Transthyretin cardiac amyloidosis (ATTR-CA) is an increasingly recognized cause of cardiac dysfunction in adults, resulting from extracellular deposition of misfolded transthyretin fibrils and progressive myocardial impairment. Clinical expression and diagnostic yield differ substantially between sexes, contributing to systematic underdiagnosis in women, who often present with subtler myocardial remodeling, heart failure with preserved ejection fraction (HFpEF)-dominant phenotypes, and nonspecific systemic manifestations that fall below conventional diagnostic thresholds, particularly in early disease stages. Female patients, particularly those with ATTRwt, tend to present at older ages and more frequently show HFpEF-dominant phenotypes and nonspecific extracardiac manifestations. Carpal tunnel syndrome (CTS) is an important extracardiac red flag for ATTR-CM, but its interpretation in women requires caution because of the high background prevalence of idiopathic CTS in the general population. Evidence also suggests sex-related differences in diastolic function, right ventricular involvement, and overall progression. Despite these biological and phenotypic distinctions, women are markedly underrepresented in trials of disease-modifying therapies, limiting conclusions about sex-specific treatment effects and leaving uncertainty about whether current pharmacologic interventions provide comparable benefit. Hormonal influences, genetic background, and age-related mechanisms, comorbidities, and diagnostic pathways may contribute to the distinctive female phenotype, but underlying mechanisms remain insufficiently defined. This narrative review examines sex-associated differences in ATTR-CA, focusing on mechanisms of underdiagnosis, principal clinical and imaging features, and implications for therapeutic response, with the goal of improving diagnostic accuracy, guiding individualized management, and ultimately enhancing outcomes for women and all affected patients worldwide in clinical practice.
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Background/Objectives: Amb a 1 is the major allergenic component of Ambrosia artemisiifolia pollen and a clinically relevant marker of genuine ragweed sensitization. Heart failure is increasingly recognized as a systemic syndrome shaped by immune activation, endothelial dysfunction, fibrosis, neurohormonal imbalance, pulmonary comorbidity, and environmental exposures. This narrative review aims to synthesize the translational evidence linking Amb a 1-specific IgE, IgE-mediated inflammation, allergic airway disease, and cardiovascular remodeling in heart failure. Methods: A targeted narrative review was performed, integrating evidence on component-resolved ragweed diagnosis, IgE-FcεRI signaling, mast cell and eosinophil biology, pollen exposure, cardiovascular inflammation, and heart failure pathophysiology. Results: No dedicated clinical studies have validated Amb a 1-specific IgE as a diagnostic, prognostic, or therapeutic biomarker in heart failure. However, adjacent evidence supports biologically plausible links between allergen-specific IgE responses and cardiovascular dysfunction, including mast cell activation, cytokine release, endothelial perturbation, oxidative stress, microvascular dysfunction, pulmonary-cardiac interaction, and myocardial fibrosis. Amb a 1-specific IgE may therefore identify a seasonally vulnerable heart failure phenotype, particularly in patients with allergic rhinitis, asthma, eosinophilic inflammation, or recurrent symptom worsening during ragweed season. A systemic/indirect pathway operating through allergic airway disease is distinguished from a postulated direct cardiac pathway; the latter remains strictly speculative, as no direct evidence demonstrates that inhaled Amb a 1 reaches or activates cardiac mast cells in vivo. Conclusions: Amb a 1-specific IgE should not currently be used to infer cardiac causality or modify heart failure therapy. Prospective, phenotype-rich, exposure-informed studies are needed to determine whether ragweed sensitization has clinically meaningful implications for heart failure endotyping, seasonal risk assessment, and cardio-allergology care. These findings may inform patient-centered heart failure management by improving the interpretation of seasonal dyspnea, allergic comorbidity, and symptom fluctuations in ragweed-endemic regions.
