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Background Cardiac Amyloidosis (CA) pertains to the cardiac involvement of a group of diseases, in which misfolded proteins deposit in tissues and cause progressive organ damage. The vast majority of CA cases are caused by light chain amyloidosis (AL) and transthyretin amyloidosis (ATTR). The increased awareness of these diseases has led to an increment of newly diagnosed cases each year. Methods We performed multiple searches on MEDLINE, EMBASE and the Cochrane Database of Systematic Reviews. Several search terms were used, such as “cardiac amyloidosis”, “diagnostic modalities cardiac amyloidosis” and “staging cardiac amyloidosis”. Emphasis was given on original articles describing novel diagnostic and staging approaches to the disease. Results Imaging techniques are indispensable to diagnosing CA. Novel ultrasonographic techniques boast high sensitivity and specificity for the disease. Nuclear imaging has repeatedly proved its worth in the diagnostic procedure, with efforts now focusing on standardization and quantification of amyloid load. Because the latter would be invaluable for any staging system, those spearheading research in magnetic resonance imaging of the disease are also trying to come up with accurate tools to quantify amyloid burden. Staging tools are currently being developed and validated for ATTR CA, in the spirit of the acclaimed Mayo Staging System for AL. Conclusion Cardiac involvement confers significant morbidity and mortality in all types of amyloidosis. Great effort is made to reduce the time to diagnosis, as treatment in the initial stages of the disease is tied to better prognosis. The results of these efforts are highly sensitive and specific diagnostic modalities that are also reasonably cost effective.

Iron deficiency (ID) is a prevalent comorbidity in heart failure (HF), affecting 37–75% of patients and contributing significantly to symptom burden and adverse outcomes independent of anemia status. Current diagnostic criteria for ID in HF include absolute deficiency (ferritin <100 μg/L) and functional deficiency (ferritin 100–299 μg/L with transferrin saturation <20%). Major clinical trials including AFFIRM-AHF, IRONMAN, HEART-FID, and FAIR-HF2 have demonstrated that intravenous iron therapy, particularly ferric carboxymaltose, reduces HF hospitalizations and improves quality of life and exercise capacity. The 2023 European Society of Cardiology guidelines recommend intravenous ferric carboxymaltose for symptomatic iron-deficient patients with heart failure with reduced ejection fraction. Despite these advances, significant knowledge gaps remain regarding optimal diagnostic approaches, the relationship between ID and ferroptosis in cardiac tissue, and the efficacy of newer iron formulations. This review synthesizes current understanding of ID in HF and highlights emerging therapeutic strategies.

Background: Dual antiplatelet therapy (DAPT) with a potent P2Y12 inhibitor is recommended for patients with acute coronary syndrome (ACS) following percutaneous coronary intervention (PCI). On-treatment platelet reactivity has been associated with ischemic endpoints and may vary between male and female patients. We, therefore, investigated sex-related differences in on-treatment platelet reactivity in ACS patients receiving ticagrelor or prasugrel. Methods: Maximal platelet aggregation by light-transmission aggregometry (LTA) and platelet surface P-selectin expression in response to arachidonic acid (AA), ADP, collagen, TRAP (a protease-activated receptor [PAR-1] agonist), and AYPGKF (a PAR-4 agonist) were assessed in 80 prasugrel- and 77 ticagrelor-treated patients 3 days after PCI. Results: In the overall study population (n = 157), women were older and had lower serum creatinine, hemoglobin, and hematocrit levels than men (all p < 0.05). Women exhibited higher ADP-inducible platelet aggregation in response to both 10 μM and 5 μM of ADP (both p < 0.05), while no sex-related differences were observed for AA-, TRAP-, collagen-, or AYPGKF-inducible platelet aggregation and agonist-inducible platelet surface P-selectin expression. In prasugrel-treated patients, women had higher ADP-inducible platelet aggregation and P-selectin expression compared with men (both p < 0.05), whereas no sex-related differences were found in ticagrelor-treated patients. In the multivariate linear regression analyses, female sex remained an independent predictor of higher platelet aggregation in response to 5 μM of ADP in prasugrel-treated patients (p < 0.05). High on-treatment residual platelet reactivity (HRPR) in response to AA was detected in four patients, and HRPR ADP was seen in seven patients, with no significant differences between female and male ACS patients (both p > 0.05). Low on-treatment residual platelet reactivity (LRPR) in response to AA was identified in 153 patients and LRPR ADP was present in 80 patients, with a higher prevalence of LRPR ADP in men (p = 0.01). Conclusions: Female ACS patients on prasugrel exhibited higher ADP-inducible platelet aggregation than male patients, while no sex-related differences were observed in patients on ticagrelor.

