Search Results (188)

Arrhythmogenic cardiomyopathies (ACMs) are a phenotypically and etiologically heterogeneous group of myocardial disorders characterized by fibrotic or fibro-fatty replacement of ventricular myocardium, electrical instability, and an elevated risk of sudden cardiac death. Initially identified as a right ventricular disease, ACMs are now recognized to include biventricular and left-dominant forms. Genetic causes account for a substantial proportion of cases and include desmosomal variants, non-desmosomal variants, and familial gene-elusive forms with no identifiable pathogenic mutation. Nongenetic etiologies, including post-inflammatory, autoimmune, and infiltrative mechanisms, may mimic the phenotype. In many patients, the disease remains idiopathic despite comprehensive evaluation. Cardiac magnetic resonance imaging has emerged as a key tool for identifying non-ischemic scar patterns and for distinguishing arrhythmogenic phenotypes from other cardiomyopathies. Emerging classifications propose the unifying concept of scarring cardiomyopathies based on shared structural substrates, although global consensus is evolving. Risk stratification remains challenging, particularly in patients without overt systolic dysfunction or identifiable genetic markers. Advances in tissue phenotyping, multi-omics, and artificial intelligence hold promise for improved prognostic assessment and individualized therapy. Full article

Background: Mobile health applications have emerged as a novel tool to support secondary prevention after myocardial infarction (MI) or percutaneous coronary intervention (PCI). However, the impact of app-based interventions on clinically meaningful outcomes such as hospital readmissions remains uncertain. Objective: To systematically evaluate the effectiveness of smartphone app-based interventions in reducing unplanned hospital readmissions among post-MI/PCI patients. Methods: A systematic search of PubMed was conducted for randomized controlled trials published between January 2020 and April 2025. Eligible studies evaluated smartphone apps designed for secondary cardiovascular prevention and reported on unplanned hospital readmissions. Risk ratios (RRs) and 95% confidence intervals (CIs) were pooled using a random-effects model. Subgroup analyses were performed based on follow-up duration and user adherence. Results: Four trials encompassing 827 patients met inclusion criteria. App-based interventions were associated with a significant reduction in unplanned hospital readmissions compared to standard care (RR 0.45; 95% CI: 0.23–0.89; p = 0.0219). Greater benefits were observed in studies with longer follow-up durations and higher adherence rates. Improvements in patient-reported outcomes, including health-related quality of life, were also documented. Heterogeneity was moderate. Major adverse cardiovascular events (MACEs) were reported in only two studies and were not analyzed due to inconsistent definitions and low event rates. Conclusions: Smartphone applications for post-MI/PCI care are associated with reduced unplanned hospital readmissions and improved patient-reported outcomes. These tools may play a meaningful role in future cardiovascular care models, especially when sustained engagement and personalized features are prioritized. Full article

Myocardial hypertrophy (MH) represents a complex and heterogeneous condition in the pediatric and young adult population. While rare in children, MH encompasses a wide spectrum of physiological and pathological entities, ranging from transient hypertrophy in the infants of diabetic mothers to progressive genetic hypertrophic cardiomyopathies (HCM) with significant morbidity and mortality. Differential diagnosis is critical, as many phenocopies—including metabolic, mitochondrial, and syndromic diseases—can mimic HCM. Echocardiography remains the first-line imaging modality, with cardiac magnetic resonance (CMR) and molecular diagnostics increasingly used for detailed characterization. Risk stratification tools, such as the HCM Risk-Kids model, support clinical decision-making but must be integrated with individualized assessment. Advances in prenatal screening and genetic testing have significantly improved outcomes, though long-term management requires multidisciplinary care. Understanding age-specific presentations and the underlying etiologies is essential for accurate diagnosis and targeted treatment. This review provides a comprehensive overview of cardiac hypertrophy from fetal life through young adulthood, with a focus on etiologies, diagnostic approaches, imaging modalities, and therapeutic strategies, and aims to guide clinicians through the evolving landscape of MH, emphasizing early recognition, comprehensive evaluation, and personalized care. Full article

