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.