Background: Chronic kidney disease (CKD) is linked to high cardiovascular morbidity and mortality. Many patients remain at risk despite standard treatment. This review assessed the renal, cardiovascular, safety, and primary care implementation outcomes of sodium-glucose cotransporter-2 (SGLT2) inhibitors in CKD, including patients with and without diabetes. Methods: This systematic review followed PRISMA 2020 guidelines. PubMed, Scopus, and Google Scholar were searched for English-language human studies published between 2016 and 2026. Reference lists of eligible articles were also manually screened. Eligible studies included randomized controlled trials and primary observational studies evaluating SGLT2 inhibitors in patients with CKD, with or without diabetes. Studies reporting renal, cardiovascular, safety, or primary care implementation outcomes were included. Data were extracted using a standardized form and synthesized qualitatively because of clinical and methodological heterogeneity. Results: Fifteen primary studies were included, comprising randomized controlled trials and observational studies. Across landmark clinical trials and real-world studies, SGLT2 inhibitors slowed eGFR decline, reduced albuminuria, and lowered the risk of kidney and heart failure hospitalization. Renal and cardiovascular benefits were observed in patients with and without diabetes. SGLT2 inhibitors were generally well tolerated, with genital mycotic infections and volume depletion being the most reported adverse events, while serious adverse events were uncommon. Real-world studies consistently identified underprescription and implementation barriers in primary care. Discussion: SGLT2 inhibitors are foundational therapies for CKD, providing consistent renal and cardiovascular benefits with an acceptable safety profile in patients with and without diabetes. However, substantial gaps remain in their implementation in primary care. Improving early identification of eligible patients, clinician awareness, and integration of guideline-directed prescribing into routine practice may help reduce CKD progression and cardiovascular events.
Parturients with pulmonary arterial hypertension (PAH) face an increased risk of morbidity and mortality surrounding the peripartum period. Patients with severe PAH and Eisenmenger syndrome have the highest risk for perioperative mortality and provide a significant perioperative challenge for anesthesiologists, necessitating a multidisciplinary approach throughout pregnancy. We present a case of an urgent cesarean section at 37 weeks of gestation in a patient with Eisenmenger syndrome, a large atrial septal defect, and supra-systemic pulmonary hypertension. Due to the patient’s severity of PAH, cardiothoracic surgery was present and placed femoral arterial and venous catheters in preparation for possible extracorporeal membrane oxygenation (ECMO) cannulation in the event of hemodynamic collapse. The procedure was performed under a carefully titrated epidural, thus avoiding general anesthesia and the dangers associated with inducing a patient with her comorbid conditions. An arterial line, internal jugular central line, and Swan-Ganz catheter were placed while the patient was awake to aid in monitoring. Additionally, transthoracic echocardiography (TTE) was used to assist in cardiac monitoring while the epidural level was gradually increased. She was maintained on vasopressin, epinephrine, and phenylephrine infusions in addition to inhaled nitric oxide. She tolerated the procedure well, and the fetus was delivered safely. Careful management across pre-epidural, post-epidural, intraoperative, and postoperative stages illustrates the dynamic adjustments and multidisciplinary communication required in this patient population. Advanced medical therapy optimization, careful neuraxial anesthesia titration, and early consideration of extracorporeal cardiopulmonary resuscitation (ECPR) together capture the critical elements of management in this complex setting.
