Heart failure (HF) remains a major global health challenge, driven by multifactorial pathophysiological processes, such as systemic congestion, endothelial dysfunction, and inflammation. While natriuretic peptides are well-established biomarkers for diagnosing and monitoring HF, they do not fully capture the complexity of vascular involvement. CD146, also known as melanoma cell adhesion molecule (MCAM), is a transmembrane glycoprotein primarily expressed on endothelial cells and involved in cell adhesion, vascular permeability, and angiogenesis. Its soluble form (sCD146), released in response to multiple pathophysiological stimuli, including venous and arterial endothelial stretch, oxidative stress, and inflammatory cytokine activation, has emerged as a promising biomarker reflecting both hemodynamic congestion and systemic endothelial stress. This review synthesizes current knowledge on the structure, regulation, and release mechanisms of CD146 and explores its clinical utility in HF. Elevated sCD146 levels have been associated with echocardiographic and radiological indicators of congestion, as well as with adverse outcomes. While promising, its application is limited by variability, lack of standardization, and confounding elevations in non-cardiac conditions, including malignancy.

Heart failure (HF) remains a major global health challenge, driven by multifactorial pathophysiological processes such as systemic congestion, endothelial dysfunction, and inflammation. While natriuretic peptides are well-established biomarkers for diagnosing and monitoring HF, they do not fully capture the complexity of vascular involvement. CD146, also known as melanoma cell adhesion molecule (MCAM), is a transmembrane glycoprotein primarily expressed on endothelial cells and involved in cell adhesion, vascular permeability, and angiogenesis. Its soluble form (sCD146), released in response to multiple pathophysiological stimuli, including venous and arterial endothelial stretch, oxidative stress, and inflammatory cytokine activation, has emerged as a promising biomarker reflecting both hemodynamic congestion and systemic endothelial stress. This review synthesizes current knowledge on the structure, regulation, and release mechanisms of CD146 and explores its clinical utility in HF. Elevated sCD146 levels have been associated with echocardiographic and radiological indicators of congestion, as well as with adverse outcomes. While promising, its application is limited by variability, lack of standardization, and confounding elevations in non-cardiac conditions, including malignancy.

In this paper, we present the case of a 68-year-old male with personal medical history of coagulopathy issues, who presented to our Emergency Room (Emergency County Hospital, Arad, Romania) with bleeding of the superior tract of the digestive system; the case was difficult to manage, thus warranting the intervention of the Department of Gastroenterology. Endoscopy was performed to localize the site of bleeding and to stop the hemorrhage. This procedure was not successful. The patient was transferred to our Intensive Care Unit where different medications, such as proton pump inhibitor, hemostatic agent and prokinetic drugs were administered. Unfortunately, our attempt to stop bleeding failed; this led us to expand our investigation. We focused on a possible hemophilia as the cause of bleeding, which was confirmed as hemophilia A through the coagulometry test after a period of three days. Patient medical history and coagulation test led us to believe that this is a very rare case of a mild hemophilia A. Finally, the correction of Factor VIII deficiency and repeated endoscopic hemostasis clip was able to stop patients bleeding and ensured a favorable clinical evolution of the patient.