Accurate assessment of pulmonary vascular resistance index (PVRi) is essential for the diagnosis and management of pulmonary arterial hypertension (PAH). PVRi depends on pulmonary blood flow (Qp), which can be determined by thermodilution or the Fick principle. However, agreement between these methods in children with PAH remains poorly characterized. We performed a retrospective single-center study of 209 cardiac catheterizations in 50 pediatric patients with WHO Group 1 PAH. Thermodilution-derived Qp was obtained in patients without significant intracardiac shunting and compared with Fick-derived Qp using reported oxygen consumption (VO2), which was obtained by direct measurement (173 procedures, 93%) or the Seckeler equation (13 procedures, 7%). Agreement between methods was assessed using Bland-Altman analysis, and multivariable linear regression was performed to identify predictors of discrepancies in PVRi. Thermodilution-derived PVRi was, on average, 2.0 Wood units·m2 lower than Fick-derived PVRi. The discrepancy increased as PVRi increased (R2 = 0.47). Differences in VO2 estimation contributed minimally to variability in PVRi compared with differences in Qp determination. Among patients who underwent serial catheterizations, thermodilution was used consistently in only 42%, whereas 58% had variable use across procedures. Thermodilution systematically yields lower PVRi than the Fick method in pediatric PAH, particularly in patients with higher PVRi. These findings highlight the importance of maintaining a consistent method of Qp determination during serial catheterizations to improve interpretation of longitudinal hemodynamic changes and clinical decision-making.
Thyroid dysfunction often delays surgery during preoperative evaluation, though evidence on perioperative risk and biochemical optimization is limited. This review explores recent literature on perioperative outcomes in hypothyroidism and hyperthyroidism, focusing on surgery delays, rapid optimization strategies, and areas of uncertainty. Observational studies and meta-analyses link subclinical hypothyroidism with adverse cardiovascular outcomes in cardiac surgeries, but evidence for non-cardiac surgeries is limited. Overt hypothyroidism is associated with complications like impaired wound healing, prolonged ventilation, and cardiovascular issues, making euthyroid state preferable before surgery, despite retrospective, heterogeneous data. For hyperthyroid patients undergoing total thyroidectomy, recent literature questions the need for biochemical euthyroid state; evidence for non-thyroid surgeries is sparse and extrapolated from thyroid surgeries. Selective use of liothyronine and therapeutic plasma exchange in severe or urgent cases shows promise, but evidence is limited and low quality. Current management of thyroid dysfunction is largely consensus-driven and based on limited evidence. Routine elective surgery optimization is advised for overt thyroid disease; however, in urgent cases, surgery after starting appropriate therapy and multidisciplinary planning is often reasonable. Future research should focus on prospective outcome data, rapid correction strategies, and the role of modern care pathways in reducing endocrine-related surgical risks.
Background: Diabetic retinopathy (DR) is the most prevalent microvascular complication of type 2 diabetes mellitus (T2DM) and a recognised marker of systemic vascular injury. Whether DR-graded independently by two experienced ophthalmologists as part of routine institutional care-is independently associated with concurrent nephropathy (urine albumin-to-creatinine ratio [UACR] ≥ 30 mg/g) and subclinical cardiac stress (N-terminal pro-B-type natriuretic peptide [NT-proBNP] ≥ 125 pg/mL) remains insufficiently examined. Methods: Retrospective cross-sectional study of 401 T2DM adults who underwent dilated fundus examination independently graded by two board-certified ophthalmologists (each ≥ 10 years' experience in diabetic eye disease) using ETDRS-based classification. Inter-physician agreement was quantified by Cohen's weighted kappa. The primary composite outcome was concurrent nephropathy and subclinical cardiac stress. Multivariable logistic regression adjusted for age, sex, HbA1c, diabetes duration, eGFR, hypertension, and pharmacological treatments. Results: The composite outcome was present in 120 (64.2%) DR-positive vs. 14 (6.5%) DR-negative patients (crude OR: 25.59 (13.78-47.51); p < 0.001; fully adjusted OR: 21.49 (11.02-41.81); p < 0.001). Inter-physician agreement was high (Cohen's weighted κ = 0.88; 95% CI: 0.83-0.93). Nephropathy alone was found in 164 (87.7%) vs. 76 (35.5%) patients (OR: 12.95 (7.71-21.75); p < 0.001), and elevated NT-proBNP in 137 (73.3%) vs. 39 (18.2%) patients (OR: 12.29 (7.65-19.76); p < 0.001). A significant trend across DR severity grades was observed (p for trend < 0.001), although the gradient was not strictly monotonic. ROC AUC = 0.837 (95% CI: 0.784-0.860). Conclusions: Ophthalmologist-graded DR was independently associated with the concurrent presence of albuminuria and elevated NT-proBNP in T2DM. Because the design is cross-sectional, these findings describe association rather than prediction or causation. They generate the hypothesis that retinal grading may help flag patients in whom cardiorenal biomarker assessment is worth considering, but prospective validation is required before any screening application.
