: Heart failure with preserved ejection fraction (HFpEF) accounts for approximately 50% of heart failure cases and is primarily characterized by impaired diastolic function, leading to increased ventricular filling pressures and symptoms like dyspnea and reduced exercise tolerance. Significant gender-specific differences are observed, with women, particularly post-menopausal, experiencing higher prevalence and distinct clinical profiles compared to men. Diastolic dysfunction in HFpEF involves altered cellular mechanisms such as reduced SERCA2a expression, impacting calcium handling and myocardial relaxation. Diagnostic strategies mainly employ echocardiography, including Doppler imaging, tissue Doppler imaging, and strain imaging, to assess ventricular relaxation and stiffness. However, early identification remains challenging, necessitating advanced tools like cardiac magnetic resonance and exercise stress testing for accurate diagnosis, especially in women who often present with subtle symptoms. Treatment options for HFpEF have traditionally been limited, but recent trials, notably EMPEROR-PRESERVED and DELIVER, demonstrated significant cardiovascular benefits using sodium–glucose cotransporter-2 (SGLT2) inhibitors. Additionally, glucagon-like peptide-1 receptor agonists (GLP-1 RAs) have shown promising results, particularly in obese patients. Despite these advances, gender differences in therapeutic response necessitate further research for personalized management strategies. Understanding sex-specific pathophysiological mechanisms and optimizing diagnostic criteria remain essential to improving prognosis and quality of life in HFpEF patients.

Adherence to exercise-based cardiac rehabilitation (CR) is essential for preventing and managing cardiovascular disease (CVD). Participation in CR reduces all-cause mortality by 27% and cardiac deaths by 31% and lowers rehospitalization rates while also improving functional capacity and quality of life. However, many patients do not start, complete, or maintain CR, resulting in reduced functional abilities, a higher risk of recurring events, and poorer long-term outcomes. This narrative review summarizes patterns of adherence to exercise and CR in CVD, with a specific focus on sex- and gender-related differences in referral, participation, and completion. We synthesize evidence on biological, psychological, and social barriers that limit engagement and describe emerging strategies, such as technology-enabled and home-based programs, multidisciplinary care, and family-centered models, to enhance adherence. Finally, we propose a practical, gender-aware framework for CR design and delivery that can be adjusted and evaluated across diverse healthcare settings to guide clinical practice and future research.

Introduction: Primary Sjögren’s (pSS) is an autoimmune disease that affects several organs, especially the heart, and raises cardiovascular risk. Investigating the associations of hemoglobin-to-red cell distribution width (RDW) ratio (HRR), vitamin D status, and cardiac function could provide valuable insights and biomarkers regarding early cardiovascular risk in patients with pSS. Method: This cross-sectional study involved 61 patients diagnosed with pSS based on ACR/EULAR criteria. Data on demographics, hematological (Hb, RDW), echocardiography, and serum vitamin D levels were collected. Echocardiograms were conducted by trained cardiologists following established guidelines, while vitamin D levels were measured using ELISA. Statistical analyses, including univariate linear regression, were performed with SPSS in order to identify whether HRR tertiles were related to cardiac function and vitamin D status. Results: A study of 61 pSS patients (mean age 59.8 years, 89% female) revealed that patients with a lower hemoglobin-to-RDW ratio (HRR ≤ 0.98) had significantly higher pulmonary artery pressures (PAPs) and lower values for the tricuspid annular plane systolic excursion (TAPSE)/PAPs ratio, contributing to poor right heart function. These associations were particularly strong in patients with insufficient levels of vitamin D (<30 ng/mL), while differences in other echocardiographic parameters remained nonsignificant between HRR groups. Conclusions: These findings underscore the clinical value of HRR as a composite biomarker that reflects the interplay between anemia, inflammation, and cardiovascular health in primary Sjögren’s disease. They also suggest that vitamin D status may be an important therapeutic consideration to mitigate cardiopulmonary risks in this population.

