Internal Medicine Resident Queen's University Kingston, Ontario, Canada
Case background: A 30-year-old woman, G3P3 presented to hospital 3 days post-cesarean section with atypical chest discomfort with associated weakness and dizziness.
In the emergency department, she was found to be in sinus bradycardia with a heart rate of 38 beats per minute and was subsequently given atropine. Following atropine administration, she developed a feeling of impending doom, accompanied by typical chest pain. An ECG performed at that time demonstrated dynamic ST-segment changes, including elevation in leads I, aVL, and aVR, along with diffuse ST-segment depression and T-wave inversion (Figure 1a). Her chest discomfort and ECG changes spontaneously resolved in the following fifteen minutes (Figure 1b) and she was transferred to the nearest cardiac tertiary care center for further work-up.
Upon arrival, her initial troponin level was 208 ng/L (normal < 9 ng/L) which was down-trending on subsequent bloodwork. A transthoracic echocardiogram (TTE) performed on the day of admission revealed mild left ventricular (LV) systolic dysfunction (LVEF 50%) with extensive wall motion abnormalities of the septal, anteroseptal, inferior, posterior, and lateral walls—ranging from hypokinesis to akinesis, suggestive of mid-cavitary Takotsubo cardiomyopathy. She underwent an invasive coronary angiogram, which demonstrated mild tapering or the proximal left main (LM) coronary artery with TIMI 3 flow (Figure 2). Given her clinical presentation, was concern for potential LM SCAD or vasospasm as the etiology of her chest discomfort and ECG changes.
A cardiac CT scan showed no evidence of an intramural hematoma to suggest SCAD. At that time, the working diagnosis was atropine-induced left coronary vasospasm complicated by Takotsubo cardiomyopathy. A repeat TTE was performed 48-hours later, which showed near-complete resolution of the wall motion abnormalities. Supporting the diagnosis of Takotsubo, the NT-proBNP rose to 6294 pg/mL (normal ≤ 125 pg/mL) in the absence of heart failure symptoms.
Given her transient, typical chest pain and ischemic changes on ECG, the patient was started on nifedipine for the prevention of coronary vasospasm in the postpartum setting and experienced symptomatic improvement with medical therapy.
At follow-up visits one and six months after discharge, she had recovered well, remained asymptomatic from a cardiac standpoint, and repeat TTEs showed normal biventricular size and systolic function (LVEF >55%) with no regional wall motion abnormalities.
Management Challenges: This case highlights the association between atropine and coronary vasospasm—a link that has been described in only a few prior case reports, particularly following spinal anesthesia due to the occurrence of sinus bradycardia. It was a challenging case, as the differential diagnosis and management of acute coronary events in the postpartum period differ from those in the general population. Notably, the postpartum differential diagnosis includes acute plaque rupture from atherosclerosis, spontaneous coronary artery dissection (SCAD), coronary thrombosis, and coronary vasospasm.
In this case, multimodality imaging was essential in tailoring management to the presumed underlying etiology of coronary vasospasm. While an isolated presentation of Takotsubo cardiomyopathy is possible, the presence of ST segment depression suggests another cardiac pathology; the InterTAK diagnostic score for Takotsubo syndrome includes the absence of ST-depression. Furthermore, on review of the coronary angiogram images, we noticed tapering of the LM coronary artery. This territory was not in accordance with her wall motion abnormalities on echocardiogram. Furthermore, while catheter-induced tapering of the LM is possible, the dynamic ECG changes were concerning for diffuse subendocardial ischemia which is suggestive of proximal LM disease.
A cardiac CT was completed to help differentiate between vasospasm and SCAD. The absence of luminal stenosis, intramural hematoma, or dissection flap, especially in a proximal coronary artery, essentially rules out SCAD. Coronary CT angiography may provide increased sensitivity for minimal atherosclerotic CAD compared to invasive coronary angiography given that high attenuation on these images which may be able to differentiate between intramural hematoma from noncalcified plaque. These features may be much more difficult to recognize with smaller coronary arteries. However, given that we were examining for her LM coronary artery, the sensitivity for detection would be higher and ultimately help differentiate between SCAD and coronary vasospasm.
The diagnostic challenges of this case were also confounded by the peripartum period as cardiac MRI would have been useful in elucidating her diagnosis. After engaging in shared decision making with the patient, we decided to forgo the MRI given the possible risks of gadolinium during the breastfeeding period. Acute coronary syndrome in the peripartum period represents a unique clinical scenario that requires careful consideration of etiology, treatment, and outpatient follow-up.