Acute myocardial infarction (AMI) in young adults, though less common than in older populations, is an emerging clinical concern with increasing incidence and diverse etiologies. Unlike classic atherosclerotic presentations, a significant proportion of AMI cases in individuals under 45 years are due to nonatherothrombotic mechanisms such as coronary vasospasm, spontaneous coronary artery dissection (SCAD), vasculitis, hypercoagulable states, and drug-induced coronary injury. This manuscript aims to explore the multifactorial nature of AMI in young adults through a focused review of current evidence and a series of illustrative clinical cases. We present and analyze four distinct cases of young patients with AMI, each demonstrating different pathophysiological mechanisms and risk profiles—including premature atherosclerosis, substance use, human immunodeficiency virus (HIV)-related coronary disease, and SCAD. Despite the heterogeneity of underlying causes, early diagnosis, individualized management, and aggressive secondary prevention were key to favorable outcomes. Advanced imaging, lipid profiling, and risk factor modification played a central role in guiding therapy. AMI in young adults requires heightened clinical suspicion and a comprehensive, multidisciplinary approach. Early intervention and recognition of nontraditional risk factors are essential to improving outcomes and preventing recurrent events in this vulnerable population. Full article

Cardiomyopathies represent a heterogeneous group of myocardial disorders, traditionally classified by phenotype into hypertrophic, dilated, and arrhythmogenic. Historically, these conditions have been attributed to high-penetrance rare variants in key structural genes, consistent with a classical Mendelian pattern of inheritance. However, emerging evidence suggests that this model does not fully capture the full spectrum and complexity of disease expression. Many patients do not harbor identifiable pathogenic variants, while others carrying well-known disease-causing variants remain unaffected. This highlights the role of incomplete penetrance, likely modulated by additional genetic modifiers. Recent advances in genomics have revealed a broader view of the genetic basis of cardiomyopathies, introducing new players such as common genetic variants identified as risk alleles, as well as intermediate-effect variants. This continuum of genetic risk, reflecting an overall genetic influence, interacts further with environmental and lifestyle factors, likely contributing together to the observed variability in clinical presentation. This model offers a more realistic framework for understanding genetic inheritance and helps provide a clearer picture of disease expression and penetrance. This review explores the evolving genetic architecture of cardiomyopathies, spanning from a monogenic foundation to intermediate-risk variants and complex polygenic contribution. Recognizing this continuum is essential for enhancing diagnostic accuracy, guiding family screening strategies, and enabling personalized patient management. Full article

Sudden cardiac death represents an unexpected death for which a strong underlying genetic background has been described. The primary causes are identified in cardiomyopathies and channelopathies, which are heart diseases of the muscle and electrical system, respectively, without coronary artery disease, hypertension, valvular disease, and congenital heart malformations. Genetic variants, especially single nucleotide variants and short insertions/deletions impacting essential myocardial functions, have shown that cardiomyopathies display high heritability. However, genetic heterogeneity, incomplete penetrance, and variable expression may complicate the interpretation of genetic findings, thus delaying the management of seriously at-risk patients. Moreover, recent studies show that the diagnostic yield related to genetic cardiomyopathies ranges from 28 to 40%, raising the need for further research. In this regard, investigating the occurrence of structural variants, especially copy number variants, may be crucial. Based on these considerations, this review aims to provide an overview of copy number variants identified in cardiomyopathies and discuss them, considering diagnostic yield. This review will ultimately address the necessity of incorporating copy number variants into routine genetic testing for cardiomyopathies and channelopathies, a process increasingly enabled by advances in next-generation sequencing technologies. Full article

Cardiotoxicity is a leading cause of mortality in the growing populations of elderly breast cancer (BC) patients. Breast cancer treatment in the elderly is highly challenging due to its heterogeneous nature and the lack of specific evidence, as this population is usually underrepresented in randomized clinical trials. Decision making requires a comprehensive approach, considering the type and stage of BC, the patient’s overall health status, life expectancy, geriatric and frailty assessment, the risk of cancer recurrence, comorbidities, cardiotoxicity risk, and the patient’s preferences. The cardiotoxic effects of BC treatments cover the whole spectrum of cardiovascular diseases: heart failure, hypertension, arrhythmias, and myocardial ischemia. Cardiotoxicity risk in these patients is defined by several factors: anticancer therapies, polypharmacy, established cardiovascular disease, comorbidities, frailty, cellular senescence, hormonal changes, and genetic predisposition. Preventive oncological and cardio-oncological strategies, as well as patients’ education, are critical for improved outcomes. Prospective clinical trials in this population are urgently needed. Full article

