Search Results (108)

Introduction: Chronic kidney disease (CKD) is associated with a high risk of cardiovascular complications and mortality. This study aimed to assess the relationship between the diurnal blood pressure (BP) profile, progression of CKD, and hypertension-mediated organ damage (HMOD) in patients with CKD stages 1–3 during a 6-month observation period. Methods: Eighty-seven patients with CKD stages 1–3 underwent 24 h ambulatory blood pressure monitoring (ABPM), echocardiography, carotid intima-media thickness (IMT) assessment, and aortic pulse wave velocity (PWV) measurement at baseline and after 6 months. Serum creatinine and the estimated glomerular filtration rate (eGFR) were evaluated using the CKD-EPI formula. Results: Based on ABPM, patients were classified as dippers/extreme dippers (D/ED, 35.6%), non-dippers (ND, 47.2%), and reverse dippers (RD, 17.2%). At follow-up, the RD group showed a significant decline in the eGFR and a lower left ventricular ejection fraction compared to D/ED. IMT values were consistently higher in RD than in D/ED at baseline and follow-up. No significant differences in PWV were observed. Conclusions: An abnormal diurnal BP profile is common in patients with CKD stages 1–3. The “reverse dipper” profile is associated with faster CKD progression, more advanced vascular remodeling, and reduced left ventricular function. The results of our study support the role of ABPM as a useful tool in assessing risk in the early stages of CKD, providing additional prognostic information beyond office blood pressure measurements. Limitations: The relatively small sample size, short follow-up period, lack of detailed data on treatment modifications, and absence of orthostatic BP assessment may limit the interpretation and generalizability of the results. Full article

Background: Left ventricular (LV) mechanics assessed by speckle-tracking echocardiography provides sensitive markers of cardiac adaptation to exercise. Different training modalities—endurance, high-intensity interval training (HIIT), and acute exercise tests—impose distinct hemodynamic loads, yet their comparative effects on LV deformation remain unclear. Importantly, acute and chronic endurance exposures may elicit divergent myocardial responses that must be interpreted separately. Methods: A systematic search of PubMed, Scopus, and EMBASE (through September 2025) identified studies evaluating LV mechanics in response to endurance, HIIT, or acute exercise among healthy or recreationally active individuals. Echocardiographic parameters of strain and torsion were extracted, and methodological quality was appraised using the NIH Quality Assessment Tool. Results: Twenty-three studies (859 participants) met inclusion criteria. Acute prolonged endurance exercise—particularly marathon and ultra-endurance events—was associated with transient, fully reversible reductions in global longitudinal, circumferential, and radial strain and torsion, despite preserved ejection fraction, reflecting short-term myocardial fatigue rather than maladaptive remodeling. In contrast, chronic endurance training maintained or improved LV mechanics without evidence of dysfunction, while HIIT interventions consistently enhanced LV systolic strain and rotational indices across diverse age groups and sexes, reflecting improved contractile efficiency and physiological remodeling. Acute exercise produced heterogeneous, load-dependent strain responses, with isometric stress increasing regional strain and maximal exertion inducing temporary global reductions. Between-study heterogeneity was moderate, methodological quality generally good, and small-study effects varied by modality, being most evident in endurance studies, borderline for HIIT, and limited for acute tests due to sample size. Conclusions: Acute endurance exercise produces transient, reversible LV deformation changes, whereas chronic endurance training preserves mechanical efficiency. HIIT reliably enhances systolic strain and torsional mechanics, and acute exercise elicits variable but physiologically meaningful responses. These findings clarify that transient post-race strain reductions reflect physiological fatigue, not chronic maladaptation, and underscore the modality-specific nature of myocardial adaptation to exercise. Full article