Cardiac resynchronisation therapy (CRT) improves prognosis in patients with heart failure (HF) however the role of ABO blood groups and Rhesus factor are poorly understood. We hypothesise that blood groups may influence clinical and survival outcomes in HF patients undergoing CRT. A total of 499 patients with HF who fulfilled the criteria for CRT implantation were included. Primary outcome of all-cause mortality and/or heart transplant/left ventricular assist device was assessed over a median follow-up of 4.6 years (IQR 2.3–7.5). Online repositories were searched to provide biological context to the identified associations. Patients were divided into blood (O, A, B, and AB) and Rhesus factor (Rh-positive and Rh-negative) groups. Mean patient age was 66.4 ± 12.8 years with a left ventricular ejection fraction of 29 ± 11%. There were no baseline differences in age, gender, and cardioprotective medication. In a Cox proportional hazard multivariate model, only Rh-negative blood group was associated with a significant survival benefit (HR 0.68 [0.47–0.98], p = 0.040). No association was observed for the ABO blood group (HR 0.97 [0.76–1.23], p = 0.778). No significant interaction was observed with prevention, disease aetiology, and presence of defibrillator. Rhesus-related genes were associated with erythrocyte and platelet function, and cholesterol and glycated haemoglobin levels. Four drugs under development targeting RHD were identified (Rozrolimupab, Roledumab, Atorolimumab, and Morolimumab). Rhesus blood type was associated with better survival in HF patients with CRT. Further research into Rhesus-associated pathways and related drugs, namely whether there is a cardiac signal, is required.

Heart failure (HF) remains a major public health challenge, while HF self-care is particularly challenging. Mobile health (mHealth)-based interventions taking advantage of smartphone technology have shown particular promise in increasing the quality of self-care among these patients, and in turn improving the outcomes of their disease. The objective of this study was to co-develop with physicians, patients with HF, and their caregivers a patient-oriented mHealth app, perform usability assessment, and investigate its effect on the quality of life of patients with HF and rate of hospitalizations in a pilot study. The development of an mHealth app (The Hellenic Educational Self-care and Support Heart Failure app [ThessHF app]) was evidence based, including features based on previous clinically tested mHealth interventions and selected by a panel of HF expert physicians and discussed with patients with HF. At the end of alpha development, the app was rated by mHealth experts with the Mobile Application Rating Scale (MARS). The beta version was tested by patients with HF, who rated its design and content by means of the Post-Study System Usability Questionnaire (PSSUQ). Subsequently, a prospective pilot study (THESS-HF [THe Effect of a Specialized Smartphone app on Heart Failure patients' quality of self-care, quality of life and hospitalization rate]) was performed to investigate the effect of app use on patients with HF over a 3-month follow-up period. The primary endpoint was patients' quality of life, which was measured with the Kansas City Cardiomyopathy Questionnaire (KCCQ) and the 5-level EQ-5D version (EQ-5D-5L). The secondary endpoints were the European Heart Failure Self-care Behavior Scale (EHFScBS) score and the hospitalization rate. A systematic review of mHealth-based HF interventions and expert panel suggestions yielded 18 separate app features, most of which were incorporated into the ThessHF app. A total of 14 patients and 5 mHealth experts evaluated the app. The results demonstrated a very good user experience (overall PSSUQ score 2.37 [SD 0.63], where 1 is the best, and a median MARS score of 4.55/5). Finally, 30 patients (male: n=26, 87%) participated in the THESS-HF pilot study (mean age 68.7 [SD 12.4] years). A significant increase in the quality of self-care was noted according to the EHFScBS, which increased by 4.4% (SD 7.2%) (P=.002). The mean quality of life increased nonsignificantly after 3 months according to both KCCQ (mean increase 5.8 [SD 15] points, P=.054) and EQ-5D-5L (mean increase 5.6% [SD 15.6%], P=.06) scores. The hospitalization rate for the follow-up duration was 3%. The need for telehealth services and remote self-care management in HF is of vital importance, especially in periods such as the COVID-19 pandemic. We developed a user-friendly mHealth app to promote remote self-care support in HF. In this pilot study, the use of the ThessHF app was associated with an increase in the quality of self-care. A future multicenter study will investigate the effect of the app use on long-term outcomes in patients with HF.

