Inflammation has emerged as an important contributor to heart failure (HF) development and progression. Current research data highlight the diversity of immune cells, proteins, and signaling pathways involved in the pathogenesis and perpetuation of heart failure. Chronic inflammation is a major cardiovascular risk factor. Proinflammatory signaling molecules in HF initiate vicious cycles altering mitochondrial function and perturbing calcium homeostasis, therefore affecting myocardial contractility. Specific anti-inflammatory treatment represents a novel approach to prevent and slow HF progression. This review provides an update on the putative roles of inflammatory mediators involved in heart failure (tumor necrosis factor-alpha; interleukin 1, 6, 17, 18, 33) and currently available biological and non-biological therapy options targeting the aforementioned mediators and signaling pathways. We also highlight new treatment approaches based on the latest clinical and experimental research.

Vitamin D emerged as an important prognostic biomarker in heart failure (HF), with currently highly debated therapeutic implications. Several trials on vitamin D supplementation in HF showed improvements in left ventricular (LV) remodeling and function and health-related quality of life (HRQoL), which did not translate into mid- to long-term beneficial effects regarding physical performance and mortality. We addressed total 25-hydroxyvitamin D (25(OH)D), serum albumin, and uric acid (UA) levels, focusing mainly on vitamin D deficiency, as potential markers of LV systolic dysfunction in HF with reduced and mildly reduced ejection fraction (HFrEF, HFmrEF). Seventy patients with LVEF < 50% were comprehensively evaluated using ECG, echocardiography, lung ultrasound (LUS), blood sampling, and the six-minute walk test (6MWT). HRQoL was also assessed using the Minnesota Living with Heart Failure Questionnaire (MLHFQ). Statistically significant positive correlations were found between LVEF, 25(OH)D, serum UA, and albumin, respectively (p = 0.008, p = 0.009, and p = 0.001). Serum UA (7.4 ± 2.4 vs. 5.7 ± 2.1, p = 0.005), NT-proBNP levels (1090.4 (675.2–2664.9) vs. 759.0 (260.3–1474.8), p = 0.034), and MLHFQ scores (21.0 (14.0–47.0) vs. 14.5 (4.5–25.5), p = 0.012) were significantly higher, whereas 25(OH)D concentrations (17.6 (15.1–28.2) vs. 22.7 (19.5–33.8), p = 0.010) were lower in subjects with severely reduced LVEF. Also, 25(OH)D was independently associated with LVEF in univariate and multiple regression analysis, maintaining its significance even after adjusting for confounders such as age, NT-proBNP, the presence of chronic coronary syndrome, hypertension, and anemia. According to our current findings, 25(OH)D is closely associated with LVEF, further supporting the need to establish correct vitamin D supplementation schemes and dietary interventions in HF. The changes in LVEF, 25(OH)D, serum UA, and albumin levels in HFrEF and HFmrEF indicate a similar pathophysiological background.

Heart failure and mental health conditions frequently coexist and have a negative impact on health-related quality of life and prognosis. We aimed to evaluate depression and anxiety symptoms and to determine the association between psychological distress and cardiac parameters in heart failure with reduced and mildly reduced ejection fraction. A total of 43 patients (33 male, mean age 64 ± 10 years) with heart failure and left ventricular systolic dysfunction (29 with HFrEF, 14 with HFmrEF) underwent comprehensive echocardiographic evaluation. All study participants completed questionnaires for the assessment of depression (PHQ-9), anxiety (GAD-7), and health-related quality of life (MLHFQ). Ten (34%) patients with HFrEF and two (14%) participants with HFmrEF had moderate-to-severe depression symptoms. Significant anxiety symptoms were more frequent in HFrEF (10 vs. 2 patients; 34% vs. 14%). Poor quality of life was also more common among patients with HFrEF (17 vs. 5 patients; 59% vs. 36%), showing higher MLHFQ scores (p = 0.009). Moreover, PHQ-9, GAD-7, and MLHFQ scores showed significant correlations between NYHA class severity and the presence of peripheral edema. The symptoms of dyspnea correlated with both PHQ-9 and MLHFQ scores. Significant correlations were observed between MLHFQ scores and a large number of clinical features, such as exercise capacity, 6MWT distance, the need for furosemide, echocardiographic parameters (LVEDVI, LVESVI, LVEF, LVGLS, SVI), and laboratory variables (albumin, GFR, NT-proBNP). In the multiple linear regression analysis, dyspnea proved to be a significant predictor of higher PHQ-9 and MLHFQ scores, even after adjusting for potential confounders. High symptom burden due to psychological distress is common among patients with HFrEF and HFmrEF. More efficient control of congestion may improve depression, anxiety symptoms, and health-related quality of life.

