Search Results (1,815)

Background: NT-proBNP is a mechanistically grounded biomarker of ventricular wall stress with established prognostic value in cardiac surgery, but its perioperative role in lung cancer resection remains incompletely characterised. Pulmonary resection imposes unique haemodynamic stressors—including one-lung ventilation-induced right ventricular afterload increase, permanent pulmonary vascular bed reduction, and ischaemia–reperfusion injury—that create a distinct biological context for natriuretic peptide elevation not represented in general surgical cohorts. Methods: A narrative review of the literature was conducted through systematic searches of PubMed, EMBASE/MEDLINE, and the Cochrane Library (January 2000–June 2026), supplemented by manual reference screening. Approximately 135 articles were included in the final synthesis. Results: Perioperative NT-proBNP elevation predicts postoperative atrial fibrillation, major adverse cardiovascular events, and long-term survival after lung resection, with effect sizes substantially exceeding those reported in general surgical populations. The PRESAGE trial established that NT-proBNP-guided prophylaxis reduces postoperative atrial fibrillation from 40% to 6% in high-risk patients. No thoracic surgery-specific NT-proBNP threshold has been prospectively validated in a multicentre setting, and approximately half the evidence base derives from BNP rather than NT-proBNP assays, precluding direct threshold synthesis. Surgical approach—particularly robot-assisted thoracoscopy—modulates postoperative biomarker elevation through OLV duration rather than inflammatory burden alone. The combination of NT-proBNP with high-sensitivity troponin identifies a dual-elevation subgroup with a MACE rate of 18.4%. Conclusions: NT-proBNP measurement is clinically actionable in thoracic surgery but requires assay-standardised, multicentre validation of population-specific thresholds stratified by resection extent and surgical approach. A dual biomarker strategy combining NT-proBNP with high-sensitivity troponin represents the most evidence-based perioperative risk stratification framework currently available. Full article

In polytrauma patients, persistent or unexplained hemodynamic instability is commonly attributed to hemorrhage, hypovolemia, or septic evolution. Compensatory neuro-cardiovascular responses may temporarily mask structural cardiac injury and delay diagnosis. Traumatic tricuspid valve injury is a rare condition in which physiological compensation and right-ventricular adaptation can initially preserve systemic perfusion but progressively impair circulatory efficiency. We report the case of a young polytrauma patient and a targeted narrative review to shed light on a rare cause of hemodynamic instability in blunt chest trauma, emphasizing that identifying the underlying mechanism of shock is crucial for adequate management. Full article

Heart failure (HF) is a systemic syndrome in which prognosis depends on cardiac dysfunction, congestion, cardiorenal and cardiohepatic interactions, inflammation, and metabolic dysregulation. The liver is exposed to elevated systemic venous pressure and reduced forward flow, and contributes to albumin and coagulation factor synthesis, bile acid metabolism, iron homeostasis, and the acute-phase response. Cardiohepatic injury involves hemodynamic stress, sinusoidal endothelial dysfunction, oxidative stress, inflammatory signaling, fibrogenesis, and altered metabolic regulation. Congestive hepatopathy is associated with right-sided HF, tricuspid regurgitation (TR), pulmonary hypertension, and elevated central venous pressure, whereas hypoxic hepatitis develops during low-output states, shock, or acute circulatory deterioration. These mechanisms may coexist, producing congestive/cholestatic, hypoperfusive/ischemic and mixed/systemic reserve profiles. Composite liver-related scores, including Model for End-Stage Liver Disease (MELD), MELD excluding International Normalized Ratio (MELD-XI), MELD with sodium (MELD-Na), MELD-Albumin and albumin–bilirubin (ALBI) score, may reflect congestion, hepatorenal dysfunction, nutritional status and reduced systemic reserve. This review summarizes hemodynamic and molecular mechanisms of cardiohepatic injury, liver-related biomarkers and composite scores, with emphases on advanced HF, left ventricular assist device (LVAD) therapy and heart transplantation. Liver-related abnormalities remain underrecognized in HF. Their serial interpretation may support risk stratification, but composite scores should complement rather than replace comprehensive clinical assessment. Full article

