSQFR < 13, SS/FSSQFR: 13–21, and SS/FSSQFR: >21. The primary endpoint was the predictive value of the FSSQFR of the composite endpoint of all-cause death, myocardial infarction, ischemia-driven revascularization, hospitalization for heart failure, and life-threatening arrhythmias after the follow-up period. Results: This study included 410 patients. SS and FSSQFR were measured for all patients. After calculating FSSQFR, the risk stratification changed in 11% of the study population; more specifically, 26.8, 32.7, and 40.5% of patients were classified as high-, intermediate-, and low-risk, respectively. After a median 30.2 (25.7–33.7) months follow-up period, we recorded 85 events of the primary outcome. The high-risk FSSQFR group compared to the low-risk group had a significantly higher rate of the primary composite outcome (HR: 1.95, 95% CI 1.33–3.34, p = 0.016). Conclusions: In our study, patients classified as the high-risk FSSQFR group had a significantly higher rate of cardiovascular adverse events.

Prompt recognition of arrhythmogenic conditions in recreational and competitive athletes is essential for clinical management and for providing appropriate exercise recommendations. We report the case of a 67-year-old athletic individual with a high burden of ventricular arrhythmias and a phenotype within the dilated/nondilated left ventricular cardiomyopathy spectrum. Genetic testing identified a likely causative variant in the Filamin C (FLNC) gene. An integrative evaluation incorporating advanced cardiac imaging, genetic analysis, and invasive electrophysiology was undertaken to optimize risk stratification and customize exercise counseling. In arrhythmogenic cardiomyopathy with confirmed or suspected genetic etiology, a multimodal evaluation is essential for accurate patient phenotyping. The impact of exercise on disease expression in specific gene variants associated with predominantly left-sided involvement remains insufficiently understood and requires further research and shared decision-making. A comprehensive multidisciplinary evaluation is key for diagnosis, risk stratification, and management of athletes with ventricular arrhythmias.

Background: The widespread use of fluoroquinolones has been associated with the formation, dissection, and rupture of aortic aneurysms. Arterial biomarkers are established predictors of cardiovascular events. The present study was designed to investigate the effect of quinolones on arterial stiffness and aortic size for the first time. Methods: We studied 28 subjects receiving short-term (<15 days) antibiotic therapy involving quinolones and 27 age- and sex-matched subjects receiving an alternative to quinolone antibiotics. The follow-up period was approximately 2 months. The study’s primary endpoint was the carotid–femoral pulse wave velocity (cfPWV) difference between the two groups 2 months after therapy initiation. Secondary endpoints were the augmentation index corrected for heart rate (AIx@75) and sonographically assessed aortic diameters 2 months after the initial treatment. Results: Subjects had similar values of arterial biomarkers, blood pressure measurements, and aortic diameters at baseline. At follow-up, no significant change was observed between the two groups regarding the hemodynamic parameters and arterial biomarkers (p > 0.05 for all), i.e., cfPWV (7.9 ± 2.6 m/s for the control group vs. 8.1 ± 2.4 m/s for the fluoroquinolones group; p = 0.79), AIx@75 (22.6 ± 9.0% for the control group vs. 26.6 ± 8.1% for the fluoroquinolones group; p = 0.09), and aortic diameters. Conclusions: To our knowledge, FRAGILES is the first study to provide insights into the possible effects of fluoroquinolones on arterial biomarkers, showing that, at least in the short term, treatment with fluoroquinolones does not affect aortic function and diameter.

Sudden cardiac death (SCD) remains a devastating but potentially preventable outcome in inherited cardiomyopathies. Although its absolute incidence is low, the possibility of preventing SCD through implantable cardioverter-defibrillators renders accurate arrhythmic risk stratification a central clinical priority. Risk prediction is evolving from phenotype-based stratification towards individualized approaches integrating genotype, imaging biomarkers, and clinical variables. This review critically evaluates available SCD risk prediction models across cardiomyopathy subtypes, including well-validated tools for hypertrophic cardiomyopathy (HCM) and arrhythmogenic right ventricular cardiomyopathy (ARVC), as well as emerging gene-specific models. We explore key methodological concepts and highlight limitations, such as data sparsity, endpoint heterogeneity, overfitting, and the lack of robust external validation. The application of fixed risk thresholds across diverse patient populations poses ethical and clinical challenges, particularly when competing risks such as heart failure or non-cardiac death are not adequately considered. Synthesis of aggregate data and graphical illustrations show how risk trajectories and mortality drivers differ by genotype and disease stage. Despite recent progress, most models are not yet embedded in routine care. Future advances will require dynamic, longitudinal, and multimodal models, designed for transparency, patient-centred decision making, and real-world implementation to meaningfully reduce mortality in cardiomyopathies.

Background: Despite the increasing use of transcatheter aortic valve procedures, many patients still require surgical aortic valve replacement (SAVR). Assessing arterial properties in patients undergoing SAVR for aortic valve stenosis can be challenging, and the existing evidence is inconclusive. Our study aimed to investigate the impact of SAVR on vascular stiffness and the quality of life, as well as the different effects of valve type on arterial properties. Methods: We included 60 patients (mean age 70.25 ± 8.76 years, 65% men) with severe symptomatic aortic stenosis who underwent SAVR. Arterial stiffness (cfPWV, baPWV) and vascular parameters (AIx@75, central pressures, SEVR) were measured at baseline, pre-discharge, and 1-year post-operation. The QOL was assessed using the generic questionnaire—short-form health survey 36 (SF-36) pre-operatively and at 1 year. Results: Post-SAVR, cfPWV increased immediately (7.67 ± 1.70 m/s vs. 8.27 ± 1.92 m/s, p = 0.009) and persisted at 1 year (8.27 ± 1.92 m/s vs. 9.29 ± 2.59 m/s, p ≤ 0.001). Similarly, baPWV (n = 55) increased acutely (1633 ± 429 cm/s vs. 2014 ± 606 cm/s, p < 0.001) and remained elevated at 1 year (1633 ± 429 cm/s vs. 1867 ± 408 cm/s, p < 0.001). Acute decrease in Alx@75 (31.16 ± 10% vs. 22.48 ± 13%, p < 0.001) reversed at 1 year (31.16 ± 10% vs. 30.98 ± 9%, p = 0.71). SEVR improved (136.1 ± 30.4% vs. 149.2 ± 32.7%, p = 0.01) and persisted at 1 year (136.1 ± 30.4% vs. 147.5 ± 30.4%, p = 0.01). SV had a greater cfPWV increase at 1 year (p = 0.049). The QOL improved irrespective of arterial stiffness changes. Conclusions: After SAVR, arterial stiffness demonstrates a persistent increase at 1-year, with valve type having a slight influence on the outcomes. These findings remain consistent despite the perceived QOL.