Case presentation:
A 59-year-old female with history of hypertension, hyperlipidemia and undifferentiated connective tissue disorder on chronic steroids presented in 2012 for intermittent chest pain following emotional stress. Her initial workup showed new onset left bundle branch block and an elevated high sensitivity troponin. She underwent urgent cardiac catheterization, revealing 100% occlusion of the first obtuse marginal branch (Figure 1, left) with attempted, but unsuccessful percutaneous coronary intervention (PCI). Left ventriculogram showed ejection fraction (EF) of 40% and severe distal inferior and inferoapical hypokinesis. The wall motion abnormalities were not explained by the coronary anatomy and were attributed to possible concomitant Takotsubo’s cardiomyopathy in the setting of acute myocardial infarction. Patient was treated medically.
Three years later in 2015, the patient presented for recurrent chest discomfort following the death of a family member. While being evaluated in the emergency room, she developed ventricular fibrillation arrest. She underwent defibrillation and was successfully resuscitated. Urgent cardiac catheterization was performed revealing a healed obtuse marginal branch (figure 1, right). However, spontaneous dissection of the small caliber first diagonal branch was visualized (figure 2, left). Echocardiogram revealed an ejection fraction 35-40%. Cardiac Electrophysiologist was consulted for possible ICD placement for secondary prevention of sudden cardiac arrest (SCA). Given her acute ischemic event was within 48 hours of her arrest, patient was treated medically with beta blockers.
The patient returned 2 years later in 2017 at the age of 64, again with substernal chest pain. On arrival, initial high sensitivity troponin was 10.3. Within thirty minutes, she suffered a ventricular fibrillation arrest. She underwent defibrillation and was successfully resuscitated. Emergent cardiac catheterization showed improved first diagonal disease when compared to 2015(figure 2, right) but the left anterior descending artery (LAD) showed severe diffuse distal narrowing (figure 3, left) compared to coronary angiogram in 2015 (Figure 3, middle) suggesting SCAD. Patient remained hemodynamically stable without signs of ongoing ischemia. Given that this was the third occurrence of SCAD, she underwent CT angiography of the head and abdomen. Findings were suggestive of fibromuscular dysplasia involving bilateral carotid and renal arteries. On the third day of the hospital course, she developed recurrent chest pain, with repeat high-sensitivity troponin greater than 40 ng/dl. Cardiac catheterization was again performed, with a worsening subtotal occlusion of the distal LAD with proximal extension of the dissection (figure 3, right). Echocardiogram was performed that showed ejection fraction to be 45% without regional wall motion abnormalities. Her symptoms eventually resolved, she remained stable and was treated conservatively. Patient did not meet standard criteria for ICD placement as both her episodes of SCA were within 48 hours of an ischemic event. Regardless, because of her propensity for recurrent SCAD as well as two prior episodes of SCA, the patient was discharged home an external cardioverter-defibrillator and eventually underwent an ICD placement as outpatient.