Background: Atrial fibrillation (AF) is the most frequent sustained arrhythmia. It increases the risk of stroke, heart failure, death, hospitalizations, and costs. Area of uncertainty: Several scores were introduced to stratify the stroke risk and need for anticoagulation in patients (pts) with AF . CHA₂DS₂-VASc, the most frequently used score, as well as other stroke risk scores have been additionally applied to estimate outcomes for different other conditions, with inhomogeneous results. To date, there has been no consensus regarding the usefulness of these scores to estimate outcomes outside of thromboembolic risk assessment, and their value in estimating different end-point outcomes is still a subject of debate. We conducted this review to investigate whether the stroke risk scores' utility can be extended for the prediction of other severe outcomes in pts with AF. Data sources: We searched PubMed database and included studies that stratified the outcome of pts with AF by different stroke risk scores. We also included studies with a separate analysis of the pts with AF subpopulation. Results: Mortality rates increased with higher CHADS₂ [from 2.28% (2.00%–2.58%) to 13.2% (8.24%–20.8%) per year] and CHA₂DS₂-VASc scores [risk ratio 1.26 (1.21–1.32), P < 0.0001 for score ≥3]. CHADS₂ and CHA₂DS₂-VASc predicted poor outcome in stroke [odds ratio (OR) ranging 1.42–6 for CHADS₂ and 1.3–7.3 for CHA₂DS₂-VASc]. Acute myocardial infarction rates increased with higher CHADS₂ [OR 2.120 (1.942–2.315) P < 0.001] and CHA₂DS₂-VASc [OR 1.63 (1.53–1.75), P < 0.001]. Limited data were reported for ABC( Age, Biomarkers, Clinical histoty) and R₂CHADS₂. No statistically significant correlation was found for major bleeding. Conclusions: CHADS₂ and CHA₂DS₂-VASc are useful tools in identifying pts with AF at higher risk for all-cause death, regardless of other pathologies. Both scores correlated with the development of acute myocardial infarction, cardiovascular hospitalization, outcome in stroke, major adverse cardiovascular events, and major adverse cardiovascular and cerebral events, but not with serious bleeding.

Introduction: Heart failure (HF) is a significant global health issue associated with high morbidity and mortality. Accurate biomarkers are crucial for predicting adverse outcomes and informing management. High-sensitivity cardiac troponins T (hs-cTnT) and I (hs-cTnI) are important prognostic indicators in HF, though their predictive value can be affected by comorbidities, particularly renal dysfunction. Objectives: This review evaluates the prognostic significance of troponin adjusted for renal function in patients with HF. Methods: A comprehensive literature search was performed in PubMed, including studies from 2011 to September 2024, using specific MeSH terms related to HF, troponin, and prognosis. Results: Thirty-two studies met the inclusion criteria, all indicating an association between troponin levels adjusted for renal function and cardiovascular mortality in HF patients (HR 1.67–3.22). High-sensitivity cardiac troponins T (hs-cTnT) and I (hs-cTnI) are independent predictors of cardiovascular mortality in acute heart failure (AHF). Increasing hs-cTnI levels, with a baseline threshold of 0.03 ng/mL, significantly correlate with mortality risk (P = .0011). Patients with hs-cTnT > 14 ng/L, > 21.5 ng/L, and > 26.5 ng/L exhibit increased all-cause mortality after adjusting for renal function. Despite these associations, the role of troponin in predicting heart failure readmissions remains inconsistent, indicating that elevated troponin levels do not reliably predict rehospitalization risk, particularly in those with advanced renal impairment. Conclusions: High-sensitivity troponins (hs-cTnT and hs-cTnI) are independent predictors of mortality in heart failure, even after accounting for renal function, while their role in predicting hospitalizations is weaker.

Background/Objectives: The coexistence of heart failure (HF) and chronic kidney disease (CKD) complicates management and worsens prognosis. NT-proBNP is a recognized biomarker for HF diagnosis and prognosis, yet its interpretation in CKD can be challenging due to confounding factors increasing its levels. This study aimed to evaluate the predictive value of NT-proBNP for all-cause long-term mortality in HF patients across various stages of renal dysfunction. Methods: Hospitalized HF patients were included in this observational, retrospective analysis. NT-proBNP levels and serum creatinine were measured on admission. The primary outcome was all-cause mortality. Patients were divided into three groups according to renal function estimated using the CKD-EPI formula: eGFR1 (>60 mL/min/1.73 m²), eGFR2 (30–60 mL/min/1.73 m²) and eGFR3 (<30 mL/min/1.73 m²). Results: The study included 716 HF patients with a mean age of 71 ± 10 years, 49% males. All-cause long-term mortality was 35% after a median follow-up of 59 months. The mortality rate increased from 29% in eGFR1 patients, to 43% in eGFR2, to 68% in eGFR3. Median NT-proBNP increased from 997 pg/mL in eGFR1 patients to 1586 pg/mL in eGFR2 to 4928 pg/mL in eGFR3. Cut-off values for predicting all-cause long-term mortality were NT-proBNP >1837 pg/mL in eGFR1 patients, >1413 pg/mL in eGFR2 and >6415 pg/mL in eGFR3. In multivariable Cox analysis, NT-proBNP was an independent predictor of all-cause long-term mortality in all eGFR groups. Conclusions: NT-proBNP on admission was an independent predictor of long-term all-cause mortality in hospitalized HF patients across all eGFR subgroups, with increasing cut-off levels in patients with renal dysfunction.

