Search Results (316)

Background: Type 2 diabetes mellitus (T2DM) is associated with subclinical myocardial dysfunction, which may occur despite preserved left ventricular ejection fraction. Left ventricular global longitudinal strain (LV GLS) is a sensitive marker of early systolic impairment and may detect subtle changes in myocardial function before conventional echocardiographic parameters become abnormal. The effect of sodium-glucose cotransporter-2 inhibitors (SGLT2i) on LV GLS in adults with T2DM remains incompletely defined. Objective: To synthesize the available evidence on the effects of SGLT2i therapy on LV GLS or LV strain in adults with T2DM. Methods: Original full-text human studies evaluating SGLT2i therapy in adults with T2DM and reporting LV GLS or LV strain were included. LV GLS was assessed primarily by speckle-tracking echocardiography, while one study used cardiac magnetic resonance feature-tracking. Reviews, conference abstracts, protocols, animal-only studies, and studies without LV strain assessment were excluded. Risk of bias was assessed using RoB 2 for randomized studies and ROBINS-I for non-randomized studies. Results: Twenty-six studies involving more than 2300 participants were included. The studies evaluated dapagliflozin, empagliflozin, ertugliflozin, canagliflozin, or mixed SGLT2i regimens across heterogeneous clinical populations, including patients with preserved ejection fraction, pre-heart failure, diabetes-related cardiomyopathy, chronic heart failure, coronary artery disease, hypertension, non-alcoholic fatty liver disease, and cardio-oncology risk. Most observational and before–after studies reported favorable changes in LV GLS after SGLT2i therapy, whereas randomized and controlled studies showed more variable findings. Several studies also reported improvements in LV remodeling, diastolic function, left atrial function, myocardial work indices, NT-proBNP, cardiometabolic parameters, or epicardial adipose tissue thickness. However, the certainty of evidence was limited by methodological heterogeneity, differences in comparator groups, variable follow-up duration, non-standardized imaging protocols, and risk of bias, particularly in non-randomized and single-arm studies. Conclusions: SGLT2i therapy may be associated with favorable changes in LV GLS in adults with T2DM, suggesting a potential beneficial effect on subclinical left ventricular systolic function. However, current evidence does not definitively establish a consistent treatment effect across all populations. Larger randomized controlled trials with standardized strain imaging protocols, predefined LV GLS endpoints, and clinically relevant follow-up are needed to determine whether SGLT2i-related improvements in LV GLS reflect true myocardial benefit and translate into improved cardiovascular outcomes. Full article

Atrial fibrillation (AF) and diabetes mellitus frequently coexist and together define a high-risk cardiometabolic phenotype. Diabetes is associated with an increased incidence of AF, although this relationship is strongly influenced by obesity, hypertension, chronic kidney disease (CKD), heart failure (HF), sleep-disordered breathing, and broader metabolic risk clustering. Once AF develops, diabetes is associated with greater thromboembolic and HF risk, impaired quality of life, cognitive vulnerability, and excess mortality. These adverse outcomes may be partly explained by a multidimensional atrial substrate, described here within the conceptual framework of diabetic atrial cardiomyopathy, in which hyperglycaemia, insulin resistance, glycaemic variability, oxidative stress, inflammation, autonomic dysfunction, microvascular disease, lipotoxicity, and epicardial adipose tissue dysfunction may contribute to atrial fibrosis, electrical heterogeneity, impaired calcium handling, mitochondrial injury, and mechanical dysfunction. Collectively, these abnormalities may facilitate AF initiation, persistence, progression, and recurrence after rhythm-control interventions. Management should therefore extend beyond rhythm control and anticoagulation alone. In individuals at increased risk of AF, priorities include cardiometabolic optimization, treatment of obesity, hypertension, CKD, HF, and sleep apnoea, lifestyle intervention, and selective rhythm surveillance. In subclinical AF, decisions regarding anticoagulation should account for AF burden, thromboembolic and bleeding risk, renal function, frailty, and patient preference. In established AF, stroke prevention, symptom-directed rate or rhythm control, cardiometabolic therapy, and longitudinal reassessment remain central. This narrative review integrates the epidemiology, mechanisms, and management of AF in diabetes across the continuum from AF risk to subclinical and clinical disease. Full article