Cardiac fibrosis is a key physiopathological process underlying the progression of virtually all heart diseases and related conditions, including myocardial infarction, pressure overload, and heart failure. Once regarded as a homogeneous and passive population, cardiac fibroblasts are now recognized as highly heterogeneous and dynamic, comprising distinct subpopulations with specialized molecular and functional identities. These subpopulations include resident fibroblasts, activated myofibroblasts, matrifibrocytes, inflammatory fibroblasts, and senescent fibroblasts, each contributing uniquely to extracellular matrix (ECM) remodeling, cytokine secretion, and intercellular crosstalk. Recent advances in single-cell transcriptomics, lineage tracing, and epigenetic profiling have revealed the plasticity and phenotypic transitions of cardiac fibroblasts in both physiological and pathological contexts. This review synthesizes current knowledge on fibroblast diversity in the adult heart, including their embryological origins and anatomical distribution, and explores how these insights could guide the development of precision anti-fibrotic therapies. We discuss a selection of emerging therapeutic strategies, including subtype-specific targeting (e.g., anti-POSTN, anti-IL1β), modulation of key signaling pathways (e.g., TGF-β, Wnt, Notch), with a brief mention also of novel approaches based on non-coding RNAs and epigenetic regulators. A better understanding of cardiac fibroblast heterogeneity holds significant potential for the design of more specific cell-type and context-tailored interventions, moving toward more effective and personalized treatments for cardiac fibrosis and its sequelae. Full article

Heart failure with preserved ejection fraction (HFpEF) represents nearly half of all heart failure cases and remains diagnostically challenging due to its heterogeneous pathophysiology and often subtle myocardial dysfunction. Conventional echocardiographic parameters, such as left ventricular ejection fraction (LVEF) and the left atrial volume index (LAVI), frequently fail to detect early functional changes. Advanced echocardiographic techniques have emerged as valuable tools for early diagnosis and risk stratification. Global Longitudinal Strain (GLS) allows for the identification of subclinical systolic dysfunction, even with preserved LVEF. Left Atrial Strain (LAS), particularly reservoir and pump strain, provides sensitive markers of diastolic function and elevated filling pressures, offering additional diagnostic and prognostic insights. Myocardial Work (MW), through non-invasive pressure–strain loops, enables load-independent assessment of contractility, while Right Ventricular Free Wall Longitudinal Strain (RVFWLS) captures early right heart involvement, often present in advanced HFpEF. The integration of these advanced parameters can enhance diagnostic precision and guide personalized treatment strategies. This review highlights the current evidence and clinical applications of strain-based imaging in HFpEF, underscoring the importance of a multiparametric, pathophysiology-oriented approach in heart failure evaluation. Full article

Background: Myocardial infarction complicated by cardiogenic shock (MI-CS) remains a critical condition with high mortality rates, despite advances in treatment. Systemic inflammation plays a significant role in MI-CS progression; however, its dynamics across different stages of the Society for Cardiovascular Angiography and Interventions (SCAI) classification remain poorly understood. This study aimed to evaluate indices of systemic inflammation—neutrophil–lymphocyte ratio (NLR), platelet–lymphocyte ratio (PLR), systemic immune-inflammation index (SII), systemic inflammation response index (SIRI), and aggregate index of systemic inflammation (AISI)—in MI-CS patients, correlating them with SCAI stages and survival outcomes. Methods: A single-center retrospective study included 132 patients with MI-CS, categorized into SCAI stages A–E. All patients were assessed for demographic, clinical, and laboratory data, procedural and treatment characteristics, MI timing, and outcomes. Complete blood count test data were used to calculate inflammatory indices and evaluate types of immune reactions. Results: PLR, SII, and AISI peaked at SCAI stage C and declined significantly at stage E, suggesting suppressed inflammation in advanced shock. SIRI emerged as a key prognostic marker for stage C patients, with elevated levels associated with larger infarct size, higher heart rate, and predominant innate immune activation. Patients with SIRI ≥ 3.34 had significantly lower two-year survival (log-rank test, p = 0.006). Conclusions: Inflammation indices, particularly SIRI, provide valuable prognostic insights in MI-CS, reflecting disease severity and heterogeneity of immune response. The decline in inflammatory indices at SCAI stage E may indicate immune suppression in extreme MI-CS, underscoring the need for personalized therapeutic strategies. Full article