Introduction: Hypereosinophilic syndrome is a rare clinical condition, and cardiac involvement confers a poor prognosis. Hypereosinophilic myocarditis is a medical emergency and targeted treatment should be started promptly even before a definitive diagnosis could be made. Case presentation: A 27-year-old female patient is hospitalized for exertional dyspnea, chest pain, and fatigue for the past 2 weeks. She also describes left leg paresthesias. Clinical examination was in normal limits. ECG showed sinus tachycardia, QS pattern in V1–V4, and diffuse flattened T waves. Laboratory tests revealed increased inflammatory markers, hypereosinophilia, elevated cardiac enzymes, high NT-proBNP. Echocardiography revealed LV dysfunction (EF 31%), while cardiac MRI showed diffuse delayed enhancement with predominant subendocardial disposition. The electromyogram was suggestive of left tibial nerve neuropathy. We interpreted the case as eosinophilic myocarditis with an urgent requirement of therapy and initiated high-dose glucocorticoid therapy and the GDMT 4-pillar heart failure treatment. We excluded common infectious, myeloproliferative syndromes, and frequent associated autoimmune diseases. With prednisone, the eosinophil count rapidly normalized and we gradually tapered the dose by 5 mg per week, however continuing with heart failure therapy. At monthly follow-up visits, there was a significant clinical improvement, with normalization of the eosinophilic count, and a near-normalization of myocardial function. The only symptom that persisted was paresthesias linked to left tibial neuropathy. Conclusion: The surprisingly rapid and favorable course of the disease offers a high index of suspicion for a toxic or a reactive transitory etiology, however still unidentified. In our case, the cause of eosinophilia remained unknown, although we managed to narrow down the possible etiologies. A surprisingly good clinical response was obtained with non-specific treatment targeting mainly hyperosinophilic myocarditis.

Background: Cardio-oncology has developed as an intersection science and practice, balancing the risks and benefits of chemotherapy treatment. Implementing a cardio-oncology program in practice is currently one of the most challenging areas of clinical medicine. In Romania, there are scarce cardio-oncology centers and no dedicated training programs. Thus, the care of these patients is highly heterogeneous and empirical, often without following guideline recommendations. Study Question: This study evaluates the awareness and knowledge of cardio-oncology diagnosis and treatment strategies among Romanian physicians. Study Design: A cross-sectional validated online survey was sent to clinicians treating oncological patients with cardiovascular (CV) risk or associated CV pathology. Measures and Outcome: The survey covered formal training, knowledge of basic cardio-oncology concepts, and therapy. Results: One hundred ninety professionals responded to our questionnaire, most being cardiologists (73.2%), 20.5% oncologists/hematologists, and the remaining had other specialties. Only 21 respondents mentioned the availability of dedicated cardio-oncology teams. Eighty percent would not prescribe prophylactic medication before starting a potentially cardiotoxic oncological treatment in patients with a normal left ventricular ejection fraction and low CV risk. Even in patients with high CV risk, 34.7% would still not prescribe medication for primary prevention of cardiotoxicity. However, most respondents (63.2%) did not consider chemotherapy in patients at high risk of CV events. Most respondents (90.5%) recommend direct oral anticoagulants for CV pathology if indicated. For acute coronary syndromes under fluoropyrimidine treatment, the responses are heterogeneous for all specialties, with a tendency to stop chemotherapy for cardiologists. Sixty-four respondents considered long QT secondary to oncologic treatment a reason to interrupt treatment, with cardiologists more likely to consider it. Conclusions: This survey highlights the heterogeneity in understanding, preventing, and treating CV toxicity. It emphasizes the lack of clear, well-implemented clinical practice algorithms in the population studied. Our survey underlines the gap between guidelines and clinical practice.

Introduction. Atrial fibrillation (AF) is the most frequent hospitalized arrhythmia. It associates increased risk of death, stroke and heart failure (HF). Stroke risk scores, especially CHA₂DS₂-VASc, have been applied also for populations with different diseases. There is, however, limited data focusing on the ability of these scores to predict HF decompensation. Methods. We conducted a retrospective observational study on a cohort of 204 patients admitted for cardiovascular pathology to the Cardiology Ward of our tertiary University Hospital. We aimed to determine whether the stroke risk scores could predict hospitalisations for acute decompensated HF in AF patients. Results. C-statistics for CHADS₂ and R₂CHADS₂ showed a modest predictive ability for hospitalisation with decompensated HF (CHADS₂: AUC 0.631 p = 0.003; 95%CI 0.560–0.697. R₂CHADS₂: AUC 0.619; 95%CI 0.548–0.686; p = 0.004), a marginal correlation for CHA₂DS_2-VASc (AUC 0.572 95%CI 0.501-0.641 with a p value of only 0.09, while the other scores failed to show a correlation. A CHADS₂ ≥ 2 showed a RR = 2.96, p<0.0001 for decompensated HF compared to a score <2. For R₂CHADS₂ ≥ 2, RR = 2.41, p = 0.001 compared to a score <2. For CHA₂DS_2-VASc ≥ 2 RR = 2.18 p = 0.1, compared to CHA₂DS₂-VASc <2. The correlation coefficients showed a weak correlation for CHADS₂ (r = 0.216; p = 0.001) and even weaker for R₂CHADS₂ (r = 0.197; p = 0.0047 and CHA₂DS₂-VASc (r = 0.14; p = 0.035). Conclusions. Among AF patients, CHADS_2, CHA₂DS₂-VASc and R₂CHADS₂ were associated with the risk of hospitalisation for decompensated HF while ABC and ATRIA failed to show an association. However, predictive accuracy was modest and the clinical utility for this outcome remains to be determined.