Atrial fibrillation (AF) and heart failure (HF) frequently coexist, but the clinical relevance of AF may differ according to whether it appears to be a potentially reversible contributor, an aggravating factor in established HF, or a marker of advanced substrate. The driver–modifier–marker lens used in this review is a provisional, nonvalidated aid to clinical reasoning and should not be interpreted as a treatment score. This narrative review was informed by dated searches of PubMed/MEDLINE, the Cochrane Library, and OpenAlex through 29 July 2026, followed by a targeted update on 30 July 2026. It considers HF with reduced, mildly reduced, and preserved ejection fraction together with AF timing, burden, ventricular-rate exposure, myocardial substrate, and reversibility. Early rhythm control may be particularly relevant when AF is recent or temporally associated with ventricular dysfunction, symptoms, decompensation, or inadequate cardiac resynchronization therapy delivery. Evidence supporting catheter ablation is most direct in suspected AF-mediated cardiomyopathy and selected HFrEF populations, whereas evidence in HFpEF more consistently supports symptom relief, improved exercise hemodynamics, and AF-burden reduction than mortality reduction. Pulmonary vein isolation remains the procedural foundation. Radiofrequency, cryoballoon, and pulsed-field ablation are effective in broad AF populations, but HF phenotype-specific prognostic superiority has not been established for any energy source. Clinical decisions should reflect the design and directness of the evidence together with expected benefit, rhythm durability, procedural risk, patient-reported outcomes, stroke prevention, guideline-directed HF therapy, risk-factor management, and patient preference. Full article

Background: The Heart Rate Recovery Index (HRRI), derived from post-exercise heart rate recovery (HRR), reflects autonomic function and cardiovascular performance. Whether HRRI reflects early myocardial dysfunction and left atrial remodelling in heart failure with preserved ejection fraction (HFpEF) has not been previously examined. The H₂FPEF score, which integrates clinical and echocardiographic parameters, is used to assess the likelihood of HFpEF. This study investigates the relationship between HRRI, H₂FPEF score, and echocardiographic markers of longitudinal systolic function, including mitral annular plane systolic excursion (MAPSE), as well as left atrial volume index (LAVI), in patients with preserved left ventricular ejection fraction. Methods: A prospective observational study included 241 patients referred for cardiac exercise testing at the Institute of Cardiovascular Diseases Timisoara and the Clinical County Hospital of Sibiu. HRRI was calculated as the ratio of heart rate acceleration time (AT) to deceleration time (DT) during exercise testing. A comprehensive echocardiographic assessment was performed on all patients. Statistical analysis involved univariate testing and multivariable logistic regression with stepwise selection. Results: HRRI was significantly lower in HFpEF patients compared with those without heart failure (1.97 ± 0.66 vs. 2.73 ± 1.08, p < 0.01). HRRI correlated significantly with exercise performance, age, H₂FPEF score, and echocardiographic markers of diastolic and longitudinal systolic dysfunction. ROC analysis identified an HRRI cut-off value of 2.25 for HFpEF detection (AUC = 0.748), while HRRI remained significantly associated with HFpEF after adjustment for the covariates included in the model. The combined HRRI–H₂FPEF score improved diagnostic discrimination compared with the H₂FPEF score alone (AUC 0.897 vs. 0.858), achieving an overall classification accuracy of 82.2%. Conclusions: In our study, HRRI is significantly reduced in HFpEF and distinguishes patients with and without heart failure. It shows associations with echocardiographic markers of diastolic and longitudinal systolic dysfunction, exercise capacity, and H₂FPEF score. Full article