Introduction: Arrhythmogenic cardiomyopathy (ACM) is a myocardial disorder characterized by fibrofatty replacement of the myocardium and is associated with heart failure and sudden cardiac death. It can involve either ventricle, including left-dominant forms defined partly by genetic findings. Methods: We investigated a consanguineous family with four affected daughters presenting with ACM, epidermolytic palmoplantar keratoderma, and woolly hair. The two eldest siblings died suddenly during childhood. The remaining two affected siblings underwent genetic analysis using autozygosity mapping and whole-exome sequencing, followed by segregation analysis. Results: Autozygosity mapping identified a shared identity-by-descent (IBD) interval at the DSP locus on chromosome 6. Exome sequencing revealed a novel homozygous nonsense variant (c.4297C>T; p.Gln1433*; rs1554108283) in exon 23 of DSP. This variant introduces a premature termination codon within the region specific to transcript variant 1, sparing transcript variant 2. Both parents were heterozygous carriers. Cardiac imaging in the affected siblings demonstrated biventricular involvement, including left ventricular systolic dysfunction and right ventricular dilatation. Skin biopsy in one patient confirmed epidermolytic palmoplantar keratoderma. Conclusions: We describe a novel homozygous nonsense variant in the transcript 1-specific region of DSP causing Carvajal syndrome, characterized by severe biventricular ACM, epidermolytic palmoplantar keratoderma, and woolly hair, in a consanguineous Arabian family with four affected sisters.
Background/Objectives: Danon disease is a rare X-linked lysosomal disorder caused by pathogenic variants in LAMP2. In women, cardiac involvement may occur later in life and may resemble sarcomeric hypertrophic cardiomyopathy (HCM), particularly when extracardiac manifestations are absent or subtle. A 42-year-old woman presented with chest discomfort in 2017 and was initially diagnosed with hypertrophic cardiomyopathy (HCM). She underwent serial 3.0-T cardiovascular magnetic resonance (CMR) over an 8-year period. Initial CMR showed left-ventricular hypertrophy, preserved left-ventricular ejection fraction (65.0%), increased native T1 and T2 relaxation times, extracellular volume (ECV) of 24.9%, and patchy apical late gadolinium enhancement (LGE extent, 12.35%). Five years later, worsening dyspnea was accompanied by increased left-ventricular mass index, higher native T1 and ECV, greater LGE extent (15.18%), and slow atrial fibrillation with ventricular ectopy on Holter monitoring. Genetic testing identified a likely pathogenic LAMP2 variant, c.928G>A (p.Val310Ile), supporting the diagnosis of Danon disease in the clinical context. During a subsequent readmission three years later with acute amaurosis and dyspnea, no definite neurologic cause was identified in the available record. Repeat CMR showed the highest recorded native T1 and ECV values and diffuse LGE with relatively less interventricular-septal involvement, particularly in the basal septum (LGE extent, 24.59%); repeat Holter monitoring showed frequent long R-R intervals and ventricular escape beats. Because of progressive imaging and electrical deterioration, implantable cardioverter-defibrillator therapy and heart-transplantation assessment were recommended, and the patient ultimately chose to proceed with pre-transplant assessment in December 2025. Conclusions: Female LAMP2-related Danon disease may initially resemble HCM, but differs from it with diffusely abnormal T1/ECV measurements. Follow up in our case revealed progressive storage cardiomyopathy with diffuse myocardial injury and clinically relevant bradyarrhythmia.