Sodium–glucose cotransporter 2 inhibitors (SGLT2i) were originally developed as glucose-lowering therapies for type 2 diabetes mellitus. However, robust clinical evidence has demonstrated substantial cardiovascular and renal protective effects that extend beyond glycemic control. Emerging data highlight their systemic influence across the cardiovascular–renal–metabolic (CRM) continuum, a conceptual framework describing the shared pathophysiological links between metabolic dysfunction, heart failure (HF), and chronic kidney disease (CKD). Despite the rapid expansion of clinical and mechanistic evidence, the integration of these insights into coordinated therapeutic implementation across cardiology, nephrology, and endocrinology remains incompletely synthesized. This structured narrative review synthesized evidence from PubMed/MEDLINE, Embase, and Google Scholar to identify relevant studies published between January 2016 and December 2025. Emphasis was placed on randomized controlled trials, meta-analyses, large observational cohorts, guideline documents, and translational mechanistic investigations evaluating pharmacologic mechanisms, clinical efficacy, and multidisciplinary applications of SGLT2i across CRM conditions. Cardiovascular and renal outcome trials consistently show that SGLT2i reduce hospitalization for heart failure, delay CKD progression, and improve major cardiovascular outcomes in both diabetic and non-diabetic populations. Mechanistically, these agents restore tubuloglomerular feedback, enhance cardiac energy efficiency through increased ketone utilization, attenuate inflammatory and profibrotic signaling pathways, and improve mitochondrial bioenergetics. These multisystem effects contribute to therapeutic benefits across HF phenotypes and CKD stages while also improving metabolic parameters such as adiposity, blood pressure, and hepatic steatosis. Collectively, current evidence supports SGLT2i as foundational disease-modifying therapies across the CRM spectrum. Future investigations should prioritize precision-based treatment approaches, biomarker-guided patient selection, and rational combination pharmacotherapy to further optimize outcomes across interconnected cardiovascular, renal, and metabolic diseases.
Aim: Takotsubo cardiomyopathy (TTC) is an acute form of systolic dysfunction triggered by physical or emotional stress, most commonly seen in postmenopausal women. Its pathophysiology involves catecholamine surge, autonomic imbalance, and microvascular dysfunction. Fibromyalgia is a chronic pain disorder observed primarily in premenopausal women characterized by autonomic dysregulation, central sensitization, and high psychiatric comorbidity—mechanisms that overlap substantially with TTC. Nevertheless, fibromyalgia has not been established as an independent risk factor for TTC. This study evaluated the association between fibromyalgia and TTC using a nationally representative sample. Methods: A retrospective case-control study was conducted using the 2022 National Inpatient Sample. Adult hospitalizations with TTC (ICD-10-CM I51.81) were identified, and a 1% random sample of non-TTC admissions served as controls. Fibromyalgia was defined by ICD-10 code M79.7. Survey-weighted multivariable logistic regression assessed the association between fibromyalgia and TTC, adjusting for demographics, comorbidities, and severity of illness. Results: Among 9,376 TTC and 65,690 control hospitalizations, fibromyalgia was present in 282 (3.0%) TTC cases and 827 (1.3%) controls. After multivariable adjustment, fibromyalgia was independently associated with TTC (OR 1.19; 95% CI 1.00–1.42, P = 0.044). This association persisted after accounting for psychiatric comorbidities. Conclusions: Fibromyalgia was associated with increased odds of TTC. These findings highlight the need for vigilance in evaluating fibromyalgia patients with chest pain and warrant further research into mechanisms underlying stress-induced cardiomyopathy.
Aim: Artificial intelligence may support syncope evaluation, but reliability of language models in structured syncope care remains uncertain. We evaluated diagnostic performance, safety, and within-case consistency of Generative Pre-trained Transformer-5 (GPT-5) in patients with transient loss of consciousness (T-LOC). Methods: This prospective cohort study included 55 patients evaluated in syncope units. GPT-5 and a syncope-expert assessed identical case information after core evaluation (CE: history-taking, physical examination, active standing test, and 12-lead electrocardiogram) and extended evaluation (EE: CE plus additional testing when indicated). An expert panel adjudicated the final diagnosis after 18 months. Outcomes were diagnostic yield, final-diagnosis inclusion rate, diagnostic precision score (DPS), cardiac diagnostic safety, and within-case consistency across five repeated GPT-5 runs. Results: Of 55 patients, 54 had complete follow-up for performance analyses. Diagnostic yield was 94% for the syncope-expert at CE and EE, and 100% and 96% for GPT-5 at CE and EE, respectively. GPT-5 included the final diagnosis in 52% (CE) and 57% (EE) of cases, versus 67% for the syncope-expert. DPS remained negative for GPT-5 at CE (mean −0.03, SD 0.54) and EE (mean −0.01, SD 0.49). Among four final cardiac syncope cases, GPT-5 selected the final diagnosis in one case and the syncope-expert in three. First-diagnosis consistency across five GPT-5 runs was 69% after CE and 74% after EE. Conclusions: GPT-5 generated diagnostic outputs frequently but showed limited precision, cardiac safety concerns, and within-case variability. Its role in syncope evaluation should remain supportive within clinician-led pathways rather than autonomous.