The right ventricle has been considered by many clinicians to be the “forgotten chamber” of the heart. In this narrative review of the literature, we aim to examine chemotherapy-induced right ventricular failure. We will discuss the clinical significance of the subject, the effects of chemotherapy on the heart, and why it is crucial to take a closer look at the right ventricle. We will present key aspects of the anatomy and physiology of the right ventricle and how it differs from the left ventricle. Furthermore, this review explains the mechanisms behind chemotherapy-induced right ventricular dysfunction, strategies for assessing the right ventricle, recent advancements in cardiac imaging, available treatment options, and future directions in therapeutic management. Full article

Cardiac amyloidosis (CA) is an infiltrative cardiomyopathy caused by extracellular deposition of misfolded proteins, most commonly immunoglobulin light chains (AL) or transthyretin (ATTR). Once considered a rare disease, CA is increasingly recognised due to improved diagnostic strategies and the availability of disease-modifying therapies. Early diagnosis is crucial, as treatment efficacy and clinical outcomes are strongly influenced by the stage of cardiac involvement. Multimodality cardiac imaging plays a central role in the diagnostic pathway, risk stratification, and evaluation of therapeutic response in CA. Echocardiography represents the first-line imaging modality and is essential for raising clinical suspicion through the identification of characteristic structural and functional abnormalities, including ventricular wall thickening, diastolic dysfunction, and distinctive strain patterns. Bone scintigraphy has revolutionised the non-invasive diagnosis of ATTR-CA, allowing accurate identification of transthyretin-related disease in the absence of monoclonal gammopathy, which needs to be excluded via serum and urinary immunofixation. Cardiovascular magnetic resonance provides advanced tissue characterisation through late gadolinium enhancement and quantitative mapping techniques, enabling detection of early myocardial involvement and robust prognostic stratification. Emerging imaging modalities, including dual-energy (spectral) computed tomography and positron emission tomography tracers, show promise in myocardial amyloid quantification and subtype differentiation, although their role is still evolving. Integration of imaging findings with clinical and laboratory parameters allows comprehensive disease assessment, facilitating early diagnosis, guiding therapeutic decisions, and improving risk stratification. This review summarises the current role of multimodality imaging in CA, highlighting its contribution from early detection to prognostic evaluation and monitoring of treatment efficacy, with particular emphasis on the emerging role of quantitative imaging in monitoring treatment response. Full article

Background/Objectives: This study aimed to evaluate the prognostic role of the extracellular volume (ECV) assessed by cardiac magnetic resonance imaging (MRI) in relation to systolic dysfunction and unfavorable remodeling of the left ventricular (LV) at 24 weeks after myocardial infarction (MI) and revascularization. Methods: The study included 154 patients aged 56 ± 8 years who had been diagnosed with their first MI. Cardiac MRI was performed at 7–10 days and after 24 weeks, including assessment of indexed volumes, LV ejection fraction (LVEF), ECV, and patterns of ischemic and reperfusion injury. The study is registered in the international clinical trials registry with the number NCT04347434 (ClinicalTrials.gov). Results: Patients were divided into two groups after 24 weeks: group 1 (n = 24) with LVEF < 50% and group 2 (n = 130) with LVEF ≥ 50%. At 7–10 days, the scar mass in group 1 was 58.5 (39.5; 69.8) g vs. 17.1 (9.2; 29.7) g in group 2 (p < 0.001); microvascular obstruction was present in 23 cases (95.8%) vs. 55 (42.3%) (p < 0.001). After 24 weeks, inter-group differences increased (p < 0.05). Global ECV and remote myocardial ECV were significantly higher in patients with LVEF < 50% both at 7–10 days and after 24 weeks compared to those with LVEF ≥ 50% (p < 0.05). Infarct zone ECV did not differ between groups. Systolic dysfunction after 24 weeks was predicted by global ECV > 38.3% (p < 0.001) and remote myocardial ECV > 33.6% (p = 0.008). Predictors of an increase in end-diastolic volume index > 12% after 24 weeks in the subgroup of patients with initial systolic dysfunction were global ECV > 42.8% (p = 0.017) and remote myocardial ECV > 35.6% (p = 0.012). Conclusions: Global ECV and ECV of the remote myocardium, which exceed a certain level established by a cardiac MRI in the acute stage of MI, are among the predictors of LVEF < 50% and unfavorable LV remodeling in the medium term. Full article

