“…Proposed mechanisms include mechanical irritation triggering a myogenic reflex [6,7], stress receptor activation [8], and platelet aggregation at the catheter tip with release of vasoactive agents [9]. Several underlying etiologies have been documented including hypercholesterolemia, ergot toxicity, exercise, L-thyroxin therapy, hyperosmolar contrast medium, nonsteroidal anti-inflammatory drugs, cigarette smoking, and alcohol [7,8,[10][11][12][13][14][15][16][17][18]. In accordance with the presence of mild coronary artery disease (CAD) in the LAD and LCx in this patient, she also fits the typical prototype of patients predisposed to coronary vasospasm as previously defined by provocative testing with ergonovine [19].…”