This review summarizes current 2D and 3D echocardiographic techniques for evaluating right heart structure and function in pulmonary hypertension (PH), emphasizing their diagnostic, prognostic, and monitoring roles. It also highlights the emerging role of myocardial strain imaging and right atrial (RA) assessment in comprehensive right heart evaluation. Recent guidelines support a multiparametric echocardiographic approach, integrating structural, functional, and hemodynamic parameters to characterize right ventricular (RV) remodeling in PH. Advanced modalities such as 3D echocardiography and speckle-tracking strain imaging enhance evaluation of RV and RA function and may enable earlier detection of dysfunction and improved risk stratification. Established 2D echocardiographic guidelines provide a strong foundation for PH assessment. Incorporating 3D RV imaging and RA/RV strain builds on these standards, improving diagnostic precision and clinical relevance. Standardization and broader adoption of these tools will be essential to optimize patient outcomes and support future PH research.

This paper aims to clarify the mechanism of action of Cardiac Contractility Modulation in heart failure treatment, synthesize key clinical evidence supporting the combination of Cardiac Contractility Modulation and implantable cardioverter-defibrillators for managing heart failure with reduced ejection fraction, and explore potential challenges and future applications pertaining to this combined therapy. Recent studies indicate that cardiac contractility modulation therapy improves ventricular function without elevating myocardial oxygen consumption, promotes recovery of diastolic and systolic function, augments myocardial contractility, and exhibits substantial efficacy in drug-refractory chronic heart failure. Additionally, cardiac contractility modulation markedly improves left ventricular function, reduces hospitalization frequency, and enhances quality of life in patients with heart failure with reduced ejection fraction and a QRS duration of 120-149 ms. It may also serve as a pivotal strategy to arrest progression of heart failure with preserved ejection fraction. Combining implantable cardioverter-defibrillators with cardiac contractility modulation addresses a critical gap in the clinical management of patients with heart failure with reduced ejection fraction. These individuals meet criteria for left ventricular assist devices but are ineligible for cardiac resynchronization therapy and fail to derive long-term survival benefits from implantable cardioverter-defibrillator monotherapy. This review demonstrates that combining cardiac contractility modulation and implantable cardioverter-defibrillators shows potential for improving outcomes in specific populations with heart failure with reduced ejection fraction by addressing limitations of single-therapy approaches. A key implication is that this combined strategy may offer a valuable therapeutic option for patients underserved by current guidelines. However, further rigorous clinical investigations are needed to fully establish its long-term efficacy, safety, and optimal patient selection criteria. These findings highlight the need for future research to refine the application of this combined therapy and expand its evidence base, which may inform future treatment guidelines for heart failure with reduced ejection fraction.

The relationship between positive affect (PA) and heart rate variability (HRV) has attracted considerable interest due to its potential implications for emotion regulation and cardiovascular health. This systematic review synthesizes current literature on the association between PA and HRV, considering resting-state, stress-reactivity and recovery contexts, as well as variations in PA conceptualization. A total of 36 studies (N = 5501) were included, spanning experimental, ambulatory, cross-sectional, and mixed designs. Elevated PA was most often associated with higher vagally mediated HRV, measured as RMSSD or high-frequency (HF) power, but results varied by context. Resting-state and trait-like PA measures showed the most consistent positive associations. In stress-induction paradigms, effects depended on the stress phase and arousal level of PA, with RMSSD emerging as a more consistent index than other HRV metrics. In real-life settings, aggregated activated PA was linked to higher RMSSD, while momentary activated PA was linked to lower RMSSD, suggesting short-term allostatic adjustments. Findings for other HRV metrics, such as LF/HF ratio, LF-HRV, and SDNN, were mixed. Overall, this review highlights the complex interplay between PA and cardiac autonomic regulation and provides directions for future research, which should aim for greater methodological consistency and clarify the temporal dynamics of the PA-HRV relationship.

Postoperative atrial fibrillation (POAF) and post pericardiotomy syndrome (PPS) are among the most common complications following cardiac surgery. This review explores their incidence, clinical features, risk factors, and shared inflammatory mechanisms. It also examines prevention and management strategies, with a focus on the relationship between PPS and POAF and remaining gaps in understanding. Pericardial inflammation and innate immune activation are central to the development of both POAF and PPS. Surgical trauma initiates cascades involving cytokines, oxidative stress, and atrial remodeling. PPS has been associated with a higher risk of atrial fibrillation in the early postoperative period. Although current prediction models do not provide optimal discrimination, several preventive strategies, including preoperative medications and surgical options, have been shown to reduce the risk of these complications. However, varying definitions and diagnostic criteria limit comparability across studies, and long-term data are scarce. POAF and PPS are associated with significant morbidity, including longer hospital stays, readmissions, and cardiovascular complications. Identifying high-risk patients is essential to guide early interventions. The overlap in pathophysiology suggests PPS may trigger POAF, but causality remains unconfirmed. Future research should focus on clarifying their relationship, assessing the durability of preventive strategies, and establishing standardized diagnostic criteria to reduce heterogeneity and improve clinical decision-making.