Background/Objectives: Polymer-free drug-eluting stents (PF-DESs) aim to mitigate long-term adverse effects associated with polymer-based platforms. However, clinical comparisons with biodegradable polymer DESs (BP-DESs) remain limited. The objective of this review is to assess the efficacy and safety of PF-DESs versus thin-struts (<100 μm) BP-DESs in patients undergoing percutaneous coronary intervention (PCI). Methods: We conducted a systematic review and meta-analysis of randomized controlled trials (RCTs) comparing PF-DESs and BP-DESs in adults undergoing PCI. PubMed, Embase, and CENTRAL were searched up to 1 February 2025. A random-effects model was used to calculate pooled risk ratios (RR) or mean differences (MD) with 95% confidence intervals (CI). Outcomes included myocardial infarction (MI), all-cause and cardiac death, target lesion revascularization (TLR), stent thrombosis, and angiographic/OCT parameters. Subgroup and sensitivity analyses were conducted for outcomes with high heterogeneity (I² > 50%). Results: Nine RCTs (n = 9597) were included. At 12 months, no significant differences were found between PF-DESs and BP-DESs for TLR (RR 1.51; 95% CI: 0.83–2.75), MI, or stent thrombosis. At 24 months, MI and all-cause death were similar between groups. A subgroup analysis showed lower cardiac death with the BioFreedom stent (RR 0.57; 95% CI: 0.35–0.90), not observed in non-BioFreedom devices. No significant differences were detected in angiographic or OCT outcomes, though heterogeneity was high. Conclusions: PF-DESs and BP-DESs demonstrated comparable clinical performance. The observed benefit in cardiac death with BioFreedom may reflect device-specific effects and merits further investigation. Full article

Background/Objectives: Previous research has established that beta-blockers significantly reduce all-cause mortality, cardiovascular mortality, and recurrent acute myocardial infarction (AMI) in patients with left ventricular dysfunction following AMI. However, their efficacy in patients with preserved left ventricular ejection fraction (LVEF) who undergo timely reperfusion and revascularization while receiving evidence-based medical management remains inconclusive. To address this uncertainty, we conducted a systematic review and meta-analysis to synthesize the available evidence on the impact of beta-blocker therapy in patients with AMI and preserved LVEF. Methods: A comprehensive literature search was conducted across PubMed, the Web of Science, and Scopus from their inception until November 2024. The search strategy incorporated three primary keywords and their corresponding Medical Subject Headings (MeSH) terms: “preserved”, “myocardial infarction”, and “beta-blocker”. Data analysis was performed using Review Manager 5.4 software. A random-effects model was applied to account for the study’s heterogeneity, while a fixed-effects model was utilized for homogeneous outcomes. Pooled odds ratios (ORs) and hazard ratios (HRs) were calculated for dichotomous outcomes, with a 95% confidence interval (CI) and a significance threshold of p < 0.05. Results: Beta-blocker therapy was significantly associated with a reduction in all-cause mortality compared to non-use, with an OR of 0.73 (95% CI: 0.61–0.88, p = 0.001) and an HR of 0.78 (95% CI: 0.67–0.91, p = 0.002). Similarly, beta-blocker administration was linked to a lower risk of cardiovascular mortality, demonstrating an OR of 0.76 (95% CI: 0.68–0.84, p < 0.00001) and an HR of 0.76 (95% CI: 0.59–0.99, p = 0.04). Furthermore, beta-blocker use was significantly correlated with a decreased risk of major adverse cardiovascular events (MACEs) compared to non-use, with an OR of 0.84 (95% CI: 0.75–0.95, p = 0.004) and an HR of 0.84 (95% CI: 0.71–0.99, p = 0.04). Conclusions: The current meta-analysis suggests a potential beneficial association between beta-blocker use and outcomes in patients with AMI and preserved LVEF, including lower rates of all-cause mortality, cardiovascular mortality, and MACEs; however, these findings should be interpreted with caution due to the observational nature of most included studies. Therefore, further randomized controlled trials (RCTs) are needed to confirm these findings, particularly in distinguishing outcomes among patients with and without heart failure. Full article

Background: Over the last 15 years, few echocardiographic studies have examined the biventricular mechanics by speckle tracking echocardiography (STE) in patients affected by chronic obstructive pulmonary disease (COPD) without advanced lung disease. We aimed to summarize the main findings of these studies and quantify the overall effect of COPD on biventricular mechanics in patients without severe airflow obstruction. Methods: Eligible studies assessing cardiac function by conventional transthoracic echocardiography (TTE), implemented with a STE analysis of left ventricular (LV)-global longitudinal strain (GLS) and/or right ventricular (RV)-GLS in COPD patients without severe airflow obstruction vs. healthy controls, were selected from the PubMed, Embase and Scopus databases. The primary endpoint was to quantify the effect of COPD on LV-GLS and RV-GLS in individuals without advanced lung disease. Continuous data [LV-GLS, RV-GLS, left ventricular ejection fraction (LVEF) and tricuspid annular plane systolic excursion (TAPSE)] were pooled as the standardized mean difference (SMD) comparing COPD cohorts with healthy controls. Results: Ten studies were included, totaling 682 COPD patients and 316 healthy controls. Overall, COPD showed a large effect on LV-GLS (SMD −1.296; 95%CI −2.010, −0.582, p < 0.001) and RV-GLS (SMD −1.474; 95% CI −2.142, −0.805, p < 0.001), a medium-to-large effect on TAPSE (SMD −0.783, 95% CI −0.949, −0.618, p < 0.001) and a small effect on LVEF (SMD −0.366, 95% CI −0.659, −0.074, p = 0.014). The I² statistic value for the LV-GLS (91.1%), RV-GLS (88.2%) and LVEF (76.7%) studies suggested a high between-study heterogeneity, while that for the TAPSE (38.1%) studies was compatible with a low-to-moderate between-study heterogeneity. Egger’s test yielded a p-value of 0.16, 0.48, 0.58 and 0.50 for LV-GLS, RV-GLS, LVEF and TAPSE studies, respectively, indicating an absence of publication bias. Meta-regression analyses excluded that the effect of COPD on biventricular mechanics might be influenced by potential confounders (all p > 0.05). Sensitivity analysis confirmed the robustness of the LV-GLS, RV-GLS and TAPSE studies’ results. Conclusions: COPD appears to be independently associated with a mild attenuation of biventricular mechanics in patients with moderate airflow limitations, despite a preserved LVEF and TAPSE on conventional TTE. STE analysis may allow clinicians to identify COPD patients with subclinical myocardial dysfunction and an increased risk of heart failure and cardiovascular complications early. Full article