Gasdermin D (GSDMD) has been identified as a potential key effector protein within the inflammatory response and is characterized as a primary executor of pyroptosis through the formation of transmembrane pores. This review evaluates the emerging role of GSDMD-mediated pyroptosis in the pathogenesis of cardiovascular diseases (CVDs), with a specific focus on its potential contributions to atherosclerosis. We examine how the activation of GSDMD by inflammasomes, such as NLRP3 and AIM2, facilitates the release of inflammatory cytokines (IL-1β and IL-18) and damage-associated molecular patterns (DAMPs). Central to this discussion is the proposed role of GSDMD in driving macrophage foam cell death and vascular smooth muscle cell (VSMC) dysfunction. These factors are associated with necrotic core expansion and increased risk of atherosclerotic plaque instability. Furthermore, GSDMD may mediate endothelial dysfunction and disrupt lipid metabolism, and is suggested to participate in systemic signaling via extracellular vesicles. Finally, we highlight the therapeutic potential of targeting GSDMD as a possible strategy to stabilize vulnerable plaques, which may offer new avenues for cardiovascular precision medicine.
Aim: Older adults with dyslipidemia often have coexisting diabetes and hypertension, requiring triple therapy with statins, antihypertensives, and oral antidiabetics. Given that statin adherence is a key metric in the Medicare STAR Ratings program, understanding statin use in this population is critical. However, prior studies have focused on adherence to statin monotherapy or composite adherence to triple therapy, with limited evidence on statin-specific patterns in this population. Methods: We conducted a retrospective cohort study using a Texas-based Medicare Advantage database (2016–2017). Adults receiving concurrent triple therapy (statins, renin-angiotensin system antagonists, and oral antidiabetics) were followed for 12 months. Statin adherence was measured monthly using the proportion of days covered (PDC) and modeled using group-based trajectory modeling (GBTM). Multinomial logistic regression, informed by the Andersen behavioral model, was used to identify sociodemographic and clinical predictors of adherence trajectories. Results: Among 7,847 patients, three distinct statin adherence trajectories were identified: near-perfect adherence (57.0%), adherent (23.6%), and rapid decline (19.4%). Female sex was associated with higher odds of rapid decline than male sex. Younger age (≤ 65 years) and having at least one prior hospitalization were significant predictors of rapid adherence decline, whereas older age and a greater number of concomitant medications were associated with lower odds of decline. Notably, about 80% of patients were adherent to statin despite lower adherence to the overall triple-therapy regimen. Conclusions: This study identified three distinct statin adherence trajectories among older adults on triple therapy. By highlighting predictors of rapid adherence decline, including female sex and prior hospitalization, these findings can help clinicians identify high-risk patients and inform targeted interventions to improve adherence and cardiovascular outcomes.
Aim: Low cardiac output syndrome (LCOS) may be improvable; hence, timely detection and intervention are essential. However, no model has been established for the prediction of LCOS onset post non-isolated coronary artery bypass grafting (CABG) surgery. Therefore, this study aimed to develop a machine-learning-based model to predict LCOS after non-isolated CABG. Methods: A total of 378 patients who underwent non-isolated CABG at Nanjing First Hospital, China, were retrospectively assessed. Five algorithms [L2 regularized logistic regression (LR), random forest (RF) classifier, extreme gradient boosting (XGB), light gradient boosting machine (LGBM), and support vector machine (SVM)] were employed. Model performance and clinical utility were evaluated using area under the curve (AUC), 10-fold cross-validation, and decision curve analysis (DCA). SHapley Additive exPlanations (SHAP) were used to assess the model’s interpretability. A web calculator was developed. Results: XGB showed superior performance and calibration (AUC: 0.933, 95% CI: 0.903–0.962; Brier score of 0.107), with excellent specificity (0.865), accuracy (0.860), and precision (0.753). In testing, XGB maintained excellent discrimination (AUC: 0.868, 95% CI: 0.799–0.936), best specificity (0.785), accuracy (0.781), and precision (0.614). DCA confirmed clinical usefulness. SHAP analysis identified the ejection fraction, left ventricular end-systolic diameter, and lactate levels as the most influential predictors. The web calculator is accessible via https://lcos-cabg-xgb-model.streamlit.app/ Conclusions: The developed web-based XGB model effectively predicts LCOS after non-isolated CABG, aiding early risk stratification and detection.
