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Spontaneous Coronary Artery Dissection in an Elderly Woman Presenting with Chest Pain and Positive Cardiac Biomarkers

Mohanad A. Alfaqih, MD1, Rosa M. Michel Ortega, MD1, Eric H. Yang, MD2

Mohanad A. Alfaqih, MD1, Rosa M. Michel Ortega, MD1, Eric H. Yang, MD2

ABSTRACT: A 68-year-old African American female with a prior medical history of hypertension and dyslipidemia presented with sudden onset pressure-like substernal chest pain. Initial ECG showed no ST or T wave abnormalities, and troponin elevation of 2.88 ng/mL. Two hours later, chest pain recurred with ECG change and increase in troponin to 11.97 ng/mL. She underwent urgent coronary angiography, which revealed left anterior descending artery dissection with thrombus. We successfully treated with balloon angioplasty followed by placement of 3 drug-eluting stents resulting in TIMI-3 flow; further testing for vasculitis was negative. Once spontaneous coronary artery dissection is diagnosed, the approach to treatment is controversial and treatment should be patient tailored.

J INVASIVE CARDIOL 2012;24(9):E193-E195

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Case Report. A 68-year-old African American female with a prior medical history of hypertension and dyslipidemia (LDL 156 mg/dL) (not on treatment) presented to our hospital with the sudden onset of pressure-like substernal chest pain lasting 10-15 minutes. The patient had no prior history of coronary artery disease, and was a non-smoker. For several days prior to admission she had difficulty with severe constipation. ECG (Figure 1) showed no ST or T wave abnormalities, and troponin elevation of 2.88 ng/mL, she received aspirin 325 mg, sublingual nitroglycerin 400 mcg, and became pain-free. She was started on intravenous heparin infusion and admitted to the telemetry unit. Two hours later, chest pain recurred. A repeat ECG (Figure 2) was significant for deep T wave inversions in the anterolateral leads, and her troponin I peaked to 11.97 ng/mL.

The patient underwent urgent coronary angiography, which revealed normal right and left circumflex coronary arteries. The left anterior descending artery had a long dissection in the mid-segment, which contained thrombus (Figures 3A and 3B). After a prolonged discussion with the patient’s family, the decision was to proceed with coronary intervention due to the ongoing symptoms and thrombotic nature of the dissection. The lesion was successfully treated with balloon angioplasty followed by placement of 3 drug-eluting stents (Xience), resulting in TIMI-3 flow (Figures 3C and 3D).

Following PCI, chest pain resolved and troponin I trended down. Testing for vasculitis, including antinuclear antibody, rheumatoid factor, sedimentation rate, and C- and P-cytoplasmic anti-neutrophil cytoplasmic antibodies was negative. Transthoracic 2D ECG demonstrated normal left ventricular (LV) ejection fraction (55%) with mildly increased LV thickness. The patient was discharged from the hospital the following day and at the 3-month follow-up remained asymptomatic.

The etiology for dissection in this patient with typical risk factors but without obstructive coronary artery disease is likely to be due to atherosclerotic plaque rupture resulting in intimal dissection.

Discussion. Spontaneous coronary artery dissection (SCAD) is defined as separation involving the intima and the media in cases involving atherosclerosis or between the media and the adventitia in cases associated with childbirth.1 It is a rare cause of acute coronary syndromes, and was first described in 1931.2 It is more common in women (70%) than in men (30%).3 It is increasingly accepted as a cause of acute myocardial infarction in younger women,4 with one-third of cases described in the peripartum period and a mean onset age of 35 years.5

Diseases that have previously been described as related to the development of SCAD include systemic lupus sclerosis, type IV Ehler Danlos, Marfan syndrome, and rheumatoid arthritis with coronary arteritis. SCAD has also been described after vigorous exercise and blunt chest trauma.6 In addition to these disease states, certain medications have also been associated with SCAD, including oral contraceptives, cocaine, and cyclosporine.