Background/Objectives: Sodium glucose co-transporter 2 inhibitors (SGLT2is) improve outcomes in heart failure; however, data in left ventricular non-compaction cardiomyopathy (LVNC) patients are limited. We sought to analyze the clinical effects of the SGLT2is dapagliflozin and empagliflozin in patients with LVNC. Methods: Thirty consecutive LVNC patients diagnosed by CMR were prospectively enrolled. Clinical, biochemical and echocardiography data were obtained at the initiation of the SGLT2is and at the 12-month follow-up. All patients were on stable guideline-directed medical therapy. A response to SGLT2i therapy was defined as an improvement in LVEF ≥ 5% at 12 months. Results: Of the 30 enrolled patients, 25 were male, with a mean age of 49 ± 16 years and few comorbidities. Dapagliflozin 10 mg was prescribed to 23 patients and empagliflozin 10 mg to 7 patients. Five patients experiened an adverse event during follow-up (one sudden cardiac death; four heart transplantations or LVAD implantations). During follow-up, significant improvements were observed in LVEF (32.1 ± 6.9% vs. 43.5 ± 9.7%; p = 0.003), LVOT VTI (14.8 ± 6.5 cm vs. 17.6 ± 3.3 cm; p = 0.008), E/e′ (14.8 ± 4.7 vs. 10.0 ± 4.1; p < 0.001), and TAPSE (2.0 ± 0.4 cm vs. 2.3 ± 0.4 cm; p = 0.012). NT-proBNP levels decreased significantly (2025 ± 2198 pg/mL vs. 582 ± 803 pg/mL; p = 0.005). Eighteen patients responded favorably to SGLT2i therapy (Group A), whereas seven showed no significant LVEF improvement (Group B). The groups did not differ significantly in age, sex, baseline creatinine, or bilirubin. Compared to Group B, Group A had a smaller baseline LV end-diastolic diameter (6.3 ± 0.8 cm vs. 7.1 ± 0.9 cm; p = 0.025) and lower NT-proBNP levels (1720 ± 1662 pg/mL vs. 4527 ± 4397 pg/mL; p = 0.02). Conclusions: In patients with LVNC, SGLT2i therapy is associated with significant reverse remodeling and functional improvement. Benefits may be greater in those with less advanced disease. Full article

Background: Left ventricular hemodynamic forces (LV HDFs) are altered in myocardial dysfunction. While infarct location and size influence post-ST-segment elevation myocardial infarction (STEMI) remodeling, their specific effects on HDFs remain unclear. This study investigated how infarct location and size impact left ventricular HDFs and assessed HDFs’ prognostic value for predicting subsequent heart failure (HF) in STEMI patients. Methods: In this retrospective study, 275 STEMI patients underwent cardiac magnetic resonance (CMR) 3–7 days after primary percutaneous coronary intervention. HDFs were derived from routine CMR cine images. Patients were stratified by infarct location (anterior vs. non-anterior) and median infarct size (IS). Key parameters—apical–basal (A-B) and lateral-septal (L-S) forces, their ratio, force direction angle (φ), and force reversal during systolic–diastolic transition—were compared. The primary endpoint was new-onset congestive HF during follow-up. Results: Compared to non-anterior STEMI, anterior STEMI showed significantly impaired A-B and L-S HDFs throughout the cardiac cycle (all p < 0.05) and was independently associated with force reversal (OR 2.31, 95% CI: 1.05–5.07). Larger IS correlated with reduced A-B HDFs and altered force distribution (increased L-S/A-B ratio, decreased φ). Force reversal predicted HF (HR: 2.10, 95% CI: 1.22–3.62) and provided incremental prognostic value beyond left ventricular ejection fraction (LVEF) alone (C-statistic: LVEF 0.680 vs. LVEF + force reversal 0.770, p = 0.034). Conclusions: Anterior infarction causes global HDF impairment and force reversal, while larger IS primarily reduces longitudinal forces and disrupts force distribution. Force reversal predicts subsequent HF and enhances prognostic value beyond LVEF. Full article

Takotsubo Cardiomyopathy (TTC), often referred to as stress-induced or “broken heart” syndrome, is characterized by transient left ventricular dysfunction predominantly involving apical hypokinesia and basal hyperkinesia in the absence of obstructive coronary artery disease. Traditionally viewed as an acute and reversible phenomenon, accumulating evidence suggests that TTC may emerge from a preexisting myocardial substrate shaped by chronic stress and hemodynamic loading. Basal Septal Hypertrophy (BSH), a morphological finding commonly observed in elderly, hypertensive, or emotionally stressed individuals, has been increasingly recognized in patients with TTC. This hypertrophic pattern, often accompanied by dynamic contractile gradients and regional perfusion mismatch, reflects a broader adaptive remodeling process conceptualized as Stressed Heart Morphology (SHM). SHM encompasses the structural and functional myocardial responses to cumulative neurohormonal and mechanical stress, with BSH representing a key imaging marker within this spectrum. Advanced echocardiographic techniques, such as tissue Doppler imaging, speckle-tracking strain analysis, and stress echocardiography, consistently reveal overlapping features between SHM and TTC, including basal hyperkinesis, septal thickening, and inducible left ventricular outflow tract obstruction. These findings support a continuum in which SHM serves as a predisposing substrate for TTC, representing a stress-provoked clinical expression within a unified myocardial stress–response framework. Full article

