Cardiology Plus最新文献

Cardio-oncology, an emerging subspecialty at the intersection of cardiology and oncology, addresses the growing cardiovascular burden among cancer patients and survivors. Advances in cancer therapies, including anthracyclines, immune checkpoint inhibitors (ICIs), chimeric antigen receptor (CAR) T-cell therapy, and targeted tyrosine kinase inhibitors (TKIs), have improved survival but also introduced diverse cardiovascular complications such as heart failure, arrhythmias, hypertension, and ischemia. These complications are influenced by traditional cardiovascular risk factors, aging, and comorbidities, underscoring the need for precision-guided risk assessment and management. Recent innovations in cardio-oncology focus on personalized risk stratification using clinical risk models, genetic profiling, and emerging biomarkers such as high-sensitivity troponin, natriuretic peptides, and microRNAs. Advanced imaging modalities, including echocardiography, global longitudinal strain analysis, and cardiac magnetic resonance, are central to early detection of subclinical injury, with artificial intelligence (AI) increasingly enabling real-time, individualized surveillance. The integration of novel biological insights, such as clonal hematopoiesis of indeterminate potential, further refines risk prediction and mechanistic understanding. Effective cardio-oncology care requires proactive, multidisciplinary strategies that span the continuum from treatment initiation to survivorship, emphasizing longitudinal monitoring, cardioprotective interventions, and patient-centered care. Despite progress, challenges remain in standardizing predictive models, validating biomarkers, and ensuring equitable access to specialized services. Looking forward, the convergence of AI-driven imaging, multi-omic data, and precision therapeutics promises to transform cardio-oncology from reactive management to proactive, personalized care, optimizing both cancer outcomes and long-term cardiovascular health.

Background and purpose: With the widespread application of immune checkpoint inhibitors (ICIs) in cancer treatment, the associated risk of developing atherosclerotic cardiovascular injury is increasing. However, the risk of cardiovascular disease after ICI treatment in patients with both coronary artery disease and malignancy remains unclear. This study aimed to investigate whether ICI treatment is associated with an increased risk of major adverse cardiovascular events (MACE) in these high-risk patients.

Methods: This single-center, retrospective cohort study included 93 patients diagnosed with coronary heart disease and malignant tumors who received ICIs or non-ICIs therapy. The primary outcome was MACE, defined as a composite of cardiogenic death, heart failure, non-fatal acute coronary syndrome, and non-fatal ischemic stroke. The association between baseline clinical parameters, including ICI exposure, and the incidence of MACE was evaluated.

Results: During a median follow-up of 14 months, MACE occurred in 32.50% of ICIs-treated patients, with a median time to event of 4 months (2.0-8.5 months), compared to 11.32% and 15.5 months (7.8-27.0 months) in non-ICIs patients. Additionally, all-cause mortality occurred in 12.50% of the ICIs-treated group and 13.21% of the non-ICIs group. Traditional cardiovascular risk factors were not associated with MACE in patients with or without ICI treatment. Multivariable regression analyses revealed an increased risk of developing MACE following ICIs therapy (hazard ration [HR]: 2.86, 95% confidence interval [95% CI]: 1.01-8.11; P = 0.048).

Conclusions: Our findings show that ICIs therapy may be independently associated with an increased risk of MACE in patients with coronary heart disease and malignancy. Further larger-scale studies are needed to validate the potential cardiotoxic risk associated with ICIs.

Coronary flow improvement and myocardial ischemia relief are the primary goals of coronary revascularization. The pioneering work of Andreas Gruntzig, who demonstrated the reduction of trans-stenotic pressure gradients following percutaneous coronary intervention (PCI), marked a major milestone in the field. Since then, a variety of invasive and non-invasive techniques for assessing coronary physiology have been developed. These methods play a pivotal role in evaluating the hemodynamic significance of coronary lesions, guiding PCI planning, optimizing post-PCI outcomes, and assessing coronary microcirculation and disease patterns. This review explores the available tools for coronary physiology assessment in the catheterization laboratory and their applications in the decision-making process for coronary revascularization. In addition, it highlights recent technological advances, such as invasive and coronary image-based computational methods. These innovations enable individualized PCI treatment, aiming for complete ischemia relief through optimized morpho-functional procedural outcomes.

