Vasospasm-Induced Takotsubo Cardiomyopathy: An Underrecognized Phenotype of Ischemia With Nonobstructive Coronary...

Coronary vasospasm is a mechanistically distinct precipitant of takotsubo cardiomyopathy (TCM) that may produce transient left ventricular (LV) dysfunction through ischemia-induced myocardial stunning rather than adrenergic excess. Vasospasm-induced TCM remains underrecognized, and this case illustrates its distinct therapeutic implications, particularly in patients with ischemia with nonobstructive coronary arteries (INOCA). A 47-year-old perimenopausal woman with chronic tobacco use, hypertension, and a prior coronary angiogram performed approximately two years prior during a non-ST-elevation myocardial infarction workup demonstrating nonobstructive coronary artery disease presented with acute-onset substernal chest pressure, diaphoresis, and dizziness. Initial electrocardiography demonstrated anterior ST-segment depressions, and point-of-care echocardiography revealed apical ballooning with impaired LV systolic function. High-sensitivity troponin was mildly elevated at 53 ng/L. During hospitalization, the patient developed recurrent chest pain with new inferolateral ST-segment elevations, prompting emergent coronary angiography. Catheterization demonstrated diffuse multivessel vasospasm of the left anterior descending and left circumflex arteries with complete resolution following intracoronary nitroglycerin, consistent with functional rather than obstructive disease. Left ventriculography confirmed apical akinesis with basal hyperkinesis, and transthoracic echocardiography documented a left ventricular ejection fraction (LVEF) of 35%. LVEF recovered to 50-55% within 48 hours, consistent with the reversible myocardial stunning characteristic of TCM. This case satisfies the International Takotsubo Diagnostic Criteria for TCM and illustrates how diffuse epicardial vasospasm can fulfill the complete clinical syndrome of TCM in the absence of a catecholamine trigger. The patient's history of recurrent nitrate-responsive angina with prior normal coronary imaging is consistent with a chronic vasospastic INOCA substrate that culminated in this acute event. In this case, calcium channel blockers and long-acting nitrates were selected to prevent smooth-muscle vasoconstriction, and beta-blockers were withheld, given the risk of paradoxical vasospasm worsening through unopposed alpha-adrenergic vasoconstriction. This case underscores the importance of mechanism-based phenotyping in TCM to guide appropriate, pathophysiology-directed therapy.