Left ventricular hypertrophy (LVH) refers to the pathological thickening of the myocardial wall and is strongly associated with several adverse cardiac outcomes and sudden cardiac death. While the biomechanical drivers of LVH are well established, growing evidence points to a critical role for cardiac and systemic metabolism in modulating hypertrophic remodeling and disease pathogenesis. Despite the efficiency of fatty acid oxidation (FAO), LVH hearts preferentially increase glucose uptake and catabolism to drive glycolysis and oxidative phosphorylation (OXPHOS). The development of therapies to increase and enhance LFCA FAO is underway, with promising results. However, the mechanisms of systemic metabolic states and LCFA dynamics in the context of cardiac hypertrophy remain incompletely understood. Further, it is unknown to what extent cardiac metabolism is influenced by whole-body energy balance and lipid profiles, despite the common occurrence of lipotoxicity in LVH. In this study, we measured whole-body and cellular respiration along with analysis of lipid and glycogen stores in a mouse model of LVH. We found that loss of the cardiac-specific gene, myosin-binding protein C3 (Mybpc3), resulted in depletion of adipose tissue, decreased mitochondrial function in skeletal muscle, increased lipid accumulation in both the heart and liver, and loss of whole-body metabolic flux. We found that supplementation of exogenous LCFAs boosted LVH mitochondrial function and reversed cardiac lipid accumulation but did not fully reverse the hypertrophied heart nor systemic metabolic phenotypes. This study indicates that the LVH phenotype caused systemic metabolic rewiring in Mybpc3^−/− mice and that exogenous LCFA supplementation boosted mitochondrial function in both cardiac and skeletal muscle. Full article

Background/Objectives: Atrial fibrillation (AF) is the most common sustained arrhythmia, with catheter ablation outcomes differing significantly between paroxysmal and persistent forms. While pulmo-nary vein isolation (PVI) remains the cornerstone of ablation, persistent AF is often associ-ated with atrial remodeling and non-pulmonary vein triggers, reducing procedural success rates and necessitating repeat interventions. However, in selected patients with minimal atrial substrate, a single PVI may achieve durable rhythm control. This case report illus-trates such a scenario in a young patient with persistent AF and tachyarrhythmia-induced cardiomyopathy (TIC). Methods: A 42-year-old previously healthy male presented with newly diagnosed persistent AF complicated by TIC and heart fail-ure (left ventricular ejection fraction [LVEF] 25%). Despite rate control, anticoagulation, guideline-directed heart failure therapy, amiodarone pretreatment, and two failed electrical cardioversions, the patient remained symptomatic. Elec-troanatomic mapping was performed to assess atrial substrate prior to radiofrequency ablation. Results: Mapping revealed no extensive low-voltage zones, indicating absence of significant atrial fibrosis. During ablation, si-nus rhythm was restored spontaneously with a single application targeting the infero-posterior aspect of the right infe-rior pulmonary vein. No additional arrhythmogenic substrate was identified. The patient maintained sinus rhythm throughout 14 months of follow-up, with marked clinical improvement, normalization of LVEF (55%), regression of atrial and ventricular enlargement, and resolution of heart failure symptoms. Quality of life, assessed by the ASTA question-naire, improved from 24 to 0 points. Conclusions: This case highlights that even in therapy-resistant persistent AF with severe structural and functional cardiac impairment, arrhythmia may be driven by discrete pulmonary vein-dependent mechanisms. Careful patient selection, particu-larly in younger individuals without advanced atrial remodeling, can identify those in whom PVI alone achieves durable rhythm control and reverse cardiac remodeling. Full article