Heart failure with preserved ejection fraction (HFpEF) is a type of heart failure in which the ejection fraction remains within the normal range (≥50%); however, patients still experience typical symptoms of heart failure. One of the most common manifestations in this population is exercise intolerance, which in some cases may be the only presenting symptom. Exercise intolerance refers to a reduced capacity to perform physical activity. Several processes, including impaired cGMP–PKG signaling, increased collagen deposition, endothelial dysfunction, increased arterial stiffness, pulmonary hypertension, and vascular remodeling, contribute to the pathophysiology of HFpEF. The disruption of these fundamental physiological processes significantly impairs exercise capacity, leading to attenuated increases in heart rate, stroke volume, and/or contractility, along with abnormal ventricular–vascular coupling during exertion. When EI is suspected, a spectrum of diagnostic modalities—from simple, low-cost tools such as the 6 min walk test to advanced imaging—can be used to evaluate its presence and its association with HFpEF. When EI in HFpEF is diagnosed, management should focus on addressing this limitation to improve quality of life and reduce morbidity and mortality. Exercise training and pharmacological therapies, such as SGLT2 inhibitors, may be beneficial in this population. In conclusion, EI is a common manifestation of HFpEF that significantly impacts patients’ quality of life. Understanding its underlying mechanisms and addressing it appropriately are essential to improving patient outcomes. Full article

Background: Fetal cardiac rhabdomyomas are strongly associated with tuberous sclerosis complex (TSC). Although many remain asymptomatic and regress spontaneously, large tumors may cause ventricular inflow or outflow obstruction, arrhythmia, impaired ventricular function, pericardial effusion, hydrops fetalis and fetal demise. Transplacental mammalian target of rapamycin (mTOR) inhibition has emerged as a potential rescue therapy. Methods: We performed a narrative review of published reports on prenatal sirolimus or everolimus therapy for fetal cardiac rhabdomyomas in suspected or confirmed TSC. Data was extracted on treatment indication, gestational age at initiation, treatment duration, fetal echocardiographic response, maternal adverse effects, delivery and postnatal outcome. Results: Available evidence consists predominantly of case reports, small case series and retrospective cohorts; no prospective controlled trials were identified. Treatment was generally initiated for progressive or hemodynamically significant disease, particularly ventricular inflow or outflow obstruction, worsening valve regurgitation, arrhythmia, pericardial effusion, ventricular dysfunction or hydrops. Therapy was usually started in the late second or third trimester and continued until hemodynamic stabilization, delivery or planned transition to neonatal treatment. Most reports described tumor regression within 1–3 weeks, accompanied by improved cardiac function and high perinatal survival. However, rebound growth after treatment withdrawal, persistent arrhythmic risk and limited long-term safety data remain important concerns. Conclusions: Prenatal mTOR-inhibitor therapy should be considered an individualized rescue or stabilization strategy for fetuses with life-threatening or progressive cardiac compromise, rather than routine treatment for all fetal rhabdomyomas. Management should be multidisciplinary and guided by fetal hemodynamics, treatment response, maternal tolerance and gestational age. Full article

Background: Severe aortic stenosis (AS) remains the most prevalent primary valvular disease in Europe and North America, causing heart failure (HF), with pulmonary hypertension (PH) occurring in up to 75% of symptomatic patients. The coexistence of AS and atrial septal defect (ASD) is rare and may generate dual mechanisms of PH, complicating both diagnosis and management. Case summary and review: We report a 78-year-old patient with symptomatic severe AS and right heart failure, in whom an unrecognized secundum ASD with significant left-to-right shunt was identified as a major contributor to persistent HF and right ventricular (RV) dysfunction. Due to prohibitive surgical risk, a staged interventional strategy was decided: transcatheter aortic valve implantation (TAVI), followed by cardiac catheterization and ultimately by percutaneous ASD closure. Marked clinical benefit with the reduction of the RV dimensions and improved systolic function were observed at one year follow-up. A focused review of the literature was conducted to contextualize the pathophysiological mechanisms, diagnostic challenges, and therapeutic strategies in patients with coexisting AS and ASD. Conclusions: This case emphasizes the importance of comprehensive hemodynamic assessment in AS complicated by PH and HF, particularly in the presence of congenital anomalies such as ASD. Full article

