Quick Fire Cases
Thomas T. Yoo, DO
Resident Physician
Loma Linda University Health Education Consortium
Thomas T. Yoo, DO
Resident Physician
Loma Linda University Health Education Consortium
Dmitry Abramov, MD
Attending Physician
Loma Linda University Medical Center
Purvi Parwani, MD FSCMR
Associate Professor of Medicine
Loma Linda University Medical Center
A 37-year-old female with a history of asthma, non-smoker without any significant family history of coronary artery disease (CAD) and no previous cardiac history presented with one day history of chest pain. Three days prior to presentation, the patient consumed concentrated coffee and immediately developed severe headache associated with nausea, vomiting, shortness of breath, and headache. She presented to emergency room where her blood pressure was recorded at 200/173 mm Hg. Computed tomography (CT) of the head was negative, and she was initially given clonidine then discharged. Two days after, she continued to note significant chest pain, fatigue, shortness of breath and headache, which had patient present to our hospital. Vital signs and physical exam were normal. She had elevated high sensitivity troponin T level of 855 ng/L (normal < 52 ng/L), followed by 652 ng/L one hour later and then 666 ng/L three hours later, and a pro-BNP 164 pg/mL. Lipid panel was normal. Urine drug screen and serum normetanephrine/ metanephrine were negative. TSH was mildly elevated at 4.13 uIU/mL. EKG showed normal sinus rhythm, T wave inversions in lead III, aVF, and V1 with poor R wave progression. CT angiogram of the chest was negative for aortic dissection and coronary CT showed normal coronary arteries without evidence of coronary artery plaque or stenosis and no pericardial effusion. Echocardiogram was unremarkable. Cardiovascular magnetic resonance imaging (CMR) was ordered due to concern for myocardial infarction with non-occlusive coronary arteries (MINOCA).
Diagnostic Techniques and Their Most Important Findings:
CMR was performed using the GE SIGNA HD XT 1.5 Tesla MR scanner. Sequences include cine and delayed myocardial enhancement. CMR findings were subendocardial late gadolinium enhancements with corresponding hypokinesis in mid anterolateral and distal/apical inferior walls (Figures 1 and 2), focal infarcts consistent with MINOCA, and calculated ejection fraction of 65%.
Learning Points from this Case:
MINOCA can be a challenging diagnosis in young patients without any previous cardiovascular history or risk factors. MINOCA on CMR leads to change in clinical decision making and pharmacotherapy. Confirmation of MINOCA may also lead to more aggressive risk factor modification as MINOCA has been associated with worse prognosis.
In the present case, given the timeline of overconsumption of coffee with sudden onset of symptoms and elevated troponin with MINOCA on CMR, we suspect our patient likely had coffee induced coronary vasospasm (CICVSM) that led to MI. CICVSM has been reported in the literature due to suspected increased sympathetic activity. We report CMR phenotype of multiple focal subendocardial delayed enhancement areas consistent with focal MIs in our patient presenting after a concentrated coffee consumption.