Coronary vasospasm, affecting both epicardial arteries and the coronary microcirculation, is a significant yet frequently underdiagnosed and undertreated cause of coronary syndromes. When promptly identified, it carries a relatively benign prognosis. Recognition can be straightforward in non-cardiology settings when triggered by known spasmogenic agents such as misoprostol (obstetrics) or 5-fluorouracil (oncology). Vasospasm may also be incidentally revealed during noninvasive functional testing, typically presenting as ST-segment elevation during early recovery phases, or after administration of agents like aminophylline following dipyridamole or β-blockers following dobutamine. In patients with high clinical suspicion but negative Holter or stress test findings, targeted provocation with ergonovine or hyperventilation protocols can safely induce vasospasm and unmask regional wall motion abnormalities, indicating epicardial involvement. Hyperventilation-Doppler echocardiography enables the detection of microvascular dysfunction through reductions in coronary flow velocity in the mid-distal left anterior descending coronary artery. A multi-stress, multi-marker functional testing approach offers a noninvasive, safe, and effective diagnostic strategy. Inducible wall motion abnormalities are specific for epicardial spasm, while Doppler-detected flow reduction is more sensitive for microvascular dysfunction. Early diagnosis is essential, as coronary vasospasm, though potentially life-threatening, is highly manageable with appropriate therapy. Management of patients with proven epicardial coronary artery or microvascular vasospasm involves starting therapy with calcium channel blockers and nitrates, and avoiding β-blockers, as they can worsen vasospasm by blocking β2-mediated vasodilation and leaving α1-mediated vasoconstriction unopposed.
Implantable cardioverter defibrillators (ICDs) play a central role in the prevention of sudden cardiac death. Although implantation is generally safe, rare but clinically significant complications may occur. One such complication is inadvertent placement of a transvenous ICD lead into the left ventricle via a patent foramen ovale (PFO), which carries a risk of systemic thromboembolism and may remain clinically silent for prolonged periods. We report a case of an ICD lead malpositioned in the left ventricle through a PFO, detected 17 months after implantation during transthoracic echocardiography performed for worsening dyspnoea. Imaging demonstrated the lead traversing the interatrial septum and mitral valve into the left ventricle. The patient underwent successful transvenous extraction and reimplantation of a new right ventricular lead without complications. This case highlights the limitations of electrocardiographic clues alone and underscores the importance of multimodality imaging and meticulous implantation technique. A focused narrative review integrates current literature regarding mechanisms, diagnostic strategies, management options, and preventive considerations.
High-sensitivity cardiac biomarkers have transformed modern cardiology by enabling earlier diagnosis and refined risk stratification in acute coronary syndromes and heart failure. However, increasing analytical sensitivity has also amplified the clinical impact of immunoassay interferences, particularly those caused by heterophile antibodies. These endogenous antibodies can interact with assay antibodies and generate false-positive or false-negative results, most notably in sandwich immunoassays used for cardiac troponins and natriuretic peptides. Persistent, clinically implausible biomarker elevations related to heterophile antibody interference have led to unnecessary invasive procedures, inappropriate pharmacologic treatment, repeated hospital admissions, and prolonged diagnostic uncertainty. Conversely, false-negative results may delay diagnosis, result in inappropriate discharge, and contribute to adverse clinical outcomes in high-risk patients. This review summarizes the immunological basis and analytical mechanisms of heterophile antibody interference, highlights cardiac biomarkers most commonly affected, and outlines key clinical red flags that should prompt suspicion. Practical laboratory strategies include polyethylene glycol precipitation as an initial approach to detect antibody-mediated interference, followed by dilution studies, heterophile blocking reagents, and cautiously interpreted alternative platform testing within assay-specific reference frameworks, together with close clinician-laboratory collaboration. Greater awareness of analytical interference is critical as cardiology becomes increasingly biomarker-driven. Integrating clinical judgment with structured laboratory verification can substantially reduce diagnostic error, improve patient safety, and prevent avoidable healthcare utilization in contemporary cardiovascular practice.
