High-density lipoprotein (HDL) cholesterol is traditionally viewed as protective against cardiovascular disease (CVD). However, emerging evidence reveals that dysfunctional HDL, characterized by impaired reverse cholesterol transport (RCT), reduced anti-inflammatory and antioxidant activities and increased endothelial dysfunction, which can contribute to coronary artery disease (CAD). Dysfunctional HDL, resulting from oxidative modifications of Apolipoprotein A-1 (Apo A-1) and enzyme inactivation, fails to effectively remove cholesterol from peripheral tissues and may promote inflammation and atherosclerosis. Genetic mutations affecting HDL metabolism further complicate its role in cardiovascular health. Studies have shown that conventional therapies aimed at raising HDL-C levels do not necessarily reduce cardiovascular events, highlighting the need for new approaches that improve HDL functionality. Therapeutic strategies such as Apo A-1 mimetic peptides, reconstituted HDL infusions, and drugs targeting specific HDL metabolic pathways are being explored. Additionally, weight loss, statin therapy, and niacin have shown potential in enhancing HDL function. The pathophysiology of dysfunctional HDL involves complex mechanisms, including oxidative stress, inflammation, and genetic mutations, which alter its structure and function, diminishing its cardioprotective effects. New functional assays, such as the cholesterol efflux capacity (CEC) and HDL inflammatory index, provide more accurate predictions of cardiovascular risk by assessing HDL quality rather than quantity. As research progresses, the focus is shifting towards therapeutic strategies that enhance HDL function and address the root causes of its dysfunction, offering a more effective approach to reducing cardiovascular risk and preventing CAD.

The current management of patients with acute coronary syndrome (ACS) and bleeding disorders, such as hemophilia, is supported by small retrospective studies or expert consensus documents. Moreover, people with hemophilia are less likely to receive invasive treatments like percutaneous coronary intervention (PCI) or coronary artery bypass grafting (CABG) for ACS compared to those without hemophilia, which could affect their cardiovascular outcomes. A multidisciplinary team with an expert hematologist is essential to properly define the therapeutic strategy, which should balance both the thrombotic and bleeding risks. We report a clinical case that illustrates an alternative revascularization strategy for hemophilic patients presenting with ACS and with a pattern of diffuse coronary atherosclerotic disease (CAD), encompassing drug-coated balloons (DCBs) in combination with spot stenting. The proposed approach might avoid a full-length drug-eluting stent (DES) implantation and also allow a short dual antiplatelet therapy (DAPT) regimen that is desirable in patients at a very high bleeding risk (HBR) like hemophiliacs. Furthermore, we have provided a review of the available literature on this topic and a focus on the main recommendations for managing ACS, in response to the presented clinical case. Finally, this article aims to share information and develop more confidence in the current guidelines on the treatment of hemophiliacs who need myocardial revascularization.

“Pinch-Off Syndrome,” first described by Hinke, is a mechanical complication of totally implantable central venous catheters inserted via subclavian venous access. It occurs when the catheter is compressed between the clavicle and the first rib. Compression can cause transient catheter obstruction and may result in rupture or even complete resection and embolization of the catheter. In this case report, we describe our experience of percutaneous transvenous removal of an embolized port-a-cath fragment within the right heart chambers following a rupture. We used the “retrieval snare” technique and subsequent reimplantation through internal jugular access. The intervention occurred in the same session and involved a multidisciplinary team for a 55-year-old man in need of adjuvant chemotherapy.