Background: Increased placental thickness has been associated with adverse perinatal outcomes and fetal functional and structural abnormalities. However, whether marked third-trimester placental thickening is associated with a distinct maternal clinical profile compared with pregnancies with normal placental thickness remains insufficiently characterized. This study aimed to compare maternal characteristics, comorbidities, medication exposure, infection history, and fetal findings between pregnancies with marked placental thickening, defined as placental thickness ≥70 mm, and gestational-age-matched control pregnancies with a placental thickness <70 mm and no documented maternal or fetal abnormalities. Methods: This retrospective matched case-control study included singleton pregnancies referred for fetal echocardiography to a tertiary referral center in Łódź, Poland, between 1 January 2022 and 14 March 2025. Placental thickness was measured sonographically in a perpendicular plane from the chorionic plate to the basal plate, excluding the umbilical cord insertion site. Only anterior and/or fundal placentas assessed at ≥28 weeks of gestation were included. Among pregnancies with recorded third-trimester placental thickness measurements, 99 cases with placental thickness ≥70 mm were identified as the thick-placenta group. A control group of 99 pregnancies with placental thickness <70 mm was selected and matched for gestational age. Control pregnancies had no documented maternal disease, no fetal structural or functional abnormalities, and no exposure to the medications analyzed in this study. Maternal demographic characteristics, body mass index, comorbidities, infection history, obstetric history, and medication use were compared between groups. Continuous variables were compared using Welch's t-test and the Mann-Whitney U test, and categorical variables were compared using Fisher's exact test. Results: The study included 99 pregnancies with marked placental thickening and 99 control pregnancies with normal placental thickness. Gestational age at examination was comparable between groups, with a mean of 35.5 weeks in controls and 35.0 weeks in the thick-placenta group (p = 0.662, Welch's t-test). Median gestational age was also not significantly different between groups (35.4 vs. 36.43 weeks; p = 0.340, Mann-Whitney U test). Mean placental thickness was significantly greater in the thick-placenta group than in controls (81.4 mm vs. 46.9 mm; p < 0.0001). Maternal age and anthropometric characteristics were comparable between groups, whereas BMI > 25 kg/m2 was more common in the thick-placenta group. In contrast to the clinically healthy control group, maternal infection was documented in 100.0% of thick-placenta cases, hormonal treatment in 97.0%, history of COVID-19 in 52.5%, hypothyroidism in 44.4%, prior miscarriage in 37.4%, aspirin or anticoagulant use in 32.3%, gestational diabetes mellitus in 25.3%, and pregnancy-induced hypertension in 7.1%. All evaluated maternal clinical factors were significantly more common in the thick-placenta group than in controls. Fetal cardiac or extracardiac dysfunction was present in 68.7% of thick-placenta pregnancies. Conclusions: In this gestational-age-matched case-control study, pregnancies with marked third-trimester placental thickening showed a distinct maternal profile compared with healthy controls with normal placental thickness. Despite comparable gestational age, maternal age, and maternal anthropometric characteristics, the thick-placenta group demonstrated a significantly higher infectious, hormonal, metabolic, and endocrine burden. These findings indicate that, in this selected tertiary referral cohort, placental thickness ≥70 mm was associated with a higher burden of maternal clinical abnormalities and fetal functional findings. Rather than representing an independent marker of placental maladaptation or maternal-fetal risk, marked placental thickening should be interpreted as a clinically relevant ultrasound finding that may prompt careful review of maternal history and targeted fetal assessment. Prospective studies are needed to determine which maternal factors are independently associated with placental thickening and to clarify their relationship with fetal function and perinatal outcomes.
Walking recovery is a central goal of geriatric rehabilitation, but it is shaped by multiple interacting factors rather than by muscle impairment alone. This mini-review examines whether sarcopenia-related weakness, low muscle quality, and reduced physical reserve identify a clinically important vulnerability phenotype relevant to delayed gait recovery in older adults after hospitalization, hip fracture, surgery, or cardiac procedures. We summarize current consensus definitions of sarcopenia, explain why muscle strength and physical performance are often more clinically informative than muscle mass alone, and review the mechanistic pathways that may connect sarcopenia with impaired walking, including anabolic resistance, inflammation, disuse, neuromuscular remodeling, trunk weakness, and cognitive-emotional modifiers. Across community, orthogeriatric, post-acute, and cardiac rehabilitation settings, sarcopenia markers are generally associated with slower gait or poorer attained mobility; however, findings for change in mobility are inconsistent, and most available studies are observational, heterogeneous, or indirect. Sarcopenia should therefore be interpreted as one potential marker of reduced reserve and mobility risk rather than as a determinant of walking recovery or evidence that sarcopenia-aware rehabilitation improves outcomes. Future work should use more consistent diagnostic frameworks and test whether a sarcopenia-aware rehabilitation integrating early strength assessment, individualized nutrition care, and multicomponent gait rehabilitation improve walking outcomes in medically complex older adults beyond current standards of care.