Heart failure with preserved ejection fraction (HFpEF) represents an increasingly prevalent clinical syndrome, driven by population ageing and the growing burden of cardiometabolic comorbidities, and is associated with significant morbidity and mortality. Due to its heterogeneous pathophysiology and the frequent absence of overt structural abnormalities, early diagnosis and accurate risk stratification remain challenging. In the current era of emerging disease-modifying therapies, the identification of sensitive imaging markers able to detect early myocardial dysfunction and refine patient characterization has become increasingly important. Speckle-tracking echocardiography has emerged as a valuable tool for the comprehensive evaluation of HFpEF, allowing the assessment of subclinical myocardial impairment beyond conventional parameters. Left ventricular global longitudinal strain (LV-GLS) identifies subtle systolic dysfunction despite preserved left ventricular ejection fraction (LVEF) and provides incremental diagnostic and prognostic information. Accordingly, LV-GLS has been incorporated into contemporary diagnostic algorithms and may represent a promising marker for monitoring disease progression and therapeutic response. Beyond the left ventricle (LV), left atrial (LA) strain has gained increasing relevance as a marker of atrial myopathy and elevated filling pressures. Left atrial reservoir strain (LARS) detects early atrial dysfunction before overt structural remodelling, improves the identification of HFpEF in patients with unexplained dyspnoea, and provides additional prognostic information, including prediction of atrial fibrillation and thromboembolic risk. Moreover, right ventricular free-wall longitudinal strain (RV-FWLS) allows early recognition of right ventricular involvement and has shown important prognostic implications, particularly in relation to pulmonary vascular dysfunction and exercise intolerance. Overall, a multi-chamber strain-based approach may improve HFpEF diagnosis, phenotyping, and risk stratification, supporting a transition toward a more personalized management strategy. Further prospective studies are needed to define the role of strain imaging in guiding therapeutic decisions and monitoring treatment response. Full article

Chimeric antigen receptor T-cell therapy and bispecific T-cell engagers have transformed treatment of relapsed and refractory hematologic malignancies, achieving unprecedented response rates. However, their clinical adoption has revealed a complex spectrum of cardiovascular toxicities, differing in frequency and pattern between the two technologies. Manifestations range from common hemodynamic perturbations—hypotension and tachycardia—to severe events, including malignant arrhythmias, left ventricular dysfunction, myocardial infarction, and cardiogenic shock. These complications seem to have different pathophysiological pathways that are yet to be completely understood: on the one hand, they are frequently intertwined with cytokine release syndrome, the hallmark immune complication of T-cell-redirecting therapies, as seen with chimeric antigen receptor T-cell therapy; on the other, a substantial proportion of cardiovascular events—particularly with bispecific T-cell engagers—occur independently of cytokine release syndrome. Proposed cardiotoxic mechanisms include on-target, off-tumor antigen recognition and consequent damage; interleukin-6-driven systemic inflammation; and off-target, off-tumor antigen cross-reactivity. Effective management requires proactive baseline risk stratification, serial cardiac biomarker monitoring, and timely immunosuppressive intervention—primarily tocilizumab—to mitigate cytokine release syndrome-driven injury. Despite rapid clinical expansion, critical gaps remain: long-term cardiovascular outcomes are poorly characterized, validated surveillance protocols are lacking, and cardiovascular endpoints are rarely included in pivotal trials. This narrative review appraises the pathophysiology, clinical spectrum, and management of cardiovascular toxicities associated with these therapies, aiming to define this emerging cardio-oncology frontier, inform multidisciplinary care frameworks and propose a clinical management algorithm. Full article