Anthracyclines are widely used chemotherapeutic agents with proven efficacy against a broad range of malignancies, but their clinical utility is limited by a well-documented, dose-dependent cardiotoxicity. While this toxicity has traditionally been attributed to direct cardiomyocyte injury, emerging evidence highlights the pivotal role of cardiac fibroblasts (CFs) in the development and progression of anthracycline-induced cardiotoxicity. This review examines the diverse effects of anthracycline focusing on doxorubicin (DOX) and CFs across the temporal phases of cardiac injury. DOX activates fibroblast-driven extracellular matrix remodeling and promotes fibrosis through enhanced collagen production and the induction of cellular senescence, thereby exacerbating early myocardial inflammation and dysfunction. Clinically, anthracycline cardiotoxicity may present as acute (within days), subacute (within weeks), or chronic progressive forms manifesting either early (within one year) or late (up to decades post-treatment). While early manifestations may be reversible with timely detection and management, late-phase cardiotoxicity is often irreversible, characterized by declining left ventricular ejection fraction and heart failure. A deeper understanding of the molecular and cellular contributions of CFs may uncover novel therapeutic targets to prevent or attenuate anthracycline-related cardiac damage. Full article

Primary aldosteronism (PA), the most common cause of secondary hypertension, is increasingly recognized as an independent driver of adverse cardiac remodeling, mediated through mechanisms beyond elevated blood pressure alone. Chronic aldosterone excess leads to myocardial fibrosis, left ventricular hypertrophy, and diastolic dysfunction via mineralocorticoid receptor activation, oxidative stress, inflammation, and extracellular matrix dysregulation. These changes culminate in a distinct cardiomyopathy phenotype, often underrecognized in early stages. Multimodality cardiac imaging, led primarily by conventional and speckle-tracking echocardiography, and complemented by exploratory cardiac magnetic resonance (CMR) techniques such as T1 mapping and late gadolinium enhancement, enables non-invasive assessment of structural, functional, and tissue-level changes in aldosterone-mediated myocardial damage. While numerous studies have established the diagnostic and prognostic relevance of imaging in PA, several gaps remain. Specifically, the relative sensitivity of different modalities in detecting subclinical myocardial changes, the long-term prognostic significance of imaging biomarkers, and the differential impact of adrenalectomy versus medical therapy on cardiac reverse remodeling require further clarification. Moreover, the lack of standardized imaging-based criteria for defining and monitoring PA-related cardiomyopathy hinders widespread clinical implementation. This narrative review aims to synthesize current knowledge on the pathophysiological mechanisms of aldosterone-induced cardiac remodeling, delineate the strengths and limitations of existing imaging modalities, and critically evaluate the comparative effects of surgical and pharmacologic interventions. Emphasis is placed on early detection strategies, identification of imaging biomarkers with prognostic utility, and integration of multimodal imaging into clinical decision-making pathways. By outlining current evidence and highlighting key unmet needs, this review provides a framework for future research aimed at advancing personalized care and improving cardiovascular outcomes in patients with PA. Full article

Background: Sex-related differences in left ventricular (LV) reverse remodeling following ST-segment elevation myocardial infarction (STEMI) remain underexplored. We aimed to investigate predictors of reverse remodeling and its association with clinical outcomes, with a focus on sex-specific differences. Methods: We enrolled 253 STEMI patients (91 women, 28%) and assessed echocardiographic parameters at baseline and six months. LV reverse remodeling was defined as a ≥15% reduction in LV end-diastolic volume (LVEDV). Multivariate logistic regression identified independent predictors of remodeling. Clinical outcomes were evaluated over a median follow-up of 17 months (IQR 14–22 months), including major adverse cardiac events (MACEs). Kaplan–Meier and Cox regression analyses were performed. Results: Reverse remodeling occurred in 43% of patients and was more frequent in men than women (47% vs. 37%, p = 0.04). Male sex (OR 0.30; 95% CI: 0.14–0.65; p < 0.0001) and baseline global work efficiency (GWE) (OR 1.64; 95% CI: 1.45–1.85; p < 0.0001) were independent predictors. Men exhibited greater reductions in LVEDV, greater improvements in LV ejection fraction, and superior myocardial work indices. Over the follow-up, patients with reverse remodeling had significantly lower MACE rates compared to those without (10% vs. 24%, p < 0.01). Cox regression demonstrated that reverse remodeling was associated with a reduced risk of MACEs (HR 0.318; 95% CI: 0.181–0.557; p < 0.0001). Conclusions: LV reverse remodeling after STEMI is associated with improved clinical outcomes and is influenced by sex-specific differences. Baseline myocardial work indices, particularly GWE, are strong predictors of reverse remodeling. Men demonstrated a more favorable remodeling profile and myocardial recovery compared to women. Full article