Artificial intelligence applied to electrocardiography (AI-ECG) has rapidly been investigated in adult cardiovascular medicine, yet translation into pediatric and congenital heart disease populations has lagged. This review summarizes contemporary AI-ECG methodologies and emerging applications in pediatric and congenital heart disease (PCHD), with emphasis on current clinical utility, technical challenges, and future opportunities for implementation. Recent studies demonstrate that deep learning models can accurately identify arrhythmias, ventricular dysfunction, and CHD from standard ECG. Convolutional neural networks remain the dominant architecture, although transformer-based foundation models and self-supervised learning approaches are increasingly being explored. AI-ECG applications in PCHD have expanded from automated interpretation toward proactive risk stratification, including prediction of ventricular dysfunction, mortality, and sudden cardiac death risk. Additional work has investigated wearable monitoring, telemetry analysis, and integration with longitudinal clinical data. Despite promising performance, most studies remain retrospective and single-center, with limited external validation and challenges related to small datasets, physiologic heterogeneity, and age-dependent ECG variation. AI-ECG has the potential to transform PCHD by improving diagnostic accuracy, enabling earlier disease detection, and enhancing longitudinal risk assessment. Broader clinical implementation will require multicenter collaboration, prospective validation, standardized datasets, and careful attention to ethical, regulatory, and equity considerations.
Cardioneuroablation (CNA), defined as endocardial catheter ablation of atrial ganglionated plexi within the intrinsic cardiac autonomic nervous system, has emerged as a mechanism-directed therapy for cardioinhibitory reflex syncope and functional bradyarrhythmias. By attenuating postganglionic parasympathetic input to the sinoatrial and atrioventricular nodes, CNA targets the autonomic substrate of cardioinhibition rather than merely treating its bradycardic consequence. Over the past two decades, the evidence base has progressed from pioneering single-center experiences to multicenter registries, systematic reviews, meta-analyses, and randomized clinical trials, with reported freedom from recurrent syncope of approximately 80-94% in carefully selected patients at medium-term follow-up. This state-of-the-art narrative review summarizes the rationale, anatomy, patient-selection principles, mapping and ablation strategies, procedural endpoints, clinical outcomes, safety profile, and emerging applications of CNA. Particular emphasis is placed on the unresolved questions that will define the future of the field: the absence, to date, of adequately powered sham-controlled efficacy data; the lack of a universally validated intraprocedural endpoint; the biological and clinical significance of vagal reinnervation; and the gap between expert-center and broader real-world outcomes. Current evidence supports CNA as a promising, anatomically grounded neuromodulatory therapy, but its transition from expert-center innovation to guideline-endorsed treatment will depend on rigorous patient selection, standardized procedural endpoints, and the results of ongoing randomized trials.
A 24 GHz radar, useful for remote vital signs monitoring, operating in linear/circular polarization (LP/CP), was developed to analyze vital signs detection performance in the presence of environmental clutter. The radar system, equipped with horn antennas with and without suitable LP-CP field polarization converters, is designed for monitoring respiratory and cardiac activity in domestic and hospital environments. A geometric optics (GO) model is introduced to show the advantages of circularly polarized (CP) radar sensors over linearly polarized (LP) ones in discriminating vital signals in scenarios where vibrating metallic panels simulate environmental disturbance (worst case). An analytical model, numerical computations, and experimental investigations highlighted the robustness of CP radar sensors in detecting vital signs in the presence of environmental clutter.
Background: Tricuspid valve surgery is indicated for severe symptomatic tricuspid valve regurgitation (TR) when performed concomitant to another cardiac operation. While percutaneous therapies for TR continue to advance, anatomic constraints may necessitate consideration of surgery in some patients. Methods: Herein, we provide a contemporary review of surgical techniques used to treat TR, which can serve as a complement to existing and emerging tricuspid valve treatment therapies. Results: We performed a literature review on established surgical tricuspid repair techniques. Conclusions: Surgical repair of the tricuspid valve is safe and feasible. While annuloplasty remains the cornerstone operative strategy, leaflet and sub-valvular techniques serve as adjuncts to help successful repair. The therapeutic paradigm for TR continues to evolve.
