Trends in Cardiovascular Medicine最新文献

This review article - which is devoted to a wide range of physicians, e.g., pathologists, clinicians, radiologists, and general practitioners - is an up-to-date clinico-pathological description of cardiac tumours. Although rare, cardiac tumours are key components in oncology practice since both their early diagnosis and appropriate management denote urgent needs. Primary cardiac tumours (PCTs) are categorized in recent WHO classifications as well as in other scientific contributions. Their incidence is around 0.02% while their prevalence is between 0.001% and 0.03%. Among PCTs, benign lesions account for 85% of cases, while malignant neoplasms for 15%. Compared to PCTs, secondary cardiac tumours are 20-30-fold more common. The most frequent PCTs in adulthood are papillary fibroelastoma and cardiac myxoma, while, in childhood, cardiac rhabdomyoma. Heart metastases may occur through direct extension, or, indirectly, via bloodstream, lymphatics or intracavitary diffusion. Thoracic cancers (e.g. from pleura, lung, breast) are the most frequent cause of cardiac metastasis followed by oesophageal and haematological malignancies. Symptoms of PCTs (e.g. arrhythmias, dyspnoea, chest discomfort, syncope) are usually the result of both their regional involvement and location. Non-invasive imaging techniques (e.g. echocardiography, MRI, CT) and biopsy are key means in delineating tumour characteristics, size, and adjacent structure involvement. Most PCTs require surgery, which is recommended to prevent life-threatening complications. While many benign cardiac neoplasms may be completely resected, the treatment of choice for malignant PCTs and metastases is a combination of surgery, radio- and/or chemotherapy, as well as new alternative treatments, which may prolong survival in a small patient subset.

Epicardial adipose tissue (EAT), a unique fat depot surrounding the heart, plays a multifaceted role in glucose and lipid metabolism, thermogenesis, and the secretion of bioactive molecules that influence cardiac structure and function. Its proximity to the myocardium allows it to contribute directly to CVDs, including coronary artery disease, arrhythmias, and heart failure. In particular, excessive EAT has emerged as a significant factor in heart failure with preserved ejection fraction (HFpEF), the most common form of heart failure, especially in individuals with obesity and diabetes. Traditional metrics like body mass index (BMI) fail to capture the complexities of visceral fat, as patients with similar BMIs can exhibit varying CVD risks. EAT accumulation induces mechanical stress and fosters a pro-inflammatory and fibrotic environment, driving cardiac remodeling and dysfunction. Pharmacological modulation of EAT has shown promise in delivering cardiometabolic benefits. Recent advancements in diabetes therapies, such as SGLT2 inhibitors and GLP-1 receptor agonists, and antilipidemic drugs have demonstrated their potential in reducing pro-inflammatory cytokine production and improving glucose regulation, which directly influences EAT. These discoveries suggest that EAT could be a significant therapeutic target, though further investigation is necessary to elucidate its role in HFpEF and other CVDs. Recent advances have identified the prokineticin/PKR1 signaling pathway as pivotal in EAT development and remodeling. This pathway regulates epicardial progenitor cells (EPDCs), promoting angiogenesis while reducing EAT accumulation and metabolic stress on the heart, particularly under high-calorie conditions. Prokineticin, acting through its receptor PKR1, limits visceral adipose tissue growth, enhances insulin sensitivity, and offers cardioprotection by reducing oxidative stress and activating cellular survival pathways. In this review, we provide a comprehensive analysis of EAT's role in CVDs, explore novel therapeutic strategies targeting EAT, and highlight the potential of prokineticin signaling as a promising treatment for HFpEF, obesity, and diabetes.

Mitral valve transcatheter edge-to-edge repair (M-TEER) has emerged as a transformative therapy for mitral regurgitation (MR), addressing the unmet needs of patients unsuitable for surgery. Landmark trials such as EVEREST II, COAPT, and MITRA-FR have established the safety and efficacy of M-TEER, in both patients with primary (PMR) and secondary MR (SMR). Recent trials, including RESHAPE-HF2 and MATTERHORN, have expanded our understanding and refueled discussions regarding patient selection and appropriate treatment indications in SMR. These trials have also contributed to the discussion regarding SMR phenotypes most appropriate for M-TEER. This review summarizes the evidence from pivotal trials, discusses patient selection, device advancements, potential future directions, and outlines ongoing trials that may shape future clinical practice.

Cardiac implantable electronic device infections (CIEDI) are an important complication of device implantation associated with significant morbidity, mortality, and cost to the healthcare system. Identifying patients at high risk of device infection is paramount to improving decision making. This includes selecting appropriate devices and implementing adjunctive infection prevention measures, such as antimicrobial envelopes. In addition to meticulous antiseptic surgical technique, several other procedure-related practices can help reduce the risk of device infection. Developing expert centers with multidisciplinary teams capable of device extraction is important to manage patients with CIEDI. In this review, we aim to provide the reader with a succinct overview of CIEDI and summarize new evidence for risk assessment, prevention, diagnosis, and infection management.

Atrial fibrillation (AF) is the most common sustained cardiac arrhythmia in patients with cardiomyopathies and its clinical management presents a significant challenge. The prevalence of AF varies among cardiomyopathies, with hypertrophic (HCM) and dilated cardiomyopathy (DCM) associated with higher rates of AF. Presence of AF portends increased risk for thromboembolism, heart failure, and cardiovascular morbidity and mortality in patients with cardiomyopathy. The complex genetic substrate in DCM and non-dilated left ventricular cardiomyopathy (NDLVC) contribute to the heterogeneity of AF burden and its sequelae among cardiomyopathy genotypes, necessitating genotype-tailored approach in AF screening and management. Given the lack of validation of traditional risk scores for AF in cardiomyopathies, current clinical recommendations emphasize the importance of comprehensive risk stratification for AF, monitoring for AF, and early initiation of oral anticoagulation for brief AF episodes in specific cardiomyopathy subtypes such as hypertrophic or amyloid cardiomyopathy. AF management includes antiarrhythmic drugs, interventional therapies such as catheter ablation, mitral valve replacement when necessary, and lifestyle modifications to attenuate AF burden and improve quality of life. This review summarizes the current knowledge on the clinical significance, prognostic implications, and treatment of AF among different cardiomyopathy subtypes. We underscore the paradigm shift in AF management advocating for an individualized, subtype-specific, and genotype-aware approach to AF in cardiomyopathies, which is instrumental in improving prognosis and patient-centric care.