Cardiac involvement in systemic sclerosis (SSc) is mechanistically heterogeneous, driven by concurrently operative processes spanning right ventricular dysfunction, pulmonary microvascular remodeling, and mitochondrial damage. The existing literature rarely synthesizes these domains simultaneously, leaving substantive gaps in mechanistic understanding and the clinical management of SSc cardiac disease. An integrative review of original primary research was conducted using PubMed, Scopus, and Web of Science. Search terms combined “systemic sclerosis,” “right ventricular dysfunction,” “echocardiographic strain,” “pulmonary microvascular disease,” “nailfold capillaroscopy,” “mitochondrial dysfunction,” “oxidative stress,” and “cardiac biomarkers.” Eligible articles were required to report original empirical findings in SSc or SSc-related pulmonary arterial hypertension populations, encompassing echocardiographic, microvascular, molecular, or biomarker outcomes. Right ventricular function is compromised across multiple echocardiographic dimensions—from an elevated myocardial performance index and impaired ventriculoarterial coupling to prognostically significant speckle-tracking strain abnormalities—independent of overt pulmonary hypertension. Pulmonary microvascular disease, quantified by nailfold capillaroscopy and flow-mediated dilation, correlates directly with cardiac magnetic resonance tissue characterization in SSc-related pulmonary arterial hypertension. Mitochondrial dysfunction involving respiratory chain impairment, abnormal fusion dynamics, and altered mitochondrial DNA (mtDNA)copy number is demonstrable across dermal fibroblasts, monocytes, and immune cell populations. Circulating cardiac biomarkers complement echocardiographic findings and predict cardiopulmonary mortality. The integrative framework linking right ventricular remodeling, peripheral vasculopathy, and mitochondrial injury offers substantially richer insight into SSc cardiac pathophysiology than any single-domain perspective can provide, with direct implications for early detection and therapeutic targeting.

Background: The hemoglobin-to-red cell distribution width ratio (HRR) is a composite hematologic biomarker that integrates oxygen-carrying capacity and inflammation-related erythrocyte variability. Its prognostic value in idiopathic pulmonary fibrosis (IPF), and its relationship with right ventricular (RV) function, have not been established. Methods: We conducted a single-center retrospective study of 198 patients with IPF. A total of 165 patients with baseline hemoglobin, red cell distribution width (RDW) and date of diagnosis available constituted the analytical cohort. An HRR cutoff (≤0.86) was derived by time-dependent Receiver Operating Characteristic (ROC) curve analysis at 5 years. All-cause mortality from diagnosis was assessed by Kaplan–Meier and Cox regression, with bootstrap internal validation. Associations between hematologic markers and TAPSE (Tricuspid Annular Plane Systolic Excursion), PAPs (pulmonary arterial systolic pressure) and TAPSE/PASP were examined by linear and logistic regression, followed by joint stratification of HRR and RV–PA coupling. Results: Over a median follow-up of 70.3 months, 57 patients (34.5%) died. Low HRR was associated with higher mortality (72.7% vs. 15.5%; adjusted HR 3.07, 95% CI 1.68–5.63; optimism-corrected HR 2.37) and improved a clinical model beyond RDW (likelihood-ratio p = 0.012). HRR was not associated with TAPSE, PAPs, TAPSE/PASP or RV–PA uncoupling. In exploratory joint stratification, mortality rose from 11.7% with both markers preserved to 100% with both abnormal (age-adjusted HR 6.47, 95% CI 2.64–15.86). At 5 years, HRR and RDW showed similar discrimination (time-dependent AUC 0.70 and 0.71), higher than TAPSE/PASP (0.61). Conclusions: HRR is a simple, inexpensive and independent predictor of mortality in IPF that is unrelated to RV–PA coupling. The two markers provide complementary prognostic information, and their combination identifies a subgroup at very high risk. These findings require external validation.