European Cardiology Review最新文献

Chronic thromboembolic pulmonary hypertension (CTEPH) is a rare major vessel pulmonary vascular disease that is characterised by fibrotic obstructions deriving from an organised clot. Recent advances in treatments for CTEPH have significantly improved outcomes. Apart from classical surgical pulmonary endarterectomy, balloon pulmonary angioplasty (BPA) and vasodilator drugs that were tested in randomised controlled trials of non-operable patients are now available. In Europe, CTEPH affects males and females equally. In the first European CTEPH Registry, women with CTEPH underwent pulmonary endarterectomy less frequently than men, especially at low-volume centres. In Japan, CTEPH is more common in females and is predominantly treated by BPA. More data on gender-specific outcomes are expected from the results of the International BPA Registry (NCT03245268).

Nuclear factor kappa-light-chain-enhancer of activated B cells (NF-κB) is responsible for the regulation of genes involved in inflammation and immune responses. NF-κB may play an important role in cardiovascular diseases (CVDs), atherosclerosis and diabetes. Several therapeutic agents used for the treatment of CVDs and diabetes, such as pimobendan and sodium-glucose cotransporter 2 inhibitors, exert anti-inflammatory effects by inhibiting NF-κB activation; anti-inflammatory therapy may have beneficial effects in CVDs and diabetes. Several pharmacological agents and natural compounds may inhibit NF-κB, and these agents alone or in combination may be used to treat various inflammatory diseases. Immunoglobulin-free light chains could be surrogate biomarkers of NF-κB activation and may be useful for evaluating the efficacy of these agents. This review discusses recent advances in our understanding of how the NF-κB signalling pathway controls inflammation, metabolism and immunity, and how improved knowledge of these pathways may lead to better diagnostics and therapeutics for various human diseases.

Cancer and cardiovascular disease are the two main causes of death worldwide in both men and women. In the past decades, survival rate in cancer patients has substantially improved due to new treatments and developments in radiation therapy (RT). In women, breast cancer (BC) is the leading cause of cancer death and thoracic RT is a main component of the treatment in many cases. Nevertheless, despite new techniques that limit the area receiving RT, cardiac damage is still an important concern in BC patients. In this review, the following aspects will be addressed: pathophysiology of postradiotherapy heart damage in women with BC; mechanisms, diagnosis and prevention/management of heart damage; and future areas of potential research for radiotherapy injury in women.

Professor Maseri pioneered the research and treatment of coronary vasomotion abnormalities represented by coronary vasospasm and coronary microvascular dysfunction (CMD). These mechanisms can cause myocardial ischaemia even in the absence of obstructive coronary artery disease, and have been appreciated as an important aetiology and therapeutic target with major clinical implications in patients with ischaemia with non-obstructive coronary artery disease (INOCA). Coronary microvascular spasm is one of the key mechanisms responsible for myocardial ischaemia in patients with INOCA. Comprehensive assessment of coronary vasomotor reactivity by invasive functional coronary angiography or interventional diagnostic procedure is recommended to identify the underlying mechanisms of myocardial ischaemia and to tailor the best treatment and management based on the endotype of INOCA. This review highlights the pioneering works of Professor Maseri and contemporary research on coronary vasospasm and CMD with reference to endothelial dysfunction, Rho-kinase activation and inflammation.

Objective: To investigate the extent to which multivessel disease, incomplete revascularisation and prescribing differences contribute to sex-based outcome disparities in patients with ST-elevation MI (STEMI) and establish whether differences in cardiac death and MI (CDMI) rates persist at long-term follow-up. Methods and results: This observational study evaluates sex-based outcome differences (median follow-up 3.6 years; IQR [2.4-5.4]) in a consecutive cohort of patients (n=2,083) presenting with STEMI undergoing percutaneous coronary intervention). Of the studied patients 20.3% (423/2,083) were women and 38.3% (810/2,083) had multivessel disease (MVD). Incomplete revascularisation was common. The median residual SYNTAX score (rSS) was 5.0 (IQR [0-9]) in women and 5.0 (IQR [1-11]) in men (p=0.369), and in patients with MVD it was 9 (IQR [6-17]) in women and 10 (IQR [6-15]) in men (p=0.838). The primary endpoint CDMI occurred in 20.3% of women (86/423) and in 13.2% of men (219/1,660) (p=0.028). Differences persisted following multivariable risk adjustment: female sex was independently associated with CDMI (aHR 1.33; IQR [1.02-1.74]). Women with MVD had CDMI more often than all other groups (p<0.001 for all). Significant sex-based prescribing differences were evident: women were less likely to receive guideline-recommended potent P2Y12 inhibitors than men (31% versus 43%; p=0.012), and differences were particularly evident in patients with MVD (25% in women versus 45% in men, p=0.011). Conclusion: Sex-based differences in STEMI patient outcome persist at long-term follow-up. Poor outcomes were disproportionately found in women with MVD and those with rSS>8. Observed differences in P2Y₁₂ prescribing practices may contribute to poor outcomes for women with MVD and incomplete revascularisation.