Heart failure (HF) is a potentially debilitating condition, with a prognosis comparable to many forms of cancer. It is often complicated by anemia and iron deficiency (ID), which have been shown to even further harm patients’ functional status and hospitalization risk. Iron is a cellular micronutrient that is essential for oxygen uptake and transportation, as well as mitochondrial energy production. Iron is crucially involved in electrochemical stability, maintenance of structure, and contractility of cardiomyocytes. There is mounting evidence that ID indeed hampers the homeostasis of these properties. Animal model and stem cell research has verified these findings on the cellular level, while clinical trials that treat ID in HF patients have shown promising results in improving real patient outcomes, as electromechanically compromised cardiomyocytes translate to HF exacerbations and arrhythmias in patients. In this article, we review our current knowledge on the role of iron in cardiac muscle cells, the contribution of ID to anemia and HF pathophysiology and the capacity of IV iron therapy to ameliorate the patients’ arrhythmogenic profile, quality of life, and prognosis.

Background/Objectives: Iron deficiency (ID) is a common and prognostically relevant comorbidity in heart failure with reduced ejection fraction (HFrEF). It contributes to reduced functional status, exercise capacity, and survival. Intravenous ferric carboxymaltose (FCM) improves symptoms, but its effect on cardiac structure and function remains incompletely understood. The aim of this study was to assess the impact of intravenous FCM on echocardiographic indices of left ventricular (LV), left atrial (LA), and right ventricular (RV) morphology and function in HFrEF patients with ID and determine whether these changes correlate with improvements in exercise capacity. Methods: This sub-analysis of the RESAFE-HF registry (NCT04974021) included 86 HFrEF patients with ID (median age 71.8 years, 83% male). Transthoracic echocardiography was performed at baseline and 12 months post-FCM. Parameters assessed included LV ejection fraction (LVEF), LV global longitudinal strain (GLS), LV diastolic function grade, LAVi, LA strain, TAPSE, and RV free wall strain (FWS). Peak VO2 was measured to assess exercise capacity. Results: LVEF improved from 29.3 ± 7.8% to 32.5 ± 10.6% (p < 0.001), LV GLS from −7.89% to −8.62%, and the LV diastolic dysfunction grade improved (p < 0.001). LAVi, peak LA strain, TAPSE, and RV FWS also showed significant improvement. Peak VO2 increased from 11.3 ± 3.2 to 12.1 ± 4.1 mL/min/kg (p < 0.001). Improvements in LVEF, RV FWS, and LV GLS were independent predictors of VO2 increase (p < 0.001, p < 0.001, and p = 0.01, respectively), explaining 42% of the variance. Conclusions: FCM therapy improves biventricular and atrial function, with echocardiographic gains correlating with an enhanced exercise capacity in HFrEF patients with ID.

