Chest pain evaluation during pregnancy or the post-partum period poses diagnostic and therapeutic dilemma. The differential diagnosis would include acute myocardial infarction, coronary spasm, dissection, myocarditis and non-cardiac chest pain. Spontaneous coronary artery dissection (SCAD) is a rare cause of acute ischaemic coronary events.1,2 It usually occurs during pregnancy or post-partum period in young women who have no traditional risk factors for cardiac disease.1,2 We present two interesting cases of post-partum acute myocardial infarction due to spontaneous dissection.
A 36-year-old Caucasian woman presented to the emergency department (ED) with complaints of chest pressure. She is a mother of two children and gave birth to a stillborn, full-term baby 5 days prior to the presentation. Her chest pain was similar to her heartburn in the past, but lasted longer. Past medical history was significant for gestational diabetes and acid reflux disease. She never smoked and has no family history of premature coronary artery disease (CAD). Her vitals were noted as blood pressure of 136/88 mmHg, heart rate of 102 beats/minute, respiratory rate of 20/minute with 99% oxygen saturation on room air. Cardiovascular examination revealed regular rate and rhythm without any significant murmurs, jugular venous distension or carotid bruit. Initial laboratory data revealed troponin of 2.32 ng/ml (normal range <0.03), creatine phosphokinase (CPK) 1,523 U/l (normal range 5–190), brain natriuretic peptide (BNP) 253 pg/ml (normal range 0–100), creatinine 0.5 mg/dl, white blood cell count 12.2 K/ul (normal range 4.5–11) and haemoglobin 12.8 gm/dl. The chest X-ray was negative for any acute process. A 12 lead electrocardiogram (ECG) showed normal sinus rhythm with subtle ST segment elevation (<0.5 mm) and T wave inversions in V5 and V6 leads. She was treated as having an acute coronary syndrome (ACS). Since her symptoms improved upon arrival to the ED, she was not taken for an emergent cardiac catheterisation. However, the next day she had recurrence of chest pain along with elevation of troponin to 102 ng/ml, CPK elevation to 3,452 U/l and her ECG demonstrated 1 mm of ST-elevation in the inferior and lateral leads suggestive of acute myocardial infarction (see Figure 1). Due to the symptoms, elevated cardiac biomarkers and abnormal ECG she was taken emergently to the cardiac catheterisation lab. Coronary angiogram showed angiographically normal coronary arteries except for a stenosed segment in the obtuse marginal (OM) branch of the left circumflex artery with varying severity and ulcerated appearance in the mid-portion of the stenotic segment. The most severe area of stenosis in the OM was visually estimated to be a 70–80% diameter stenosis (see Figure 2). Distal to the stenosis, the OM branched with no narrowing in the branch vessels. Left ventricular angiography demonstrated severe hypokinesis of the lateral and infero-lateral segments, with an ejection fraction of 40-45%.
Since the patient did not have atherosclerotic plaques elsewhere, and the appearance was consistent with a possible spontaneous dissection, we elected to first study the OM with intravascular ultrasound (IVUS) to evaluate the underlying pathology. A 6F CLS 3.5 Runway guide catheter and an Asahi Prowater wire (Abbott Vascular, Santa Clara, California , US) was advanced smoothly across the stenotic lesion in the OM and advanced without difficulty to the distal segment. The IVUS probe was advanced distal to the lesion and an automatic pullback was performed per standard protocol. Images showed extensive dissection involving the OM branch and proximal circumflex artery with no appreciable atherosclerotic plaque. There was a tear noted in the mid-segment of the OM and extensive area of intramural haematoma throughout the entire segment of the stenosis (see Figure 3). The haematoma had the appearance of partially clotted blood in some regions. Revascularisation was then performed with direct stenting, utilising three XIENCE V (everolimus eluting coronary stent, Abbott Vascular) drug-eluting stents (DES). The final angiogram revealed a satisfactory result with good stent deployment and with thrombolysis in myocardial infarction (TIMI) grade 3 flow. After stenting, IVUS showed full of the stents to the wall along the entire length of stenosis. Her post-cardiac catheterisation course was uncomplicated. She was started on aspirin, clopidogrel and beta-blockers. She continued to do well at follow up outpatient visits without any recurrence of symptoms.
A 35-year-old female who was 7-day post-partum presented to the ED with ‘ripping and tearing’ retrosternal chest pain at rest that lasted for an hour. During her pregnancy she was diagnosed with pre-eclampsia and gestational diabetes. Other risk factors include family history of premature CAD and 10-pack-years of smoking. On arrival to the ED she was haemodynamically stable with heart rate of 85 beats/minute, blood pressure of 143/88 mmHg and temperature of 98°F. Her physical exam was unremarkable except for mild obesity. Initial ECG was within normal limits. Laboratory data were significant for troponin of 0.5 ng/ml (normal range <0.03), and high sensitive C-reactive protein (hS-CRP) of 1.2 mg/dl (normal range <3mg/dl). Her other laboratory results were unremarkable. She was admitted to the hospital and her chest pain was treated with analgesics. She did not have recurrence of chest pain after she arrived to the floor. Repeated cardiac enzymes showed a troponin level of 6.41 ng/ml (normal range <0.03). At approximately the time that the second troponin was completed, she became symptomatic with chest pain. At this point, treatment for acute non-ST elevation myocardial infarction (NSTEMI) was initiated with intravenous heparin, oral beta-blockers and a statin. She received aspirin in the ED, which was continued. She underwent urgent coronary arteriography, which showed a 75% diameter stenosis of the mid-portion of the left anterior descending (LAD) artery. The angiographic appearance was suggestive of a spontaneous dissection, with no apparent atherosclerotic lesions in other vessels. Left ventricular angiography showed minor anterior wall motion hypokinesis, but with a well-preserved overall ejection fraction of 55%. A 6 French CLS 3.5 Runway guide catheter was placed in the left main coronary artery and a 0.014 Balance Middle Weight wire was advanced across the lesion and into the distal LAD. Optical coherence tomography (OCT) (St Jude Medical, Saint Paul, Minnesota, US) assessment of the mid-segment of the LAD using standard technique demonstrated an extensive dissection of the mid-LAD, associated with an intramural haematoma. The lesion was treated with direct stenting using a 3.5 x 38 mm Xience Xpedition (everolimus eluting coronary stent, Abbott Vascular, Abbott Park, Illinois, US) DES. Following placement of the first stent from in the mid-LAD, the proximal segment still appeared hazy. Therefore, OCT evaluation was repeated and showed that the lumen was clearly narrowed,