To discuss the optimal timing of staged chronic total occlusion (CTO) percutaneous coronary intervention (PCI) in patients presenting with acute coronary syndromes (ACS), multiple CTOs and after a CTO modification procedure. In patients with acute coronary syndromes CTO PCI should be performed as part of a complete revascularization strategy within a few weeks or months from the initial presentation. In patients who undergo CTO modification procedures, such as subintimal tracking and re-entry (STAR) earlier re-intervention (within 1-2 months) is better than later re-intervention. Staged intervention is preferred in most patients who need PCI of more than one CTO to minimize the risk of complications. The optimal timing of CTO intervention as part of a complete revascularization strategy remains unknown, as does the optimal timing of repeat intervention after a CTO modification procedure, though earlier is likely better than later in both cases. PCI of more than one CTO in the same patient should also be staged for safety reasons.

The Fontan procedure, a palliative surgery for single-ventricle congenital heart disease, often leads to multisystem complications. Elevated bile acids and reduced vitamin D3 levels, frequently observed in this population, may share a harmful bidirectional relationship. This review examines their interplay and therapeutic relevance. Fontan-associated liver disease and potential gut dysbiosis contribute to altered bile acid metabolism, with elevated circulating secondary bile acids impairing cardiovascular, hepatic, musculoskeletal, and immune functions. Recent evidence suggests that bile acid accumulation hinders vitamin D absorption and metabolism. In turn, vitamin D deficiency exacerbates systemic inflammation and fibrosis while reducing bile acid detoxification via diminished vitamin D receptor signaling. The dysregulation of bile acid and vitamin D pathways may create a vicious cycle driving Fontan-associated multisystem dysfunction. Interventions targeting this axis-such as vitamin D supplementation and bile acid modulation-may offer novel strategies to mitigate organ injury and improve long-term outcomes in this high-risk population.

To provide an overview of human induced pluripotent stem cell (hiPSC)-derived cardiovascular lineages and describe their impact on drug testing in vitro. hiPSCs have garnered tremendous interest over the last decade due to their potential for unlimited proliferation and differentiation into cardiovascular lineages. Technologies using tissue engineering, 3D bioprinting, and organ-on-a-chip platforms composed of hiPSC derivatives can produce cardiovascular tissue mimetics that enhance drug screening applications. hiPSC-derived cardiovascular lineages advance drug screening efforts by using autologous cells that are more therapeutically relevant. Established approaches to reproducibly generate hiPSC-derived cardiovascular lineages and their subsequent organization into 3D constructs more accurately mimic the physiological organization of cardiac tissue, leading to improved identification of potential drug targets for therapeutic testing.

Cardiovascular disease (CVD) remains a leading cause of morbidity and mortality worldwide, with occupational factors emerging as significant yet modifiable risk factors. This comprehensive review evaluates the association between various occupational exposures-including job stress, long working hours, shift work, physical activity at work, and exposure to hazardous substances-and CVD risk. Using the GRADE framework, we assessed the strength of evidence for each risk factor. Job stress, long working hours, night shift work, and carbon monoxide exposure demonstrated moderate evidence linking them to increased CVD risk, while occupational noise, air pollutants, and extreme temperatures had limited evidence. Physical activity at work and exposure to toxic metals showed inconclusive findings due to inconsistencies and indirectness in study populations. This review suggests that evaluating occupational exposures is essential for the early identification and management of individuals at elevated cardiovascular risk, and emphasizes that workplace interventions and health policies should prioritize reducing specific risk factors-such as job stress, long working hours, and hazardous exposures-to prevent CVD at both individual and population levels.

This review explores the unique anatomy and pathophysiology of pericardial fat (including both epicardial adipose tissue [EAT] and paracardial fat), its clinical significance, and its potential role as a therapeutic target. It addresses key questions regarding the contribution of EAT to cardiometabolic conditions such as coronary artery disease, heart failure, atrial fibrillation, and ventricular arrhythmias, and explores interventions that reduce EAT to possibly improve cardiovascular outcomes. Recent studies have established EAT as a metabolically active, pro-inflammatory fat depot directly affecting the myocardium and coronary arteries. Imaging and metabolomic studies have advanced the assessment of EAT burden. Clinical evidence supports lifestyle modification, pharmacologic therapies including GLP-1 RA and SGLT2i, and bariatric surgery to effectively reduce EAT volume. Emerging data link EAT reduction with improved cardiac function and arrhythmia risk, although causality remains unclear. EAT is a modifiable cardiometabolic risk factor associated with adverse outcomes in coronary artery disease, heart failure, atrial fibrillation, and ventricular arrhythmias. Targeting EAT through cardiometabolic risk reduction strategies may improve prognosis. Future research should focus on determining whether reducing EAT directly improves clinical outcomes.