Donation after circulatory death has emerged worldwide as a safe and effective alternative pathway to increase the donor pool. However, organs undergo a variable period of warm ischemia during the agonal phase and the cardiac arrest before graft procurement, and the heart is particularly vulnerable to injury provoked by warm ischemia and subsequent reperfusion. Several reperfusion strategies are currently available for the recovery and assessment of heart function in these donors, with promising early and long-term results. Nevertheless, each technique implies specific financial, logistical and ethical challenges, translating into a heterogeneous landscape of protocols across European and non-European countries. Additionally, no randomized clinical trials have been published to assess the superiority of one technique over the other, and current clinical evidence is based on retrospective registry data and single-center observational studies.
Patients with congenital heart disease (CHD) represent a special healthcare challenge due to their high complexity, which accompanies them throughout all life stages. Consequently, this population faces increased morbidity and mortality rates, often linked to hemodynamic shifts in pulmonary flow or cardiac output. These risks are further compounded by potential arrhythmias and heart failure decompensation, which may lead to the progressive progression toward advanced stages of the disease. Unfortunately, standard outpatient follow-up is often not capable of responding to the continuous monitoring needs presented by these patients and their families. This selective review frames information on the wearable devices that have emerged as a key solution for continuous and remote monitoring. Beyond clinical tracking, research is increasingly focusing on their role in assessing physical activity-a critical determinant of health outcomes in the CHD population. This review examines the existing literature on wearable technology in both pediatric and adult patients while also addressing the current limitations that hinder their integration into routine clinical practice.
Myocardial strain imaging, derived from speckle-tracking echocardiography (STE), has evolved from a research tool into a reproducible technique for detecting subclinical myocardial dysfunction. Recent advances in automated contouring and artificial intelligence have improved feasibility, reproducibility, and analysis speed, making multichamber strain assessment increasingly accessible in perioperative practice. Perioperative cardiovascular complications, including myocardial injury after non-cardiac surgery (MINS), postoperative atrial fibrillation (POAF), and heart failure, are associated with substantial postoperative morbidity and mortality. Conventional echocardiographic parameters, particularly left ventricular ejection fraction (LVEF), lack sensitivity for detecting early myocardial dysfunction. By quantifying myocardial deformation, strain imaging identifies subtle abnormalities in ventricular and atrial mechanics before conventional echocardiographic abnormalities become evident. Among available parameters, left ventricular global longitudinal strain (LV-GLS) and left atrial reservoir strain (LASr) provide the strongest evidence for perioperative risk stratification, with impaired values independently associated with MINS and POAF, respectively. Right ventricular strain (RV-GLS, RV-FWLS) and right atrial reservoir strain (RASr) remain promising but less standardized parameters supported mainly by observational data. Despite these advances, several barriers continue to limit widespread implementation, including vendor variability, the lack of standardized thresholds, and the absence of validated transesophageal echocardiography (TEE)-specific reference values. Importantly, current evidence supports myocardial strain primarily as a tool for risk stratification rather than for guiding therapy. No randomized trial has demonstrated that strain-guided perioperative management improves clinical outcomes, and its incremental value beyond established perioperative tools, including clinical risk scores, biomarkers, and conventional echocardiography, remains to be established. This review aims to provide a practical framework for the perioperative use of myocardial strain by summarizing the current evidence, clarifying its methodological limitations, simplifying its acquisition and interpretation for non-expert users, distinguishing established clinical applications from future research directions, and identifying the key evidence gaps that must be addressed before strain-guided strategies can be incorporated into routine perioperative care.
