Abstract
A myocardial bridge has traditionally been considered a benign condition characterized by an atypical intramyocardial route of a segment of one of the major coronary arteries. However, the clinical complications of myocardial bridges can be dangerous. These potential complications include acute coronary syndromes, arrhythmias, ventricular dysfunction, and sudden death. Myocardial bridges are suspected to be adjuvant of Kounis syndrome, which is defined as an acute coronary syndrome caused by an allergic reaction. Due to high epidemiologic prevalence, clinical suspicion of a myocardial bridge should be considered in atypical and typical presentations of chest pain, especially in patients with low-risk factors for atherosclerotic disease. A male in their late 30’s presented with non-ST elevation myocardial infarction suspected to be secondary to Kounis syndrome after gadobenate dimeglumine contrast media was used for an imaging study. His clinical presentation was further complicated when he was found to have a mid-left anterior descending coronary artery myocardial bridge.
Highlights
Kounis syndrome is defined as an acute coronary syndrome caused by allergic, hypersensitivity, and anaphylactoid reaction.[1]
The type II variant involves coronary vasospasm leading to plaque erosion or rupture in patients with quiescent pre-existing coronary artery disease leading to acute myocardial infarction
Kounis syndrome should be considered in patients presenting with chest pain and a clinical presentation consistent with acute coronary syndrome who have recently been treated for allergic reaction, as an acute coronary syndrome presentation follows the anaphylactoid reaction
Summary
Kounis syndrome is defined as an acute coronary syndrome caused by allergic, hypersensitivity, and anaphylactoid reaction.[1]. The type I variant involves acute coronary syndrome caused by coronary artery vasospasm in patients without pre-existing coronary artery disease and no elevation in cardiac enzymes. The type II variant involves coronary vasospasm leading to plaque erosion or rupture in patients with quiescent pre-existing coronary artery disease leading to acute myocardial infarction. The patient developed urticaria, chest tightness, and laryngospasm He was treated with epinephrine, intravenous steroids, and antihistamines in the emergency department with relief of symptoms and discharged home with oral steroids and antihistamines. Anticoagulants are a class of medications commonly referred to as blood thinners They are used to prevent coagulation of blood and to prolong the clotting time.[5] Coronary angiography was performed as the patient was having persistent chest pain despite optimal medical therapy and supportive care including nitrates and anti-anginal agents. The patient was discharged home after three days with a steroid taper, amlodipine, and metoprolol with subsequent uneventful ambulatory follow-up
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