Inadequate vein access is a frequent obstacle during cardiac implantable electronic device (CIED) upgrade procedures; thus, bail-out strategies are employed. A 71-year-old male with dilated cardiomyopathy bearing a 7-year-old right-sided dual-chamber pacemaker was scheduled for upgrade to an implantable cardioverter defibrillator. The case presented two main challenges—first, pacemaker dependency, and second, an occluded right subclavian vein. In a shared decision-making approach, the decision was made to “abandon” the right-sided ventricular lead in situ, reposition the right-sided atrial lead by tunneling over the sternum into the left pectoral area, and implant a new left-sided defibrillator lead. During the 2-year follow-up our patient remained clinically stable and the CIED fully functional. Herein, beyond case presentation we also elaborate on individualized alternative treatment strategies for patients with venous access site occlusion in a literature review. Full article

Background: Meta-analyses suggest an association between patent foramen ovale (PFO) and white-matter hyperintensities (WMH), but pooled effect sizes do not clarify applicability to routine transthoracic echocardiography (TTE) or provide patient-level risk estimates. Objective: The objective of this study was to evaluate the association between TTE-detected PFO and MRI-defined WMH in routine practice and to develop a practice-anchored framework (PAMAP) that translates literature-derived evidence into individualized risk. Methods: We performed a retrospective, single-center, propensity-matched analysis of 149 adults undergoing TTE and brain MRI (37 PFO-positive, 112 controls). The primary endpoint was WMH (Fazekas ≥ 1). PAMAP synthesized 12 studies; 4 eligible studies were pooled using random-effects meta-analysis to derive a locked shunt coefficient (OR 3.65). The locked model used age and shunt (H); embolic context (E), and atrial stress (A) were neutral until refit. Transportability was assessed at the cohort level (expected vs. observed prevalence) and patient level (calibration, discrimination), followed by a minimal prespecified refit. Results: WMH was more frequent in PFO-positive versus control participants (54% vs. 32%). Literature-based expected prevalence approximated observed prevalence, supporting transportability. The locked model showed acceptable performance (calibration intercept 0.106; slope 0.912; Brier 0.188; AUC 0.756). A parsimonious refit improved performance (Brier 0.176; AUC 0.783), with the shunt term remaining significant (OR 2.45, 95% CI 1.23–4.88). Conclusions: PAMAP translates meta-analytic associations into a transportable patient-level risk framework. In routine TTE-defined PFO populations, the WMH association is preserved, suggesting that incidental PFO may mark early subclinical cerebral injury and enabling calibrated, individualized risk assessment. Full article

Left ventricular (LV) extracellular volume fraction (ECV) quantified by cardiac computed tomography (CT) reflects diffuse myocardial fibrosis. In patients with atrial fibrillation (AF) and reduced LV ejection fraction (LVEF), distinguishing tachycardia-induced cardiomyopathy from underlying myocardial disease remains challenging. The prognostic value of ECV for predicting reverse remodeling (RR) after catheter ablation for AF remains uncertain. We retrospectively analyzed 102 patients with LVEF ≤ 50% on echocardiography who underwent cardiac CT before AF ablation between May 2015 and April 2025. RR was defined as a ≥15% reduction in LV end-systolic volume with recovery of LVEF > 50%, or an absolute increase in LVEF of ≥15%. RR occurred in 49 patients (48%). ECV was significantly lower in patients with RR than in those without (31.2 ± 3.5% vs. 37.6 ± 7.8%, p < 0.001). Receiver operating characteristic analysis identified an optimal cutoff of 34.8% (area under the curve 0.77; sensitivity 88%; specificity 62%, p < 0.001). In multivariable logistic regression analysis, lower ECV remained independently associated with RR (odds ratio 0.84; 95% confidence interval 0.75–0.95; p = 0.006). CT-derived ECV was associated with RR after AF ablation in patients with reduced LVEF and may provide additional information for clinical decision-making. Full article

Hypertrophic Cardiomyopathy Phenotype (HCM-Ph) is the most common group of myocardial disorders in cats. It has been the subject of research worldwide with prevalence rates ranging from 8% to 34%. However, there is no data available on its occurrence in Morocco. This study aimed to investigate the prevalence of HCM-Ph in apparently healthy cats in Morocco, describe the epidemiological and echocardiographic findings of affected cats and to compare patients in ACVIM stages B1 and B2. A total of 81 apparently healthy cats underwent echocardiographic screening. The overall prevalence of HCM-Ph was 9.88% (95% CI: 4.36–18.54%). The median age was four years (IQR 3.5–5.5) and a male overrepresentation (75%) was noted. Affected cats exhibited various echocardiographic patterns of left ventricular hypertrophy, normal left ventricular diameters, preserved fractional shortening and different degrees of left atrial enlargement. Cats in B2 stage were older and had more myocardial hypertrophy compared to cats in B1 stage, highlighting the potential role of wall thickness in clinical staging and risk assessment. Subclinical HCM-Ph is relatively common in apparently healthy cats in Morocco. Veterinarians should be aware of its clinical importance, as despite the fact that it presents no clinical signs, it can have fatal cardiovascular outcomes. Full article