Feline hyperthyroidism is the most frequent endocrinopathy in adult and senior cats, frequently leading to cardiac changes characterised by a hypertrophic cardiomyopathy (HCM) phenotype, which may partially reverse with appropriate treatment. However, the structural and molecular alterations in the myocardium can persist and closely resemble those observed in hypertrophic cardiomyopathy. Despite this clinical overlap, protein expression patterns in the hearts of hyperthyroid cats remain poorly understood. This study aimed to evaluate the myocardial expression of desmin, a key contractile protein, as well as calreticulin and interleukin-10 proteins involved in cardiac remodelling and response to injury. Left ventricular samples were obtained from 16 hyperthyroid cats, 12 cats with HCM, and 10 healthy controls. Immunohistochemical staining was performed to assess the expression patterns of the selected proteins. Our findings revealed that, despite median left ventricular dimensions not being significantly different from ones observed in healthy animals, cats with hyperthyroidism exhibited similar alterations in desmin and interleukin-10 expression to those seen in HCM-affected cats. These changes were associated with cardiomyocyte degeneration and coronary artery narrowing, suggesting a shared pathway of myocardial injury independent of the primary disease. Full article

Background/Objectives: Surgical aortic valve replacement effectively relieves left ventricular afterload and promotes reverse remodeling in patients with severe aortic stenosis. The Perceval prosthesis offers a hybrid approach, combining complete annular decalcification with sutureless deployment. This design allows for reduced operative times and potentially larger effective orifice areas. However, comparative data with conventional stented bioprosthetic valves remain limited, particularly regarding reverse remodeling, hemodynamic performance, and long-term clinical outcomes. Methods: In this retrospective cohort study, 115 patients underwent aortic valve replacement with either the Perceval valve (n = 44) or conventional stented bovine pericardial valves (n = 71). Results: The Perceval group showed a 100% procedural success rate with no in-hospital mortality, significantly shorter cardiopulmonary bypass and cross-clamp times, larger effective orifice areas, and a lower incidence of patient–prosthesis mismatch. Both groups demonstrated favorable left ventricular mass regression and reverse remodeling. The rates of paravalvular leakage, permanent pacemaker implantation, and redo aortic valve replacement were comparable between groups. Multivariate Cox regression identified the follow-up indexed left ventricular mass as an independent predictor of major adverse cardiac and cerebral events. Conclusions: In this study, the Perceval valve was associated with promising hemodynamic characteristics and procedural efficiencies, particularly in cases with small aortic annuli and during minimally invasive procedures. The valve was associated with reverse ventricular remodeling and clinical outcomes that appeared similar to those of conventional stented bioprostheses. These observations suggest it may represent a potential alternative option for surgical aortic valve replacement in appropriate clinical scenarios. However, randomized control trials are needed to confirm these associations. Full article

Purpose: Although biomarkers of myocardial fibrosis and inflammation have been proposed as potential modulators of response to cardiac resynchronization therapy (CRT), their clinical utility and interaction with echocardiographic parameters remain incompletely understood. This study aims to assess the dynamic changes in these biomarkers, their relationship with echocardiographic variables, and their association with structural response to CRT. Methods: We retrospectively evaluated 86 consecutive patients referred for CRT with symptomatic heart failure, left ventricular (LV) ejection fraction ≤ 35%, QRS width ≥ 130 ms and LBBB morphology. We measured sST-2, Gal-3, NTpro-BNP and eGFR at baseline and after 1 year of CRT. An echocardiographic reduction of LV end-systolic volume ≥ 15% was used to define a patient as a responder to CRT. Results: The mean baseline and follow-up values of Gal-3 (responders: 24.1 [16.8;32] ng/mL, non-responders: 30 [20;39.3] ng/mL, p = 0.03) and sST2 (responders: 28.5 [20;36] ng/mL, non-responders: 34.5 [25;37.7] ng/mL, p = 0.03) were lower in responders than non-responders. Responders showed a significant reduction between baseline and follow-up values of ΔGal-3 (−12.1% vs. −2.5%, p = 0.04), ΔsST2 (−30.8% vs. 2.2%, p < 0.001), ΔNT-proBNP (−16.4% vs. 5.2, p = 0.04) and ΔeGFR (6.7 ± 24.3% vs. -6.3 ± 27.9%, p = 0.03). At the multivariate analyses, baseline Gal-3 [cut-off: 38.5 ng/mL, AUC: 0.63, p = 0.03, (OR 7.13 [1.12;45.41], p = 0.03), together with TAPSE > 17.5 mm (OR 10.86 [3.15;37.44], p < 0.001) significantly correlated with the structural response to CRT in several prediction models. Among echocardiographic parameters, TAPSE remained the strongest predictive factor of positive response to CRT at the univariate and multivariate analyses. Conclusions: In patients with heart failure and reduced ejection fraction undergoing CRT, Gal-3 and TAPSE are significantly associated with a positive structural response to CRT. Full article