Heart failure (HF) is still one of the most common causes of death today. The vast majority of heart diseases end up leading to HF, which therefore has a high prevalence in the adult population (on average 1–2%), and which increases enormously (over 10%) after the age of 65, becoming the most frequent cause of hospitalization for these subjects. It is therefore necessary to increase efforts to deepen our understanding of the pathophysiological mechanisms that lead to HF and its worsening, particularly with regard to hormonal-metabolic derangements as contributors to HF development and progression. This, in the hope of being able, in the near future, to intervene on them, reducing the prevalence of this pathology and its economic impact on countries’ healthcare spending. To this aim, we performed a narrative review of the scientific literature on the interactions between both insulin and the growth hormone/insulin-like growth factor-1 axis and the cardiovascular system, and in particular, to verify the role that these hormones may play in the development and negative progression of HF.
The Gerbode defect is characterized by a high ventricular septal defect associated with a defect in the septal leaflet of the tricuspid valve, allowing blood to enter the right atrium from the left ventricle. It accounts for approximately 0.08% of intracardiac shunts and may be congenital or acquired. We describe a rare case of Gerbode defect secondary to tricuspid valve endocarditis. A 58-year-old male patient presented with acute infective endocarditis due to Staphylococcus aureus, related to central venous access. Echocardiography showed a tricuspid valve with thickened leaflets and a small mobile image on the atrial side of the septal leaflet, as well as moderate to severe regurgitation. After completion of the antibiotic regimen with resolution of the infectious condition, the patient was discharged asymptomatic, and a new echocardiogram showed no vegetation on the tricuspid valve. During outpatient follow-up, he presented dyspnea on mild exertion, and consecutive echocardiograms showed moderate tricuspid insufficiency and significant pulmonary hypertension with a pulmonary artery systolic pressure of 83 mmHg (reference: 30 mmHg). He underwent right and left cardiac catheterization, which showed a Gerbode defect, and a transesophageal echocardiogram showed a shunt in the subaortic region measuring 6 to 8 mm, with a maximum gradient of 56 mmHg. He underwent elective surgery to correct the Gerbode defect and tricuspid valve repair, with a good clinical result. The Gerbode defect is rare, and the diagnosis can be challenging because it simulates other conditions. Treatment consists of closing the defect when it generates refractory symptoms or complications. The reported case was surgically corrected, with a good result and favorable evolution.
Polycystic ovary syndrome (PCOS) is a common endocrine–metabolic condition that carries a higher cardiovascular risk than currently reflected by traditional screening tools. Emerging evidence suggests that resting tachycardia and autonomic dysfunction may serve as early, non-invasive indicators of cardiovascular dysregulation in this population. This review synthesizes current data on resting heart rate (RHR), heart rate variability (HRV), and direct autonomic markers in women with PCOS, drawing from human studies published between 2000 and 2025. Across 32 eligible studies, most reported increased sympathetic activity, reduced parasympathetic tone, elevated RHR, and impaired HRV patterns observed even in normal-weight or metabolically mild PCOS phenotypes. These alterations correlate with endothelial dysfunction, arterial stiffness, and subclinical atherosclerosis, underscoring their cardiovascular relevance. Mechanistic insights highlight the contributions of insulin resistance, hyperandrogenism, inflammation, adipokine imbalance, chemoreflex sensitization, and altered cortisol metabolism to autonomic disruption. Despite consistent findings, methodological variability in HRV protocols and inadequate adjustment for major confounders limit definitive interpretation. RHR, due to its simplicity and accessibility, including through wearable devices, holds promise as a supportive early risk signal; however, it should not be used in isolation. Future studies must adopt standardized autonomic measurements, including diverse cohorts, and evaluate whether modifying autonomic markers translates into improved cardiometabolic outcomes. Integrating RHR and HRV with metabolic and endocrine markers may enhance early cardiovascular risk stratification in women with PCOS.