Atherosclerotic cardiovascular disease (ASCVD) is the most common cause of death globally. Increasing amounts of highly diverse ASCVD data are becoming available and artificial intelligence (AI) techniques now bear the promise of utilizing them to improve diagnosis, advance understanding of disease pathogenesis, enable outcome prediction, assist with clinical decision making and promote precision medicine approaches. Machine learning (ML) algorithms in particular, are already employed in cardiovascular imaging applications to facilitate automated disease detection and experts believe that ML will transform the field in the coming years. Current review first describes the key concepts of AI applications from a clinical standpoint. We then provide a focused overview of current AI applications in four main ASCVD domains: coronary artery disease (CAD), peripheral arterial disease (PAD), abdominal aortic aneurysm (AAA), and carotid artery disease. For each domain, applications are presented with refer to the primary imaging modality used [e.g., computed tomography (CT) or invasive angiography] and the key aim of the applied AI approaches, which include disease detection, phenotyping, outcome prediction, and assistance with clinical decision making. We conclude with the strengths and limitations of AI applications and provide future perspectives.

Background: Cardiac magnetic resonance (CMR) combined with late gadolinium enhancement (LGE) has revealed a non-negligible increased incidence of myocardial fibrosis (MF) in athletes compared to healthy sedentary controls. Objective: The aim of this systematic research and meta-analysis is to investigate and present our perspective regarding CMR indices in athletes compared to sedentary controls, including T1 values, myocardial extracellular volume (ECV) and positive LGE indicative of non-specific fibrosis, also to discuss the differences between young and veteran athletes. Methods: The protocol included searching, up to October 2021, of MEDLINE, EMBASE, SPORTDiscus, Web of Science and Cochrane databases for original studies assessing fibrosis via CMR in athletes. A mean age of 40 years differentiated studies' athletic populations to veteran and young. Results: The research yielded 14 studies including in total 1,312 individuals. There was a statistically significant difference in LGE fibrosis between the 118/759 athletes and 16/553 controls ( Z = 5.2, P < 0.001, I 2 = 0%, P I = 0.45). Notably, LGE fibrosis differed significantly between 546 (14.6%) veteran and 140 (25.7%) young athletes ( P = 0.002). At 1.5T, T1 values differed between 117 athletes and 48 controls ( P < 0.0001). A statistically significant difference was also shown at 3T (110 athletes vs. 41 controls, P = 0.0004), as well as when pooling both 1.5T and 3T populations ( P < 0.00001). Mean ECV showed no statistically significant difference between these groups. Conclusions: Based on currently available data, we reported that overall LGE based non-specific fibrosis and T1 values differ between athletes and sedentary controls, in contrast to ECV values. Age of athletes seems to have impact on the incidence of MF. Future prospective studies should focus on the investigation of the underlying pathophysiological mechanisms.

End-stage heart failure is a condition in which the up-regulation of the systemic and local renin-angiotensin-aldosterone system (RAAS) leads to end-organ damage and is largely irreversible despite optimal medication. Left ventricular assist devices (LVADs) can downregulate RAAS activation by unloading the left ventricle and increasing the cardiac output translating into a better end-organ perfusion improving survival. However, the absence of pulsatility brought about by continuous-flow devices may variably trigger RAAS activation depending on left ventricular (LV) intrinsic contractility, the design and speed of the pump device. Moreover, the concept of myocardial recovery is being tested in clinical trials and in this setting LVAD support combined with intense RAAS inhibition can promote recovery and ensure maintenance of LV function after explantation. Blood pressure control on LVAD recipients is key to avoiding complications as gastrointestinal bleeding, pump thrombosis and stroke. Furthermore, emerging data highlight the role of RAAS antagonists as prevention of arteriovenous malformations that lead to gastrointestinal bleeds. Future studies should focus on the role of angiotensin receptor inhibitors in preventing myocardial fibrosis in patients with LVADs and examine in greater details the target blood pressure for these patients.