Background/Objectives: Cardiovascular diseases are the most prevalent comorbidities in patients with acromegaly (APs). Acromegalic cardiomyopathy is the leading cause of mortality in APs. This study aimed to assess changes in morphology and function of the left heart in naïve APs 12 months after the beginning of acromegaly treatment and to explore the effects of disease activity and body composition parameters on changes in the left heart. Methods: This prospective study involved 34 APs and 34 healthy controls (CON) matched for age, gender, and BMI. DXA and 2D echocardiography were performed at diagnosis and 12 months after the beginning of the treatment. Results: In APs, the prevalence of left ventricular (LV) hypertrophy was 70%. LV mass index (LVMI) was greater in APs compared to CON (124 vs. 86 ± g/m², p < 0.001), but with no difference in size and systolic function of the LV. APs presented with increased left atrium volume (LAVI) and with diastolic dysfunction of the LV. Twelve months after the beginning of acromegaly treatment, IGF-1 levels decreased significantly (p < 0.001), and biochemical control of disease was achieved in 73.52% of APs. We found that in all APs, LAVI and LVMI decreased (all p < 0.05), and diastolic function of the LV improved without changes in systolic function. In multiple analyses, the changes in body surface area (β = −0.444, p < 0.001) and in lean body mass (β = −0.298, p = 0.027) were independent predictors of reverse remodelling of LVMI after the treatment. Conclusions: This study confirmed remodelling reversal of the left heart structure, followed by an improvement in diastolic function in naïve APs 12 months after the beginning of acromegaly treatment. Full article

Background/Objectives: Cardiac resynchronization therapy (CRT) with fusion pacing (“LV only”), also known as fusion-CRT (f-CRT), represents a feasible alternative to cardiac resynchronization therapy (CRT) with biventricular pacing (BiVP), not only in cases of BiVP failure, but also as a primary therapy option due to its potential benefits over traditional CRT. Fusion pacing may be particularly beneficial in selected patients and understanding the structural and functional differences between responders could guide future optimization strategies. This study provides a descriptive comparison between super-responders (SRs) and non-super-responders (NSRs) undergoing fusion-CRT. Methods: Patients with RA/LV-only pacing systems or biventricular CRT systems operating predominantly in LV-only pacing mode due to intrinsic RV conduction were included. A follow-up protocol was conducted for all patients at 6 months and then annually. Data from the most recent follow-up were used for statistical analysis. Super-responders (SRs) were those with substantial reverse remodeling, quantified by a ≥30% reduction in LVESV and a stable LVEF of ≥45% at follow-up. Although SRs were defined based on these reverse remodeling criteria, separate analyses of additional echocardiographic parameters (e.g., left atrial dimensions) were performed to independently assess the broader impact of fusion-CRT on cardiac structure and function. Results: Among 71 patients, 55 were non-super-responders (NSRs) and 16 were super-responders (SRs), with a mean follow-up of 43.2 months. SRs were predominantly female and had smaller left ventricular (LV) dimensions: LVEDd (6.30 cm vs. 6.80 cm, p = 0.02), LVEDV (185 mL vs. 240 mL, p = 0.03), LVESV (132.5 mL vs. 175 mL, p = 0.03), and a higher LVEF (p = 0.03). The follow-up LVEF was positively correlated with changes in LVESV (ρ = 0.557, p < 0.001), but not with NYHA class changes (ρ = 0.184, p = 0.125). Larger baseline LV and left atrial (LA) volumes were associated with a reduced follow-up LVEF (LVESV: ρ = −0.426, p < 0.001; LVEDV: ρ = −0.394, p < 0.001; LAv: ρ = −0.374, p = 0.001). Both groups showed improvement in the NYHA class (p < 0.001, p = 0.007). MR improved significantly in SRs (p = 0.02) and worsened slightly in NSRs (p = 0.13), while TR worsened significantly in the NSRs group (p = 0.03). Conclusions: Our findings highlight key differences in clinical and echocardiographic parameters between SRs and NSRs following fusion-CRT. These observations may contribute to a better understanding of response patterns and inform future prospective studies aiming to optimize patient selection and timing of therapy. Full article