Redesigning cardiovascular services at the local level is a pressing task for decentralized health systems facing the rising burden of chronic cardiovascular disease. In northern Modena (Emilia-Romagna, Italy), a post-restructuring reorganization exposed the limits of hospital-centric models and the need for integrated, patient-centered care. In 2021, Santa Maria Bianca Hospital, Mirandola—a first-level, non-interventional facility serving a largely rural population—launched a program to build a digitally integrated, prevention-oriented cardiology network. This review distills that field experience into a scalable framework for organizing peripheral cardiovascular services. The Mirandola Cardiology Network evolved along six operational domains: (1) reactivation of the cardiology unit with community outreach; (2) expansion of outpatient services and telecardiology; (3) a day hospital platform for chronic heart failure management; (4) digital transformation of the echocardiography service; (5) development of an advanced imaging center integrating coronary computed tomography (CT) angiography and planned cardiac magnetic resonance imaging (MRI); and (6) consolidation of professional education, research, and network-wide governance. By combining digital tools, non-invasive imaging, and multidisciplinary collaboration, the model established continuity of care across inpatient, outpatient, and community settings while improving access to diagnostics and appropriateness of care. Although prospective or comparative outcomes are not presented, process indicators and implementation milestones suggest scalability and sustainability, with potential to reduce avoidable admissions and streamline clinical pathways. The Mirandola experience shows that innovation in cardiology is feasible in peripheral settings when investment in technology, governance, and training is aligned with a coherent, value-based vision. It offers actionable guidance for decentralized systems seeking to implement digitally enabled, community-focused cardiology consistent with contemporary recommendations on territorial care and chronic disease management.
Left ventricular pseudoaneurysm is a rare acquired cardiac abnormality that frequently occurs after myocardial infarction or a previous cardiac procedure. Blunt chest trauma accounts for this uncommon entity in sporadic cases. However, this disease does not have any specific clinical findings, so it is necessary to monitor the suspected patient closely. The standard noninvasive techniques for diagnosing left ventricular pseudoaneurysms are transthoracic echocardiography and thoracic computed tomography. Untreated ventricular pseudoaneurysms carry a considerable risk of rupture, ranging from 30% to 45%. So, an urgent surgical treatment is often required. Herein, we aimed to present a 34-year-old male who underwent emergency surgery as a result of cardiac perforation three hours after a traffic accident and developed a giant left ventricular pseudoaneurysm 19 months after discharge. The giant pseudoaneurysm was successfully repaired. This case highlights the need for long‑term surveillance after blunt cardiac trauma to detect late pseudoaneurysm formation.
Background: Heart failure (HF) remains a growing global health problem, with nearly half of all cases attributed to HF with preserved ejection fraction (HFpEF) and its precursor, left ventricular diastolic dysfunction (LVDD). Although echocardiography is the diagnostic gold standard, its high cost and limited availability restrict its use for large-scale screening. In contrast, the electrocardiogram (ECG) is inexpensive and widely accessible. Recent advances in artificial intelligence (AI) have created opportunities to leverage ECG data for the early detection of cardiac dysfunction. The objective of this study was to systematically review and meta-analyze the diagnostic performance of AI-based ECG models for detecting cardiac dysfunction. Methods: The QUADAS-2 tool was used to assess the risk of bias. Pooled sensitivity and specificity were estimated using a bivariate random-effects model, with heterogeneity quantified using the I2 statistic. Pre-specified subgroup analyses were conducted according to clinical endpoint and AI model type. Results: Following Preferred Reporting Items for Systematic Reviews and Meta-Analyses (PRISMA) guidelines, nine eligible studies evaluating AI algorithms applied to ECG data for the detection of HFpEF were identified. Considerable methodological and population heterogeneity was observed across studies. Risk of bias was generally low for reference standards, although concerns were noted in patient selection. The pooled specificity of AI-ECG models was high at 0.83 [95% confidence interval (CI): 0.74–0.89], while pooled sensitivity was 0.82 (95% CI: 0.70–0.90). Both estimates demonstrated extremely high heterogeneity (I2 > 96%). Subgroup analyses by endpoint and model type did not explain this variability. Discussion: AI-enhanced ECG models show good diagnostic accuracy, specifically in ruling out cardiac dysfunction due to their high specificity. However, the high and unexplained heterogeneity across these studies limits the immediate generalizability of the results. Large, prospective validation studies across diverse populations are essential before these models can be confidently adopted into routine clinical practice.
