Journal of Cardiovascular Development and Disease最新文献

Background: Ticagrelor is a reversible, direct inhibitor of the platelet adenosine diphosphate (P2Y12) receptor, widely used in combination with acetylsalicylic acid (ASA) as dual antiplatelet therapy (DAPT) in patients with acute coronary syndrome (ACS) to prevent cardiovascular events. Despite its well-established efficacy, ticagrelor may cause adverse effects ranging from common ones (e.g., bleeding, dyspnea) to rare but potentially serious reactions such as bradyarrhythmias. These rare events are likely related to elevated adenosine levels secondary to inhibition of the human equilibrative nucleoside transporter 1 (hENT1).

Methods: We describe two clinical cases of ticagrelor-associated bradyarrhythmia observed in patients following ACS. Both cases were analyzed in terms of clinical presentation, ECG findings, management strategy, and outcomes after discontinuation of the drug.

Results: The first case concerns a 67-year-old woman with non-ST-segment elevation myocardial infarction (NSTEMI) who developed complete atrioventricular block (third degree) with a 45 s asystolic pause and syncope. The second case involves a 67-year-old man with anterior ST-segment elevation myocardial infarction (STEMI) who experienced recurrent sinus pauses lasting up to 5 s. In both cases, symptoms resolved following ticagrelor discontinuation and theophylline administration. No recurrence of arrhythmia was observed after switching to prasugrel.

Conclusions: Ticagrelor-induced bradyarrhythmias, although rare, represent an important and reversible adverse effect that clinicians should be aware of, particularly during the early post-ACS phase. Prompt recognition and drug withdrawal may prevent severe outcomes and avoid unnecessary interventions such as pacemaker implantation. Further studies are warranted to identify patient-specific risk factors predisposing to ticagrelor-related conduction disturbances.

This study used a rat model of coronary artery reperfusion imaged with preclinical 7-tesla magnetic resonance imaging (7T-MRI) to evaluate cardiac function, myocardial deformation, and the impact of infarction-to-reperfusion time. Wistar rats were assigned to control (n = 6), 20 min infarction (n = 10), 30 min infarction (n = 6), and 40 min infarction (n = 6) groups. Myocardial infarction occurred in all infarction groups but not in controls. Imaging included short- and long-axis slices. Cardiac function was assessed using end-diastolic volume, end-systolic volume, and left-ventricular ejection fraction. Myocardial deformation was analyzed by circumferential strain, radial strain (RS), and longitudinal strain (LS, four-chamber and two-chamber) using feature tracking. The 30 and 40 min infarction groups showed significant reductions in cardiac function and strain compared to the controls. RS decreased significantly between the control and 20 min infarction groups (40.6 ± 4.7% and 34.0 ± 4.1%, p < 0.05). No significant LS difference was observed between 30 and 40 min. Consequently, RS detects early myocardial changes (20 min), whereas LS may reflect compensatory contractility in severe infarction. Preclinical 7T-MRI provides valuable insights into the impact of infarction duration on cardiac function and myocardial deformation.

Background: Intraoperative iatrogenic aortic dissection (IAD) is an uncommon but serious complication of cardiac surgery, and available evidence remains limited, with most reports based on small series. This study summarizes our experience in a high-volume cardiovascular center and compares the findings with published data.

Methods: We retrospectively reviewed 31 consecutive IAD cases treated at Anzhen Hospital from 2020 to 2024, assessing patient characteristics, operative details, and postoperative outcomes.

Results: IAD was identified intraoperatively in 90.3% of patients, with ascending aortic involvement in 80.6%. The main procedures included ascending aorta replacement (45.2%) and hemiarch replacement (22.6%). Mean cardiopulmonary bypass time was 342.6 ± 133.8 min, and 38.7% required circulatory arrest. Major postoperative complications were low cardiac output syndrome (61.3%), neurological injury (25.8%), and acute kidney injury (45.2%). Overall mortality was 38.7%. Review of 17 original studies (1998-2025; >2000 patients) showed a pooled mortality of 32.8%. Patients in our cohort had higher operative risk and more complex procedures, which may partly explain the higher complication and mortality rates.

Conclusions: IAD remains a major intraoperative challenge. Prompt recognition and individualized surgical strategies are essential. These findings provide further insight into intraoperative iatrogenic dissection and may help inform operative and perioperative decision-making.

DES encodes the muscle-specific intermediate filament protein desmin, which is highly relevant to the structural integrity of cardiomyocytes. Mutations in this gene cause different cardiomyopathies including dilated cardiomyopathy. Here, we functionally validate DES-p.L112Q using SW-13, H9c2 cells, and cardiomyocytes derived from induced pluripotent stem cells by confocal microscopy in combination with deconvolution analysis. These experiments reveal an aberrant cytoplasmic aggregation of mutant desmin. In conclusion, these functional analyses support the re-classification of DES-p.L112Q as a likely pathogenic variant leading to dilated cardiomyopathy.