Background/Objectives: Digoxin, a positive inotropic agent with a narrow therapeutic window, is used in heart failure but carries toxicity risks. This study aims to characterize the profile of digoxin-associated adverse drug reactions reported in the EudraVigilance database, focusing on drug-drug interactions, dosing errors, and off-label use. Methods: Descriptive and disproportionality analyses were performed on Individual Case Safety Reports (ICSRs) until 25 January 2026. Digoxin was compared with other inotropic agents by calculating the Reporting Odds Ratio and 95% confidence intervals. Results: Digoxin recorded 11,426 ICSRs, with a predominance in patients aged 65-85 years (46.4%) and over 85 years (25.1%). Higher reporting probabilities were identified for the terms "Drug interaction" and "Overdose" compared to other inotropes. Fatal outcomes were reported in 19 cases related to drug interactions and 41 cases related to overdose. Consistent disproportionality signals were found for gastrointestinal, renal, and nervous system disorders. Off-label use was reported in 0.8% of cases and was associated with unfavorable clinical outcomes. Risks are exacerbated by polypharmacy and renal decline in elderly patients. Conclusions: Digoxin toxicity and cardiac complications are the primary drivers of reported morbidity. This risk profile highlights the need for the rigorous clinical monitoring, precise dose adjustments and heightened vigilance regarding drug-drug interactions.
Smart wearable electrocardiogram (ECG) monitoring enables continuous cardiac assessment beyond clinical settings, but ECG signals are often degraded by baseline wander, muscle artifacts, and electrode motion artifacts. At present, pure end-to-end spiking neural networks (SNNs), with the advantage of low computational complexity, have rarely been explored for ECG noise suppression, particularly under dynamic conditions. To address this gap, this study proposes Direct-Coding-Physics-Aware Spiking Neural Network (DCPA-SNN) for wearable ECG denoising. The proposed method integrates a direct-coding SNN, channel attention, residual noise learning, and a physics-aware multi-domain loss function to preserve diagnostically important waveform structures. Clean ECG signals from the MIT-BIH Arrhythmia Database and real-noise segments from the MIT-BIH Noise Stress Test Database were used to construct single-noise and mixed-noise evaluation scenarios with input SNRs ranging from -6 dB to 4 dB to reflect the noise characteristics of wearable devices. Experimental results demonstrate that DCPA-SNN achieves robust denoising performance under different noise conditions. In the mixed-noise scenario, which serves as the primary evaluation setting of this study, the average denoised SNR reached 5.80 dB, with an average SNR improvement of 6.80 dB, while the R-peak detection rate increased from 90.71% to 95.72%. These results demonstrate that the proposed model, DCPA-SNN, provides a promising approach for wearable ECG denoising with potential for low-power deployment.
Post-infarction left ventricular aneurysm is an uncommon but severe mechanical complication of transmural myocardial infarction, particularly in patients with delayed presentation or incomplete myocardial salvage. It may lead to profound distortion of left ventricular geometry, adverse remodelling, intraventricular thrombosis, mitral regurgitation, pulmonary hypertension, and advanced heart failure. We report the case of a 65-year-old male patient referred two months after a late-presenting anterior ST-segment elevation myocardial infarction caused by proximal occlusion of the left anterior descending coronary artery. At admission, the patient presented with severe decompensated heart failure, low-output status, multiorgan dysfunction, and a left ventricular ejection fraction of 12%. Transthoracic echocardiography and cardiac magnetic resonance imaging demonstrated a giant apical left ventricular aneurysm involving approximately 75% of the ventricular cavity, partial intraluminal thrombosis, extensive transmural scarring in the left anterior descending territory, and imaging features suggestive of a chronic contained free-wall rupture/pseudoaneurysmal component. Following multidisciplinary evaluation, the patient underwent surgical ventricular reconstruction using an endoventricular circular restoration technique guided by an intraventricular balloon sizer, combined with left internal thoracic artery bypass grafting to the left anterior descending artery. The early postoperative course required temporary inotropic, vasopressor, inhaled nitric oxide, and intra-aortic balloon pump support, followed by progressive haemodynamic recovery. The patient was discharged on postoperative day seven with functional improvement to NYHA class II. At six-month follow-up, he remained clinically stable without overt signs of heart failure, and echocardiography showed preserved ventricular geometry and improvement of left ventricular ejection fraction to 45%. This case highlights the potential role of carefully planned, balloon-guided surgical ventricular reconstruction in selected patients with giant post-infarction left ventricular aneurysms and end-stage heart failure when residual viable myocardium is present.