Background and purpose: Unfractionated heparin (UFH) is the most commonly utilized rapid-onset anticoagulant, valued for its potency and reversibility with protamine. However, UFH and protamine are associated with significant side effects, including increased morbidity and mortality, and concerns about sustainability due to the environmental impact of large-scale pig farming for heparin production. This study evaluates an alternative anticoagulant strategy using a factor IXa (FIXa) aptamer paired with a matched oligonucleotide antidote, comparing its efficacy and safety to heparin-protamine in a rat extracorporeal membrane oxygenation (ECMO) model.

Methods: Twenty-four Sprague-Dawley rats were randomized into two groups: one receiving heparin (600 IU/kg) and protamine (1 mg/100 IU heparin), and the other receiving a cholesterol-modified FIXa aptamer (10 mg/kg) and its antidote (50 mg/kg). Coagulation parameters, platelet counts, inflammatory markers, cardiac function, and histopathology were assessed during and after 60 minutes of ECMO.

Results: The FIXa aptamer effectively maintained circuit patency without clot formation, comparable to heparin. The antidote rapidly reversed the aptamer's anticoagulant activity, similar to protamine's reversal of heparin. Notably, the aptamer-antidote group demonstrated superior outcomes, including improved mean arterial pressure (58 ± 6 mmHg vs. 54 ± 3 mmHg at 30 minutes; 59 ± 8 mmHg vs. 51 ± 5 mmHg at 3 hours post-ECMO) and cardiac function (shortening fraction: 60 ± 16% vs. 42 ± 8%; P = 0.01). Additionally, the aptamer group exhibited better platelet preservation (platelet count decrease: -288,000 ± 121,000/μL vs. -404,000 ± 89,000/μL; P = 0.03). Inflammatory profiles were similar between groups, except for a transient increase in interleukins 10 (IL-10) in the aptamer group. Histopathological analysis revealed no significant differences in myocardial lesions.

Conclusions: The antidote-controlled anti-FIXa aptamer represents an alternative anticoagulant strategy that may prove useful for managing patients with a history of heparin-induced thrombocytopenia (HIT) and myocardial dysfunction associated with protamine administration.

Cardiovascular diseases remain the leading cause of death worldwide. Despite significant progress and the development of numerous effective drugs, substantial morbidity and mortality persist. This review highlights one potentially fruitful avenue for discovering novel therapeutics: leveraging ribonucleic acid (RNA) to tip the immunological balance toward tissue repair. Decades of research have primed the three disciplines of cardiology, immunology, and RNA drug development, to bring potent intersectional therapies to the clinic. We discuss both coding and non-coding RNA interventions across multiple cell types, such as monocytes, macrophages, and T cells, throughout different cardiovascular diseases. Altogether, advanced RNA-based medicines targeting the immune system are primed to transform how cardiovascular diseases are treated.

As ischemic heart disease (IHD) remains the leading cause of mortality worldwide, there is an urgent need for innovative therapies that go beyond symptom management. The irreversible damage to cardiac tissue following myocardial infarction (MI) and the limited regenerative and proliferative capacity of adult cardiomyocytes (CMs) present significant challenges to the development of treatments capable of restoring cardiac function. This review focuses on emerging modified and non-modified messenger ribonucleic acid (mRNA)-based therapies, which offer targeted and transient protein expression. The studies reviewed here address three major therapeutic strategies: cardiac regeneration, aimed at inducing CM proliferation to restore lost cardiac muscle; cardiac protection, centered on anti-apoptotic and anti-inflammatory methods to mitigate further tissue damage; and cardiovascular regeneration, focused on promoting angiogenesis and restoring vascular integrity after injury. By examining mRNA and modified mRNA (modRNA) therapies across these three approaches, this review showcases mRNA's promising role in advancing muscular and vascular regenerative and protective therapeutics for IHD.

[This retracts the article DOI: 10.1097/CP9.0000000000000061.].