Aims: Chronic kidney disease (CKD) is associated with adverse cardiovascular outcomes, yet few contemporary studies stratify outcomes by specific CKD stages in the era of modern percutaneous coronary intervention (PCI) techniques and new-generation drug-eluting stents (DESs). We aim to assess the relationship between CKD and post-PCI outcomes in an updated, stage-specific, and long-term cohort.

Methods: We retrospectively analyzed 11,489 patients who underwent PCI between 2010 and 2020. Kidney function was classified as preserved (eGFR ≥ 60 mL/min/1.73 m²), stage III CKD (eGFR 30-59), or stage IV/V CKD (eGFR < 30) using the CKD-EPI equation. The primary endpoint was a composite of all-cause mortality, non-fatal myocardial infarction (MI), and target vessel revascularization (TVR) at 1 year; secondary endpoints included individual components and outcomes through 5 years. Associations were evaluated using multivariable Cox regression.

Results: Stage III and stage IV/V CKD were present in 18% and 5.6% of patients, respectively. At 1 year, both stage III (HR 2.13, p < 0.01) and stage IV/V CKD (HR 4.91, p < 0.01) were associated with higher risk of the composite endpoint. Mortality rose sharply with CKD severity (33% in stage IV/V vs. 4% in preserved renal function), and MI risk was significantly higher in stage IV/V CKD. These associations persisted after 5 years. Unadjusted TVR risk was higher in stage IV/V CKD but lost significance after adjustment.

Conclusions: CKD, particularly in advanced stages, is independently associated with increased mortality and MI after PCI, with effects persisting in the long term. While advanced CKD showed higher unadjusted TVR risk, this was not independent after adjustment. These findings support individualized treatment strategies and extended follow-up in PCI patients with CKD.

Mediastinal radiotherapy plays a central role in the treatment of several malignancies, particularly Hodgkin lymphoma and breast cancer. However, exposure to thoracic radiation is associated with long-term cardiovascular complications, among which valvular heart disease (VHD) is increasingly recognized. Radiation-induced VHD typically presents after a latency period of 10-20 years and is characterized by progressive valve fibrosis, thickening, and calcification, most commonly affecting the left-sided valves. Management of radiation-induced VHD generally follows standard guidelines but remains challenging due to extensive calcification and coexisting radiation-related cardiac or pulmonary injury. A history of thoracic radiotherapy is associated with increased perioperative risk and may negatively impact surgical outcomes, which often alters the risk-benefit balance and favors less invasive therapeutic approaches. Advances in the transcatheter approach have expanded treatment options for this high-risk population; however, data on long-term outcomes remain limited. Evolving dose-reduction techniques, such as deep-inspiration breath-hold, intensity-modulated radiotherapy, and proton therapy, together with predictive dosimetric models, aim to minimize future cardiac toxicity. Given the delayed onset and progressive nature of radiation-associated VHD, structured long-term surveillance is essential to enable early detection and timely intervention in cancer survivors at risk.

Over the past decades, coronary revascularization has evolved dramatically with the introduction of bioresorbable scaffolds (BRSs), designed to provide temporary vessel support, elute antiproliferative drugs, and then fully resorb, ideally restoring natural vasomotion and eliminating long-term foreign-body reactions. Early enthusiasm for first-generation polymeric devices, such as the Absorb bioresorbable vascular scaffold, was tempered by increased rates of scaffold thrombosis and late adverse events, largely attributed to thick struts, suboptimal implantation techniques, and unpredictable degradation kinetics. Subsequent developments in polymeric (e.g., MeRes-100, NeoVas) and metallic magnesium-based scaffolds (e.g., Magmaris) have focused on thinner struts, improved radial strength, and refined resorption profiles. Clinical trials and meta-analyses, including ABSORB, AIDA, BIOSOLVE, and BIOSTEMI, reveal that optimized procedural strategies, especially the "PSP" approach (Prepare-Size-Post-dilate) and routine intravascular imaging, substantially reduce thrombosis and restenosis rates, aligning outcomes closer to those of contemporary drug-eluting stents (DESs). Nonetheless, challenges persist regarding inflammatory responses to degradation by-products, mechanical fragility in complex lesions, and patient selection. Ongoing innovations include hybrid polymer-metal designs, stimuli-responsive drug coatings, and AI-assisted imaging for precision implantation. While early-generation BRSs demonstrated both promise and pitfalls, next-generation platforms show steady progress toward achieving the dual goals of transient scaffolding and long-term vessel restoration. The current trajectory suggests that bioresorbable technology, supported by optimized technique and material science, may soon fulfill its original vision; offering safe, effective, and fully resorbable alternatives to permanent metallic stents in coronary artery disease. This review provides an updated synthesis of the design principles, clinical outcomes, and procedural considerations of drug-eluting bioresorbable scaffolds (BRSs). It integrates recent meta-analytic evidence and emerging insights on device mechanics, including the influence of strut thickness on radial strength and the potential role of non-invasive imaging in pre-implantation planning. Special focus is given to magnesium-based scaffolds and future directions in patient selection and implantation strategy.