Cor triatriatum sinister is a rare congenital heart disease characterized by an additional fibromuscular membrane in the left atrium. Cardioembolic stroke is a rare complication of cor triatriatum sinister, especially among women. We hereby describe the case of an 18-year-old female patient, without a past medical history, presenting with cardioembolic stroke in the territory of the right posterior cerebral artery. During extensive diagnostic work-up, nonrestrictive cor triatriatum sinister and patent foramen ovale were diagnosed using transthoracic and transesophageal echocardiography. In clinical practice, it is important to identify congenital cardiac defects as potential substrates for cardioembolism in young patients. In our case, cor triatriatum sinister presenting as ischemic stroke was diagnosed, which is an uncommon finding, especially in young females. Determining the optimal management strategy for patients with cor triatriatum sinister complicated by cardioembolic stroke requires a multidisciplinary approach.

Background/Objectives: Low-grade systemic inflammation, characteristic of heart failure (HF), is a nonspecific inflammatory syndrome that affects the entire body. Macrophage migration inhibitory factor 1 (MIF-1) is a pro-inflammatory cytokine, a key mediator of the innate immune response, and may serve as a potential biomarker of monocyte homing and activation in HF with reduced and mildly reduced ejection fraction (HFrEF, HFmrEF). Methods: We evaluated 70 hemodynamically stable patients with left ventricular EF (LVEF) < 50% by means of echocardiography and blood sampling. Results: We report significant correlations between MIF-1, LVEF (r = −0.33, p = 0.005), LV global longitudinal strain (LVGLS, r = 0.41, p = 0.0004), and tricuspid annular plane systolic excursion (TAPSE, r = −0.37, p = 0.001). MIF-1 levels in HFrEF patients were relatively higher, but not significantly different from those observed in HFmrEF. MIF-1 showed significant associations with TAPSE to systolic pulmonary artery pressure ratio (TAPSE/sPAP, p < 0.0001). Also, patients with TAPSE/sPAP < 0.40 mm/mmHg had significantly higher levels of MIF-1 (p = 0.009). Moreover, ischemic cardiomyopathy (ICM) was more frequent in patients with MIF-1 concentrations above 520 pg/mL (57.1% MIF-1^hi vs. 28.6% MIF-1^lo, p = 0.029). In terms of congestion, MIF-1 showed significant associations with the presence of peripheral edema (p = 0.007), but none was found with self-reported dyspnea (p = 0.307) and New York Heart Association (NYHA) class (p = 0.486). Also, no relationship was reported with N-terminal pro-B-type natriuretic peptide concentrations (NT-proBNP, r = 0.14, p = 0.263). However, the six-minute walk distance was greater in individuals in the MIF-1^lo group when compared to those in the MIF-1^hi group (404.0 ± 127.4 vs. 324.8 ± 124.1 m, p = 0.010). Conclusions: Beyond identifying inflammatory biomarkers related to disease severity, linking MIF-1 to various pathophysiological mechanisms may highlight the active involvement of the monocyte-macrophage system in HF. This system holds notable significance in congestion-related conditions, acting as a major source of reactive oxygen species that perpetuate inflammation.

Introduction : A rare complication of mitral valve surgery is the injury of the circumflex artery due to their close anatomical proximity resulting in a perioperative myocardial infarction and subsequent fibrosis with increased risk of developing ventricular arrhythmias. Case presentation : We hereby describe the case of a 74-year-old male patient who underwent minimally invasive mitral valve replacement surgery for severe mitral regurgitation two weeks prior to presenting to the emergency department with dyspnea, palpitations and slight thoracic discomfort. He was diagnosed with recurrent sustained monomorphic ventricular tachycardia due to inferior wall myocardial infarction. Angioplasty of the culprit lesion was attempted, but the procedure failed due to the elastic recoil of the vessel. Our patient received antiarrhythmic therapy and an implantable cardioverter-defibrillator for secondary prevention of sudden cardiac death, with no further recorded episodes of ventricular tachycardia. Conclusion : Although injury of the circumflex coronary artery during mitral valve surgery is described as rare, we strongly believe that increasing awareness of the potential risks involved can further prevent fatal complications.