Congenital pericardial agenesis (CPA) is a rare anomaly that is often considered a benign incidental finding but may present with nonspecific symptoms and mimic structural heart disease. Its clinical relevance remains incompletely defined, particularly regarding the distinction between a harmless anatomical variant and a clinically significant condition. We present a retrospective two-center case series of four patients with imaging-confirmed CPA, combined with a narrative review of the literature aiming to evaluate the clinical spectrum, diagnostic challenges, and management implications of CPA. The clinical presentation of our patients was heterogeneous, ranging from incidental findings to chest discomfort and dyspnea. In all cases, initial echocardiography suggested alternative diagnoses, including right ventricular cardiomyopathy, atrial septal defect, or pericardial disease, leading to diagnostic uncertainty. Definitive diagnosis was established using multimodality imaging, particularly cardiac magnetic resonance and computed tomography, which demonstrated characteristic features such as cardiac levoposition and interposition of lung parenchyma. Three patients had complete left pericardial agenesis and one had a partial defect. All patients were managed conservatively, without complications during follow-up. Full article

Background: The care of patients with transthyretin amyloid cardiomyopathy (ATTR-CM) is often fragmented and routine datasets rarely capture real-world clinical trajectories and reasons for diagnosis. We introduce a novel approach, called forensic data acquisition and pathway analysis, to examine the real-world experiences of patients with ATTR-CM in our district general hospital. Methods: We retrospectively evaluated inpatient and outpatient healthcare records for our hospital between 2019 to 2025 as a part of a quality improvement project. Results: We identified 26 cases of confirmed or likely wild-type ATTR-CM and four hereditary cases from two families carrying the S77Y variant and estimate the prevalence of transthyretin cardiac amyloidosis to be 1 per 10,000 patients. Many red flags were present in patients, including carpal tunnel syndrome (63.3%) and lumbar spinal stenosis (26.7%), as well as echocardiographic features of left ventricular hypertrophy (86.7%), left atrial dilatation (76.7%), right ventricular hypertrophy (43.3%), and a dense or speckled myocardial appearance (43.3%). Among patients with wild-type disease, the most frequent trigger for further investigation was the presence of suspicious features on transthoracic echocardiography, accounting for 13 cases. Incidental abnormalities detected on cardiac MRI contributed to another six diagnoses. In two patients, non-invasive imaging did not provide sufficient diagnostic certainty, and myocardial biopsy was required to confirm ATTR-CM. Conclusions: Forensic data acquisition and pathway analysis provides a powerful approach for revealing real-world clinical activity in ATTR-CM, exposing diagnostic patterns and missed opportunities that remain hidden in routine datasets. Full article

Infiltrative cardiomyopathies comprise a heterogeneous spectrum of hereditary and acquired diseases characterised by the accumulation of pathological substrates within the myocardium, ultimately resulting in progressive impairment of cardiac function and the development of heart failure. Across these conditions, atrial fibrillation is a frequent and clinically relevant complication, contributing to symptom burden, heart failure progression, and thromboembolic risk. Structural, functional, and electrical atrial remodelling, collectively referred to as atrial cardiomyopathy, emerges as a common pathophysiological substrate linking myocardial infiltration to atrial fibrillation and adverse cardiovascular outcomes. Multi-modality cardiac imaging enables comprehensive assessment of atrial cardiomyopathy, offering mechanistic insights into the atrial substrate of atrial fibrillation, with potential impact on the clinical management of this group of diseases. This review summarises contemporary evidence on atrial fibrillation in infiltrative cardiomyopathies, with a particular focus on the role of non-invasive multimodal imaging in the evaluation of atrial cardiomyopathy. Full article