Background and Objectives: Post-term pregnancies are associated with increased risks of perinatal complications. This study aimed to evaluate potential cardiac electrophysiological changes in pregnant women by comparing the QRS duration, interval of corrected QT (QTc), and frontal QRS-T angle [f(QRS-T)] between term and post-term pregnancies. Materials and Methods: In this observational prospective study, 120 pregnant women were enrolled—60 term (37–41 weeks) and 60 post-term (≥42 weeks). All participants underwent standard 12-lead electrocardiography (ECG) and caesarean section with spinal anaesthesia. The QTc interval, QRS duration, and frontal QRS-T angle were measured. Demographic parameters such as age, gestational week, height, and weight were recorded. The SPSS software was used to analyse the data with p < 0.05 as the threshold for significance. Results: Post-operative QTc interval (417.3 ± 20.5 vs. 410.2 ± 14.5, p = 0.032) and f(QRS-T) (28 [16–55] vs. 22 [14–34], p = 0.042) were significantly higher in the post-term group than in the term group. When the change in the f(QRS-T) angle was analysed, there was a significant widening of this angle in the post-term group (from 21 [11–37] to 28 [16–55], p = 0.002). The increased f(QRS-T) angle reflects greater heterogeneity in ventricular depolarisation and repolarisation, which may indicate sub-clinical myocardial stress or altered autonomic regulation in the post-term period. Although no overt arrhythmias were observed, subtle changes in P-wave morphology and QT dispersion were more prevalent in the post-term group. Conclusions: Prolonged QRS duration and an increased f(QRS-T) angle in post-term pregnancies can reflect the underlying changes in cardiac electrophysiology related to prolonged gestation. These ECG parameters may serve as non-invasive indicators of sub-clinical cardiac stress, which could be relevant for anaesthetic risk assessment and perinatal management. Full article

Heart failure with preserved ejection fraction (HFpEF), marked by cardiac diastolic dysfunction, contributes to half of all heart failure cases globally and poses a significant public health challenge. Effective therapies for HFpEF are rare, largely due to its complex and heterogeneous pathophysiology, which often involves multiple comorbidities. Berberine (BBR), an isoquinoline alkaloid, has demonstrated beneficial effects on multiple metabolic and cardiovascular disorders; however, its impact on cardiac diastolic dysfunction in HFpEF remains poorly understood. In this study, we utilized a rat model of HFpEF induced by a sustained high-fat/high-sucrose (HFHS) diet to explore the impact and mechanisms of BBR on diastolic dysfunction. The results revealed that BBR administration effectively alleviated cardiac diastolic dysfunction and alleviated extracardiac comorbidities, including increased weight, impaired glucose tolerance, hypercholesterolemia and hypertension, in rats fed an HFHS diet. Furthermore, BBR mitigated myocardial inflammation, oxidative stress, microvascular endothelial dysfunction, and notably restored the disturbed NO-cGMP-PKG pathway. Additionally, BBR reduced myocardial fibrosis and inhibited the abnormally activated TGF-β/Smads signaling. Moreover, BBR attenuated the systemic inflammation and corrected immune dysregulation in an HFHS diet-fed rats. Our study suggests that BBR exhibits multi-beneficial effects in the prevention and management of HFpEF, demonstrating its potential as a holistic therapeutic candidate for HFpEF. Full article