Catecholaminergic polymorphic ventricular tachycardia (CPVT) is a rare but potentially life-threatening inherited arrhythmia disorder, often presenting in childhood or adolescence. Early and accurate diagnosis is critical, as untreated CPVT carries a high risk of sudden cardiac death, particularly in young individuals. This case underscores the importance of maintaining a high index of clinical suspicion and employing a systematic diagnostic approach. We highlight the value of integrating clinical history, family background, and targeted investigations in evaluating young adults presenting with sudden cardiac arrest. Prompt recognition and diagnosis of CPVT may be lifesaving and have significant implications for both patients and their families.
Background: Myosin inhibitors have been shown to improve exercise capacity and symptoms, as well as reduce the left ventricular outflow tract (LVOT) gradient. This study explores the efficacy of mavacamten versus aficamten in hypertrophic cardiomyopathy (HCM) patients. Methods: From the inception to October 2024, the electronic databases [Cochrane Central Register of Controlled Trials (CENTRAL), PubMed, and ClinicalTrials.gov] were searched. Using a random-effects model and a frequentist framework, specific effect sizes [mean difference (MD) and risk ratio (RR)] were pooled. Results: This network meta-analysis included six randomized controlled trials (RCTs). A total of 826 individuals with HCM were included; 443 of them received a cardiac myosin inhibitor, while 383 received placebo. Comparison of aficamten versus mavacamten through a common comparator, placebo, showed that aficamten caused a lesser decrease in resting LVOT gradient than that of mavacamten [MD = 14.74, 95% CI (3.02; 26.47)]. Therefore, mavacamten ranked higher (P-score = 0.9966) than aficamten (P-score = 0.5034) in decreasing resting LVOT gradient. Aficamten significantly reduced left ventricular ejection fraction (LVEF) in contrast to mavacamten [MD = –5.59, 95% CI (–10.43; –0.75)]. According to P-score ranking, mavacamten (0.5053) ranked higher than aficamten (0.0059). For New York Heart Association (NYHA) class improvement, there was no statistically significant difference between the two groups [MD = –0.37, 95% CI (–1.79; 1.06)]. But P-score ranked mavacamten (0.8466) higher than aficamten (0.6533). Discussion: Mavacamten ranked superior to aficamten in HCM management. However, this ranking is based not on the absolute clinical benefit but on the network point estimates. Additionally, due to a larger body of clinical evidence supporting mavacamten, it has a clear advantage in terms of reliability. Therefore, more direct trials comparing the two drugs would be required to confirm which one is better and provide conclusive evidence.
Rheumatoid arthritis (RA) confers an elevated cardiovascular disease (CVD) risk through systemic inflammation, arterial stiffness, and myocardial dysfunction. The ratio of carotid-femoral pulse wave velocity (PWV) to left ventricular global longitudinal strain (LV-GLS) has been proposed as a novel index of ventricular-arterial coupling. This study investigated whether a one-year physical activity intervention improves the PWV/LV-GLS ratio in RA patients without known CVD. Eighteen participants with RA from the prospective PARA 2010 study underwent baseline and one-year assessments. PWV was measured by oscillometry, and LV-GLS by speckle-tracking echocardiography. Physical activity was promoted through supervised circuit training and additional moderate-to-vigorous activity. At one year, very active participants [≥ 1,000 metabolic equivalent of task (MET)-minutes/week, n = 10] showed a relative reduction in PWV/LV-GLS ratio compared with baseline, while no change was observed in less active participants (< 1,000 MET-minutes/week, n = 8). Between-group comparison at follow-up demonstrated significantly lower PWV/LV-GLS ratio in very active versus less active patients (p < 0.05). No significant between-group differences were observed when PWV and LV-GLS were analyzed separately. In conclusion, a high level of physical activity was associated with improved ventricular-arterial coupling, reflected by a lower PWV/LV-GLS ratio, in RA patients. These findings support a potential dose-dependent effect of physical activity on subclinical cardiovascular function in RA. The clinical trial was registered at http://www.isrctn.com, unique identifier: ISRCTN88886304.
