ST-Elevation Myocardial Infarction from Spontaneous Coronary Artery Dissection.

Spontaneous coronary artery dissection (SCAD) is a rare but life-threatening condition which occurs due to non-traumatic separation of the coronary artery wall. It is more common in women, with an unclear, non-atherosclerotic mechanism. We report a unique case of spontaneous coronary artery dissection presenting as ST-elevation myocardial infarction (STEMI). A 54-year-old woman presented with fever and recurrent abscess. On presentation, she was tachycardic, tachypneic and hypoxic, requiring nasal cannula. Physical exam was notable for healing a wound on the right lower back, status post incision and drainage, with no erythema, edema, ecchymosis or purulent drainage. Laboratory investigations were remarkable for anemia. EKG showed sinus tachycardia with no ST-segment changes. Her hospital course was complicated by septic shock, renal failure, and acute hypoxic respiratory failure requiring intubation. Following extubation, she complained of sudden-onset, severe chest pain. EKG showed ST-elevations in the lateral and inferior leads, with an elevated high-sensitivity troponin level. Cardiac catheterization revealed SCAD involving the mid to distal right posterior descending artery (RPDA) with TIMI-3 flow in the distal RPDA. Given vessel tortuosity and poor target for stenting, was medically managed with dual antiplatelet therapy, a beta-blocker and an eptifibatide infusion for 12 h post-procedure. Extensive rheumatological workup negative. She remained hemodynamically stable with no new ST changes on subsequent EKGs. This is an uncommon medical emergency requiring prompt recognition, appropriate management and early intervention to prevent unfavorable patient outcomes.

1. Background

Spontaneous coronary artery dissection (SCAD) is a rare but life-threatening condition occurring due to non-traumatic separation of the coronary artery wall. It is more common in women, with an unclear, non-atherosclerotic mechanism.1,2 We report a unique case of SCAD presenting as ST-elevation myocardial infarction (STEMI).

2. Case presentation

A 54-year-old woman presented to the emergency room with a chief complaint of fever and recurrent abscess. Her past medical history was remarkable for hypertension, hyperlipidemia, and tobacco use. She was recently hospitalized for a superficial back abscess, with a course complicated by acute hypoxic respiratory failure secondary to an undifferentiated lung injury, one month prior to her current presentation. On presentation, she was tachycardic (117–129 beats/min), tachypneic (20–22 breaths/min), and hypoxic (saturating 90%), requiring oxygen supplementation via nasal cannula. Physical examination was notable for a healing wound on the right lower back that had undergone incision and drainage during her prior hospitalization, with no residual erythema, edema, ecchymosis, or purulent drainage. Laboratory diagnostics were notable only for normocytic, normochromic anemia (hemoglobin 10.9 gm/dL, reference range: 11–14.5 gm/dL; MCV 86.4 FL, reference range: 81–100 FL; MCH 28.6 pg, reference range: 27–31 pg). A 12-lead electrocardiogram (EKG) showed sinus tachycardia without acute ST-segment changes. A plain film radiograph of the chest revealed reduced lung volumes with no infiltrates. An ultrasound of the back revealed a fluid-filled skin tract leading to a 5×3×4.5 cm collection in the right posterior bladder wall filled with pus or blood products indicating a vesicocutaneous fistula.

Her hospital course was complicated by septic shock requiring high dose vasopressors leading to acrocyanosis (resolved upon vasopressor cessation), renal failure (requiring continuous renal replacement therapy), and recurrent acute hypoxic respiratory failure requiring intubation owing to development of acute respiratory distress syndrome (ARDS). A plain film radiograph of the chest showed bilateral airspace opacities possibly due to multifocal pneumonia, pulmonary edema, or pulmonary hemorrhage. A CT scan of the chest confirmed findings consistent ARDS with diffuse ground glass and interstitial opacities. She was treated with broad spectrum antibiotics (vancomycin and piperacillin/tazobactam) as her wound cultures grew Staphylococcus aureus and there was concern for possible toxic shock syndrome. Her blood cultures remained negative, and she eventually showed clinical improvement.