Background: Coronary artery calcium score (CACS) is a well-established marker of coronary atherosclerotic burden and cardiovascular risk. While its association with left ventricular dysfunction has been extensively investigated, the relationship between CACS and right ventricular (RV) function remains insufficiently explored. This study aimed to evaluate the association between CACS and echocardiographic RV function parameters and to explore the discriminatory ability of CACS for identifying patients meeting predefined echocardiographic thresholds of RV dysfunction in patients with suspected stable coronary artery disease (CAD). Methods: This retrospective observational study included 96 patients who underwent coronary computed tomography angiography and transthoracic echocardiography within a 3-month interval. CACS was calculated using the Agatston method. RV function was assessed using tricuspid annular plane systolic excursion (TAPSE), right ventricular fractional area change (RV-FAC), and tissue Doppler-derived systolic velocity (S′). Correlation analyses, subgroup comparisons, multivariable linear regression, receiver operating characteristic (ROC) analyses, decision curve analysis (DCA), and calibration analyses were performed. Results: CACS demonstrated significant inverse correlations with TAPSE (r = −0.42, p < 0.001), RV-FAC (r = −0.36, p = 0.002), and S′ (r = −0.31, p = 0.006). Patients with higher CACS values exhibited progressively impaired RV systolic function. In multivariable regression analyses, higher CACS remained associated with lower TAPSE, RV-FAC, and S′ after adjustment for age, hypertension, and diabetes mellitus. Exploratory ROC analyses demonstrated moderate discriminatory performance, with AUC values ranging from 0.70 to 0.76. DCA suggested a potential net benefit across a range of threshold probabilities, while bootstrap calibration analysis demonstrated acceptable agreement between predicted and observed outcomes. Conclusions: In this retrospective single-center cohort, higher CACS values were associated with lower conventional echocardiographic measures of right ventricular systolic function. However, given the selected study population, relatively small sample size, limited clinical and instrumental characterization, potential residual confounding, and absence of external validation, these findings should be considered exploratory. The present data do not establish CACS as a clinical predictor of right ventricular dysfunction or support its use for clinical decision-making. Full article

Background: Left ventricular systolic dysfunction (LVSD) is a precursor to heart failure arising from diverse cardiac conditions. Although echocardiography remains the reference standard for LVSD diagnosis, its routine use in the emergency department (ED) may be constrained by cost, time, equipment availability, and the need for specialized expertise. We evaluated the diagnostic performance of an artificial intelligence-based electrocardiogram analysis model (AI-ECG model) for detecting LVSD in patients presenting to the ED. Methods: This retrospective observational study included patients treated at a single tertiary hospital between 2020 and 2022 who underwent 12-lead electrocardiography within 24 h of ED admission and echocardiography within 30 days. Electrocardiographic data were analyzed using AiTiALVSD version 1.00.00, with a predefined cutoff score of 9.7 used to classify patients as being at high or low risk of LVSD. Diagnostic performance was assessed using standard discrimination and classification metrics. Results: Among 4529 included patients, 531 had LVSD. The AI-ECG model demonstrated high discrimination, with an area under the receiver operating characteristic curve (AUROC) of 0.934 (95% confidence interval [CI]: 0.923–0.945). Performance remained robust in patients with a shock index ≥ 0.9 (n = 453; AUROC, 0.895; 95% CI: 0.854–0.937) and in those with hypotension (n = 75; AUROC, 0.885; 95% CI: 0.786–0.984). Conclusions: The AI-ECG model accurately identified LVSD in ED patients in this cohort despite heterogeneous acquisition conditions and retained good discrimination in hemodynamically unstable subgroups, although findings in the smaller hypotensive subgroup should be interpreted as exploratory. Full article