Kounis syndrome is a multisystem and multidisciplinary disease affecting the circulatory system that can be manifested as spasm and thrombosis. It can occur as allergic, hypersensitivity, anaphylactic, or anaphylactoid reactions associated with the release of inflammatory mediators from mast cells and from other interrelated and interacting inflammatory cells, including macrophages and lymphocytes. A platelet subset with high- and low-affinity IgE surface receptors is also involved in this process. Whereas the heart, and particularly the coronary arteries, constitute the primary targets of inflammatory mediators, the mesenteric, cerebral, and peripheral arteries are also vulnerable. Kounis syndrome is caused by a variety of factors, including drugs, foods, environmental exposure, clinical conditions, stent implantation, and vaccines. We report a unique case of a 60-year-old male with a past medical history of allergy to human albumin, alcoholic cirrhosis, and esophageal varices, who was admitted due to multiple episodes of hematemesis. Due to low hemoglobin levels, he was transfused with 3 units of red blood cells and fresh frozen plasma without any adverse reactions. On the third day of hospitalization, severe thrombocytopenia was observed and transfusion of platelets was initiated. Immediately following platelet infusion, the patient developed chest discomfort, skin signs of severe allergic reaction, and hemodynamic instability. The electrocardiogram revealed ST segment elevation in the inferior leads. Given the strong suspicion of Kounis syndrome/allergic coronary spasm, the patient was treated with anti-allergic treatment only, without any anti-platelet therapy. The clinical status of the patient gradually improved and the electrocardiographic changes reverted to normal. Based on these findings, Kounis hypersensitivity-associated acute coronary syndrome, specifically, type I Kounis syndrome, was diagnosed. Although platelet transfusion can be a life-saving therapy, each blood transfusion carries a substantial risk of adverse reactions. The aims of this report are to expand the existing knowledge of patient responses to blood transfusion and provide information on the incidence of various severe transfusion reactions to all blood components and especially to platelets. To the best of our knowledge, Kounis syndrome induced by platelet transfusionhas never been previously reported. Hypersensitivity to platelet external membrane glycoproteins in an atopic patient seems to be the possible etiology. Despite that Kounis syndrome remains an under-diagnosed clinical entity in everyday practice, it should always be considered in the differential diagnosis of acute coronary syndromes.

Cardiac wasting, a complex and understudied phenomenon, is observed in up to 40% of patients with advanced cancer, contributing to 20-30% of mortality within this cohort. This condition represents a significant determinant of impaired quality of life and increased mortality, highlighting its clinical importance. Numerous pathophysiological mechanisms have been identified in clinical and pre-clinical research as key drivers in the development and progression of cardiac wasting, including elevated circulating inflammatory cytokines, enhanced catabolic processes, hormonal dysregulation, dysfunction of the growth hormone-insulin-like growth factor I (GH-IGF-I) axis, oxidative stress, psychosocial factors, myosin heavy chain isoform switching, and, critically, cardiotoxic effects of anticancer therapies. Clinically, cardiac wasting manifests through a spectrum of symptoms and consequences, including muscle wasting, heart failure-like symptoms, impaired global longitudinal strain (GLS), and structural and functional alterations in the heart, particularly within the left ventricle. These cardiac alterations contribute to progressive cardiovascular decline. Preclinical and clinical studies have confirmed these observations across various models and patient cohorts, demonstrating significant cardiac changes, such as a 33% reduction in cardiomyocyte cross-sectional area, up to 21% decrease in left ventricular mass and 11% reduction in heart weight, and a 50% reduction in left ventricular axon length. Additionally, fibrosis in pre-clinical studies, preservation of left ventricular ejection fraction in some studies, and mild decreases in others, along with an 8.1% reduction in GLS and a 12.1% loss in left ventricular wall thickness, are observed, in conjunction with elevated circulating levels of interleukin-6 (IL-6). Given the substantial morbidity and mortality associated with cardiac wasting in advanced cancer, it is imperative to incorporate comprehensive cardiac assessment into routine follow-up care, refine patient stratification strategies, employ advanced diagnostic technologies in clinical trials, and prioritize research into the cardiovascular impacts of cancer treatments. A concerted focus on advancing the field of cardio-oncology is essential for mitigating the adverse outcomes of cardiac wasting in this vulnerable patient population.