A 45-year-old obese postmenopausal female with a history of coronary artery disease (CAD), hypertension, hyperlipidemia, diabetes, and chronic angina was brought to the Emergency Department midsummer after a motor vehicle accident (MVA) in which she was the restrained driver. While stationary, she was struck by another vehicle from behind at a high rate of speed with immediate airbag deployment. Though the patient did not lose consciousness at the scene and had self-extricated prior to EMS arrival, she requested hospital transport for further evaluation of chest, neck, and back pain. On initial evaluation, the patient complained of chest pain primarily across her left chest and shoulder in a seatbelt-type distribution, though she did also endorse some bilateral chest wall pain, diffuse midline neck pain, and low back pain.
In addition to her cardiac risk factors, her medical history was significant for anxiety, gastroesophageal reflux disease (GERD), migraines, and fibromyalgia. Her home medications included escitalopram, buspirone, pantoprazole, ranitidine, aspirin, clopidogrel, evolocumab, and isosorbide mononitrate. She had an extensive surgical history including a total abdominal hysterectomy, bilateral salpingo-oophorectomy, coronary artery bypass grafting (CABG), and placement of coronary stents. She denied current use of tobacco, alcohol, or illicit drugs. She had just been admitted to the hospital for unstable angina a few months prior, at which time cardiac catheterization was performed, demonstrating three patent bypass grafts: right internal mammary artery (RIMA) to left anterior descending artery (LAD), left internal mammary artery (LIMA) to obtuse marginal artery, and a saphenous vein graft from the proximal aorta to the proximal right coronary artery (RCA). One saphenous vein graft from the posterior descending artery (PDA) to the posterolateral ventricular artery segment was occluded, though this was not a new finding as it was first discovered to be occluded several years ago. Both previously placed drug-eluding stents in the second marginal and left circumflex arteries were widely patent. The catheterization also demonstrated severely diseased and diffusely calcified coronary arteries, with 95% occlusion in the proximal LAD and 100% occlusion in both the first marginal artery and the mid to distal RCA. Of note, her stenosis had worsened since her last catheterization one year earlier, which showed 70% occlusion in the mid-LAD, 90% occlusion in the distal LAD, and 90% occlusion in the mid to distal RCA. No intervention was performed during either catheterization procedure.
Physical exam revealed that the patient was in notable distress and had diffuse midline spinal and paraspinal tenderness, as well as chest wall tenderness. Her pulse was 100/minute, temperature 37.6 C, blood pressure 157/119 mmHg, respiratory rate 16 breaths/min, and SpO2 99% on room air. Chest radiographs and head computed tomography (CT) scans were unremarkable, and the aorta had a normal course and caliber on thorax CT scan. Electrocardiogram (EKG) was also unremarkable, without any ST depression or elevation, T wave inversions, or QTc prolongation noted. Laboratory workup revealed an elevated troponin-T level at 0.564 [normal <0.010]. The patient was not hyponatremic. Three hours later, her troponin-T level decreased to 0.459. BNP, CK, and lactate levels were not obtained.
Cardiac contusion secondary to blunt chest trauma from the MVA was suspected as the initial diagnosis. The patient was admitted to the acute cardiology service and underwent a transthoracic echocardiogram the following morning, which demonstrated reduced systolic function with an ejection fraction of 35%, diffuse areas of mid to apical hypokinesis, and hyperkinesis in the anterior and inferior basal segments (Figure 1). Previous echocardiograms completed three months and one year prior to this episode did not show these abnormalities; those studies lacked wall motion abnormalities and demonstrated normal systolic function with ejection fractions of 60% and 65%, respectively. Thus, these new wall motion abnormalities and reduced systolic function in conjunction with elevated cardiac enzymes, a normal electrocardiogram, and the patient's clinical presentation were consistent with a diagnosis of stress-induced cardiomyopathy.
She was started on a beta blocker and discharged the next day. A follow-up echocardiogram four months later demonstrated return of systolic function with an improved ejection fraction of 55% and normal wall motion, indicating complete resolution.