Following extubation, she complained of sudden-onset, severe chest pain. An EKG at that time revealed ST-elevations in the inferolateral leads (Fig. 1), with an elevated high-sensitivity troponin (6793 ng/L; reference range: 0–34 ng/L). Left heart catheterization revealed SCAD involving the mid to distal right posterior descending artery (RPDA) with TIMI-3 flow in the distal RPDA (Fig. 2), along with distal inferoapical severe hypokinesis and preserved left ventricular (LV) systolic function. Given vessel tortuosity, she was medically managed with dual antiplatelet therapy, a beta-blocker, and an eptifibatide infusion for 12 h post-procedure. A transthoracic echocardiogram was performed after cardiac catheterization, which revealed a hyperdynamic LV systolic function, with an ejection fraction of 65–70% and no apparent wall motion abnormalities. Rheumatologic workup including antinuclear antibodies, anti-neutrophil cytoplasmic antibodies, double-stranded DNA antibodies and ribonucleoprotein antibodies was negative. She remained hemodynamically stable with no new ST-segment changes on subsequent EKGs.

Fig. 1

12-lead EKG revealing acute ST-elevation myocardial infarction, with ST-elevations noted in the lateral and inferior leads.

Fig. 2

Coronary angiography (A) Non-obstructive disease of the left coronary distribution including the left anterior descending (LAD) artery, circumflex (LCx) artery and their branches. (B) Right dominant coronary system with right coronary artery (RCA) giving off the posterior descending artery (RPDA), with an area of moderate to severe tortuosity in the mid RPDA. (C) Focal spontaneous coronary artery dissection involving the mid to distal RPDA (box) and an area of moderate narrowing, with TIMI-3 flow in the distal RPDA (arrow).

3. Discussion and conclusion

SCAD is a rare yet life-threatening entity. It may present as acute coronary syndrome; however, it only accounts for 1–4% of acute myocardial infractions. 1,2 SCAD is more commonly seen in women with an average age of approximately 30 years. Risk factors for cardiovascular disease and connective tissue disorders such as Marfan’s syndrome or Ehlers-Danlos are important predisposing factors.3,4 It is important to differentiate SCAD from atherosclerotic disease by coronary angiography for appropriate management. The majority of the dissections involve the left anterior descending artery (LAD), however the right coronary artery (as seen in our case) may also be involved, though this is less common and more often seen in men.3

SCAD can also be seen in postpartum due to the hyperdynamic changes of pregnancy. Another entity that has been associated with SCAD is fibromuscular dysplasia (FMD), a nonatherosclerotic arteriopathy. Anatomical variations which lead to increased coronary artery tortuosity have also shown strong linkage.1,5,6 If fibromuscular dysplasia is diagnosed, it is crucial to follow up with brain imaging (magnetic resonance imaging, computed tomography, optical coherence tomography, or intravascular ultrasonography).1,5

Treatment of SCAD is patient specific, dependent upon patient factors, presentation, and associated comorbidities. General consensus recommends that a conservative approach (aspirin, anti-platelet agent, beta-blocker) to allow the natural healing of the vessel has favourable outcomes.4 Percutaneous intervention has not been shown to improve outcomes, as recurrence can be seen in other vessels.2,5 Our patient had no known connective tissue disorder and was not peripartum. She did have a complicated hospital course with septic shock and acute hypoxic respiratory failure; however, it remains unknown as to whether severe acute or chronic illnesses contribute to SCAD. Nevertheless, other states of catecholamine excess including severe exercise and cocaine abuse have been associated with SCAD, suggesting a potential common pathophysiologic mechanism.4

We describe a complex clinical case of SCAD clinically presenting as STEMI. This is an uncommon medical emergency requiring prompt recognition, appropriate management, and early intervention to prevent unfavourable outcomes. In the case above, we demonstrate the rapid response and prompt timing of intervention, leading to an accurate diagnosis and appropriate management.