Background: The minimally invasive approach is increasingly recognized as the standard for surgical management of mitral valve disease. Advances in endoscopic visualization and surgical instrumentation have enhanced precision while minimizing trauma, improving both functional and esthetic outcomes. This study presents a single-center experience with total endoscopic mitral valve repair (MVR) performed using two- or three-dimensional video-assisted technology.

Methods: Between October 2022 and September 2025, 239 patients underwent total endoscopic MVR at our institution. Demographic, operative, and postoperative data were collected and analyzed.

Results: Median age was 63 years, with 64.4% male. Median logistic EuroSCORE and EuroSCORE II were 2.53 and 0.83, respectively. Most patients were NYHA class II (54.4%), and 47.7% had pulmonary hypertension. Mitral annuloplasty was performed in 99.2% of cases; 78.6% received Gore-Tex chordae, 6.3% underwent posterior leaflet resection, and 11.7% edge-to-edge repair. Conversion to sternotomy occurred in 0.4%. In-hospital mortality was 1.3%; stroke occurred in 0.4%. Postoperative atrial fibrillation developed in 26.8%, while major complications such as sepsis (2.1%) and renal failure requiring dialysis (1.3%) were infrequent. Median ventilation time was 5 h, ICU stay was 2 days, and hospital stay was 7 days. Pre-discharge echocardiography showed ≤mild regurgitation in 99.2%.

Conclusions: Total endoscopic MVR using two- or three-dimensional video assistance is safe, feasible, and yields excellent clinical, functional, and cosmetic results, with low morbidity and rapid recovery.

Hypertrophic cardiomyopathy (HCM) is a common and deadly cardiac disease characterized by enlarged myocytes, increased myocardial wall thickening, and fibrosis. A majority of HCM cases are associated with mutations in the β-myosin heavy chain (MYH7) converter domain locus, which leads to varied pathophysiological and clinical manifestations. Using base-editing technology, we generated mutant human-induced pluripotent stem cell-derived cardiomyocytes (hiPSC-CMs) harboring HCM-causing myosin converter domain mutations (MYH7 c.2167C>T [R723C]; MYH6 c.2173C>T [R725C]) to define HCM pathogenesis in vitro. In this study, we integrated transcriptomic analysis with phenotypic and molecular analyses to dissect the HCM disease mechanisms using MYH6/7 myosin mutants. Our KEGG analysis of bulk RNA-sequencing data revealed significant upregulation of transcripts associated with HCM in the mutant hiPSC-CMs. Further, in-depth transcriptomic analysis using Gene-Ontology (GO-term) analysis for biological process showed upregulation of several transcripts associated with heart development and disease. Notably, our analysis showed robust upregulation of cytoskeletal transcripts, including actin-cytoskeleton networks, sarcomere components, and other structural proteins in the mutant CMs. Furthermore, cellular and nuclear morphological analysis showed that the MYH6/7 mutation induced cellular hypertrophy and increased aspect ratio compared to the isogenic control. Immunostaining experiments showed marked sarcomere disorganization with lower sarcomeric order and higher dispersion in the mutant hiPSC-CMs, highlighting the remodeling of the myofibril arrangement. Notably, the MYH6/7 mutant showed reduced cortical F-actin expression and increased central F-actin expression compared to the isogenic control, confirming the cytoskeletal remodeling and sarcomeric organization during HCM pathogenesis. These pathological changes accumulated progressively over time, underscoring the chronic and evolving nature of HCM driven by the MYH6/7 mutations. Together, our findings provide critical insights into the cellular and molecular underpinnings of MYH6/7-mutation-associated disease. These findings offer valuable insights into HCM pathogenesis, aiding in future therapies.

Left main (LM) coronary artery disease remains a critical and high-risk clinical entity with considerable prognostic impact. While surgical revascularization has long been the standard of care, advances in percutaneous coronary intervention (PCI) techniques have significantly improved outcomes, challenging traditional treatment paradigms. Nevertheless, PCI in LM lesions continues to be associated with increased rates of repeat revascularization. This has underscored the importance of precise procedural planning and stent optimization, for which intravascular imaging is central. Among available modalities, intravascular ultrasound (IVUS) is well-established and widely endorsed in clinical guidelines for LM PCI. Optical coherence tomography (OCT), although increasingly utilized in other coronary settings, has a more limited but growing body of evidence in LM disease. This review explores the evolving application of OCT in LM interventions, focusing on its capabilities in plaque characterization, vessel sizing, stent selection, and identification of failure mechanisms such as malapposition and underexpansion. In addition, it discusses the utility of OCT in guiding bifurcation strategies and provides a comparative assessment with IVUS, integrating the most recent clinical data.