The term allergic angina, introduced for the first time by Nicholas Kounis in 1991, initially referred to the coexistence of acute coronary syndromes with allergy or hypersensitivity. At present, it is believed that Kounis syndrome is a particular case of systemic disease, with multiorgan arterial involvement generated during immediate hypersensitivity reactions. Myocardial bridging (MB), a condition that can induce coronary artery spasm, has long been regarded as a benign condition. Since both pathologies are associated with arterial spasm, Kounis syndrome and MB are considered to be confounding pathologies for acute coronary syndromes, and their association is quite a rare finding. To date, there are no precise data on the epidemiology, and the population affected by Kounis syndrome seems to be highly heterogeneous. Since this is a rare disease, even less is known about possible different phenotypes, including MB overlap. We report a case of type I variant Kounis syndrome associated with MB with no evidence of coronary artery disease, occurring as late presentation, following a severe systemic reaction (anaphylaxis) induced by a Hymenoptera sting. At present, only two other cases of type I and one case of type II Kounis syndrome occurring in patients with myocardial bridging have been described.

Acute coronary syndromes (ACS) are a major cause of mortality worldwide, and although interventional treatment has significantly improved mortality and morbidity related to ischemic heart disease, there is constant concern about optimizing drug treatment. In this regard, multiple studies have been conducted on inflammation in myocardial infarction (MI), starting from its implications in the atherosclerosis process. The aim of this review is to analyse the current evidence related to the subject and the correlation between the inflammatory state at presentation and the prognosis of patients with MI, identifying key points, possible therapeutic limitations, and future research directions. Both innate and acquired immune components are involved in the inflammatory cascade, with an increase in inflammatory cell and cytokine levels. To analyse the degree of inflammation and determine when it is excessive, numerous inflammatory markers have been studied, from acute phase proteins such as high-sensitivity C-reactive protein (hsCRP) and fibrinogen, to the ratios between inflammatory cells and interleukins involved in the main inflammatory pathways. Their association with post-infarction mortality and morbidity has been observed, but they must be integrated into the clinical context for the selection of patients who would benefit most from their reduction. New anti-inflammatory therapies are being studied in light of these findings, and progress is expected. Early trials with non-selective anti-inflammatory drugs have highlighted the importance of selective inhibition so as not to disrupt healing, and drugs are now being studied that target specific pathways that are exacerbated in infarction and lead to excessive remodelling. Several inflammatory pathways have been investigated but the results are inconclusive in terms of improving prognosis, requiring further studies to formulate future therapeutic indications.

(1) Background: Interleukin-6 (IL-6) links innate immune activation to myocardial injury and adverse outcomes after acute myocardial infarction (AMI), yet the relationship between local intracoronary and systemic peripheral IL-6, and their prognostic value, remains unclear. (2) Methods: This prospective single-center study aimed to compare intracoronary and peripheral venous IL-6 and other inflammatory biomarkers in AMI, included 83 consecutive STEMI (ST-elevation myocardial infarction) or NSTEMI (non ST-elevation myocardial infarction) patients undergoing coronary angiography. Paired intracoronary and peripheral venous samples were obtained before revascularization and analyzed for IL-6, CRP, and ferritin, and correlated with LVEF (left ventricle ejection fraction), NT-proBNP, and a 30-day composite endpoint (death or heart failure hospitalization). (3) Results: Peripheral IL-6 exceeded intracoronary levels in 86.7% of patients (p < 0.001), with both peripheral IL-6 and the venous-to-coronary difference higher in STEMI than NSTEMI. IL-6 in both compartments correlated inversely with LVEF and positively with NT-proBNP and troponin I. Patients reaching the composite endpoint (10.8%) had markedly higher IL-6 and CRP. ROC analysis showed discriminatory ability for the endpoint by intracoronary and peripheral IL-6. (4) Conclusions: Intracoronary and peripheral IL-6 are associated with infarction phenotype, ventricular dysfunction, and short-term outcomes in AMI, supporting its role as an early prognostic biomarker.