Background: Genetic testing in hypertrophic cardiomyopathy (HCM) yields variable positivity rates. Identifying clinical predictors of positive genetic tests could improve pre-test counseling and refine expectations about diagnostic yield. Methods: We analyzed consecutive genotyped HCM probands from a contemporary multicenter cohort across four Italian tertiary centers. Genotype positivity was defined as the presence of ≥1 pathogenic or likely pathogenic variant (ACMG classes 4–5). Multivariable logistic regression identified predictors of genotype positivity. Sensitivity analyses assessed the incremental value of left atrial volume index (LAVI) ≥ 34 mL/m² and the mode of first clinical presentation. Results: Among 274 genotyped probands (median age at diagnosis 54 years; 62% male), 86 (31%) were genotype-positive (38% MYBPC3, 29% MYH7). Age at diagnosis <40 years (OR 2.38, 95%CI 1.26–4.51, p = 0.008), family history of sudden cardiac death/major ventricular arrhythmias (OR 2.34, 95%CI 1.16–4.84, p = 0.019) and family history of non-ischemic cardiomyopathy (OR 1.92, 95%CI 1.04–3.54, p = 0.038), were independently associated with genotype positivity whereas arterial hypertension was inversely associated (OR 0.42, 95%CI 0.23–0.77). Maximal left ventricular wall thickness > 20 mm and gender were not predictive of genotype positivity. Inclusion of LAVI modestly improved the model performance (AUC 0.769, p = 0.016, ΔAUC +0.024; DeLong p = 0.016) but without leading to meaningful patient reclassification. Conclusions: Genotype positivity in HCM links to earlier onset and family history; traditional severity markers and initial presentation may not independently suggest genetic causality. These findings may help shape a personalized approach to genetic counseling in HCM. Full article

Background: Flecainide has remained largely excluded from use in structural heart disease for more than three decades, mainly because of the Cardiac Arrhythmia Suppression Trial, which showed excess mortality in post-myocardial infarction patients treated for ventricular ectopy. However, the influence of this trial has extended well beyond the population actually studied, fostering a broad safety paradigm that may not fully reflect contemporary clinical practice. Aim: This review aims to re-examine the role of flecainide in structural heart disease by examining the historical basis for its restriction and contrasting it with emerging contemporary evidence across specific structural substrates. Discussion: Flecainide remains one of the most effective antiarrhythmic drugs for rhythm control in atrial fibrillation and for the suppression of selected ventricular arrhythmias in patients without overt structural abnormalities. Emerging observational and early prospective data suggest that, in carefully selected patients with stable coronary artery disease without active ischemia, preserved left ventricular function, arrhythmogenic right ventricular cardiomyopathy, and premature ventricular complex-induced cardiomyopathy, flecainide may provide meaningful antiarrhythmic benefit without a clear signal of excess proarrhythmia or mortality. Advances in cardiac imaging, ischemia assessment, and phenotypic risk stratification further support a more individualized approach to candidate selection. Conclusions: Flecainide should not be considered uniformly contraindicated across all forms of structural heart disease. Rather than supporting indiscriminate use, the available evidence supports a mechanistically informed and phenotype-specific reassessment of its role in selected patients. Prospective studies are needed to determine whether current guideline restrictions remain justified in the modern era. Full article

Emery–Dreifuss muscular dystrophy (EDMD) is a rare inherited neuromuscular disorder within the spectrum of nuclear envelope diseases, classically characterized by early musculo-tendinous contractures, slowly progressive myopathy, and cardiac involvement dominated by conduction disease and arrhythmias, with variable evolution toward cardiomyopathy and heart failure. This narrative review provides a comprehensive and clinically actionable synthesis of cardiovascular manifestations across EDMD genotypes and phenotypes, outlining pragmatic diagnostic and therapeutic pathways for real-world care. A targeted literature search was performed in PubMed, Embase, and Web of Science, focusing on studies addressing cardiovascular involvement in EDMD. Relevant original studies, case series, registries, guideline documents, and high-quality reviews were selected and synthesized narratively, with particular emphasis on diagnostic strategies, risk stratification, and management approaches. Cardiac involvement in EDMD encompasses a broad and heterogeneous spectrum, including atrial disease and conduction disturbances, ventricular arrhythmias, dilated cardiomyopathy, thromboembolic complications, and sudden cardiac death. Phenotypic expression varies according to the underlying genetic substrate, with distinct atrial- and ventricular-dominant trajectories. Early recognition and structured cardiovascular surveillance are essential to guide timely intervention, including anticoagulation, device therapy, and heart failure management. Despite growing awareness, significant gaps remain in risk prediction and standardized management strategies. EDMD represents a paradigmatic model of cardiomyopathy characterized by prominent electrical instability and systemic involvement. A structured, genotype- and phenotype-informed approach centered on early surveillance, proactive arrhythmia and thromboembolic risk management and timely device therapy may improve clinical decision-making in real-world settings. Future perspectives include the integration of precision medicine and the development of gene- and pathway-targeted therapies, with the potential to shift from symptomatic management toward disease-modifying strategies. Full article

Traditional cardiovascular assessment has historically focused on the isolated evaluation of either atrial or ventricular structure and function. However, the left atrioventricular coupling index (LACI) represents a paradigm shift by moving beyond single-chamber metrics to quantify the dynamic interaction between the left atrium and left ventricle. Defined as the ratio of left atrial end-diastolic volume to left ventricular end-diastolic volume, LACI integrates structural and functional aspects of cardiac performance. This comprehensive review examines the physiological basis of how the left atrium and ventricle operate as an integrated hemodynamic unit. We detail current measurement methodologies, including two- and three-dimensional echocardiography, cardiac computed tomography, and cardiac magnetic resonance imaging, which serves as the reference standard. Furthermore, the review explores the pathophysiological mechanisms driving atrioventricular uncoupling, specifically mechanical dysfunction, electromechanical desynchrony, and hemodynamic alterations. Extensive clinical evidence demonstrates LACI’s robust independent prognostic value across diverse cardiovascular conditions, such as heart failure, myocardial infarction, cardiomyopathies, and atrial fibrillation. Observational data suggest that LACI provides a promising prognostic value beyond established risk assessment tools by combining the assessment of both chambers’ interdependence. Finally, we outline future directions for clinical translation, highlighting the necessity for standardized measurement protocols, the integration of artificial intelligence, and the potential of LACI as a target for personalized therapeutic strategies. Full article

Mitral transcatheter edge-to-edge repair (M-TEER) has emerged as a cornerstone in the management of severe mitral regurgitation, serving as a robust, low-risk alternative to conventional mitral valve surgery. Although thromboembolic risk remains a critical clinical challenge, that varies significantly across the clinical continuum, from pre-procedural substrates to post-procedural management. This review highlights the role of atrial cardiomyopathy in creating a prothrombotic milieu even prior to intervention, while during the procedure, device time emerges as a potentially dominant independent predictor of embolic burden, marking the periprocedural window as the period of peak hazard. Furthermore, this article addresses the notable disparity between the near-universal presence of subclinical ischemic lesions on magnetic resonance imaging and the infrequent incidence of overt neurological deficits. As the post-procedural phase is considered, we discuss the shift from standardized antithrombotic protocols to individualized strategies and the potential role of concomitant left atrial appendage occlusion. Ultimately, integrating these stage-specific clinical and procedural determinants with emerging technologies—like digital twins and artificial intelligence—represents a promising frontier for mitigating embolic risks, optimizing procedural planning and patient safety in the evolving landscape of mitral valve interventions. Full article

Introduction: Hypertrophic cardiomyopathy (HCM) is a common myocardial disease worldwide and is associated with heart failure symptoms and sudden cardiac death. In a subset of patients, it may produce dynamic left ventricular outflow tract obstruction (LVOTO) and systolic anterior motion (SAM)-related mitral valve dysfunction through drag forces and altered mitral–septal geometry. In contrast, subaortic stenosis caused by a subaortic membrane is an uncommon congenital lesion that may lead to fixed subvalvular LVOTO in adulthood. The coexistence of these entities is rare and can substantially complicate diagnosis and management. Case presentation: A 51-year-old woman with HCM, paroxysmal atrial fibrillation, and heart failure presented with acute decompensation and cardiogenic shock. After initial hemodynamic stabilization and cardioversion for atrial fibrillation with rapid ventricular response, multimodality imaging with transthoracic and transesophageal echocardiography, coronary computed tomography angiography, and cardiac magnetic resonance demonstrated dual LVOTO, with a dynamic component related to HCM/SAM physiology and a fixed component caused by an elongated subaortic membrane, accompanied by severe SAM-related mitral regurgitation. Echocardiography showed a resting peak LVOT gradient of 49 mmHg, increasing to 85 mmHg with the Valsalva maneuver. After exclusion of obstructive coronary artery disease and evaluation for selected phenocopies, the patient underwent septal myectomy, subaortic membrane resection, and adjunctive mitral valve plication. Early postoperative echocardiography showed reduction in the maximum provoked LVOT gradient to 38 mmHg and improvement of mitral regurgitation from severe to mild. At 3-month follow-up, she remained in sinus rhythm, improved to New York Heart Association functional class II, and had no documented readmissions for heart failure. Conclusions: Combined fixed and dynamic LVOTO due to concomitant subaortic membrane and HCM is exceedingly rare. Accurate diagnosis requires a high index of suspicion and a multimodality imaging strategy to define the obstructive mechanisms and support mechanism-based surgical management and avoid incomplete treatment when a coexisting fixed lesion is present. Full article