Our patient presented with chest pain, which is the most common presentation of patients with SCAD.3,7 Review of the literature shows that SCAD involving the LAD occurs in 48% of cases.3 Multiple modalities including cardiac CT, intravascular ultrasound (IVUS), and coronary angiography have been used to diagnose SCAD. The advantages of IVUS are that it enables assessment of the length and morphology of the intramural dissection, and allows accurate positioning of coronary stents during interventional treatment.8 Coronary CT continues to be the best modality to follow-up on SCAD cases that were managed medically since it provides non-invasive imaging of coronary artery disease.

In the case of our patient there was no need to use alternative modalities because the diagnosis was confirmed using angiography. A retrospective analysis of patients with SCAD showed that the combination of coronary angiography and IVUS is a superior diagnostic strategy to the other methods.3

Once SCAD is diagnosed the approach to treatment is controversial, and includes medical therapy, percutaneous intervention, or coronary artery bypass grafting. In the study by Ito et al they considered medical treatment appropriate in stable patients, with no ongoing ischemia, and limited dissection on angiogram.7 This stems from the possibility that stent implantation with percutaneous coronary intervention (PCI) can cause propagation of the dissection/intramural hematoma. Medical therapy for SCAD is similar to the treatment of acute coronary syndrome and it involves the use of anti-ischemia medication (beta blocker, nitrates) and antithrombotic therapy (heparin, aspirin, clopidogrel, and glycoprotein IIb/IIIa inhibitors). The use of antithrombotic therapy is still debatable, as some authors advocate for it while others are against it. The theory behind advocating for it is that it will help decrease thrombus formation in the false lumen allowing for more normal blood flow through the true lumen. Yet the downside of using antithrombotic therapy is that it may increase bleeding in the false lumen causing an expansion of the intramural hematoma resulting in decreased flow through the true lumen.8

Retrospective analysis done by Shamloo et al showed that 60% of SCAD cases that were initially managed conservatively either remained the same or progressed. Furthermore Shamloo et al demonstrated that patients who underwent aggressive treatment with CABG or PCI at the time of diagnosis had lower mortality rates compared to those managed medically. It was shown that the success rate of PCI stenting is more than 90%.8 coronary artery bypass grafting is reserved for cases of left main involvement, multivessel involvement, or failed PCI.

This discussion stresses the point that treatment of SCAD must be tailored to each individual case. The factors that favor a more aggressive treatment strategy include evidence of ongoing ischemia, proximal left anterior descending artery, or persistence of dissection in an artery after prolonged medical treatment.8,9 In our patient's case she still experienced pain after heparin drip and morphine and acute changes were observed in ECG with increased troponin so she underwent placement of 3 stents and currently, after 3 months, is asymptomatic. 

References

  1. Romero-Rodríguez N, Fernández-Quero M, Villa Gil-Ortega M, et al. Spontaneous coronary dissection and its long-term prognostic implications in a cohort of 19 cases.  Rev Esp Cardiol. 2010;63(9):1088-1091.
  2. Pretty HC. Dissecting aneurysm of coronary artery in a woman aged 42. Br Med J. 1931;1:667.  
  3. Shamloo BK, Chintala RS, Nasur A, et al. Spontaneous coronary artery dissection: aggressive vs. conservative therapy. J Invasive Cardiol. 2010;22(5):222-228.
  4. Mahenthiran J, Revankar R, Koka V, Hoo J, Shenoy M. Spontaneous coronary artery dissection presenting as acute myocardial infarction. J Natl Med Assoc. 2000;92(2):87-90.
  5. Sharma AD, Sreeram G, Slaughter TF. Spontaneous coronary artery dissection in a healthy 24-year-old woman. J Cardiothorac Vasc Anesth. 2000;14(3):312-313.
  6. Masuda T, Akiyama H, Kurosawa T, Ohwada T. Long-term follow-up of coronary artery dissection due to blunt chest trauma with spontaneous healing in a young woman. Intensive Care Med. 1996;22(5):450-452.
  7. Ito H, Taylor L, Bowman M, Fry ET, Hermiller JB, Van Tassel JW. Presentation and therapy of spontaneous coronary artery dissection and comparisons of postpartum versus nonpostpartum cases. Am J Cardiol. 2011;107(11):1590-1596.
  8. Vrints CJ. Spontaneous coronary artery dissection. Heart. 2010;96(10):801-808.
  9. Cini R, Iezzi F, Sordini P, Pasceri V. Spontaneous left main coronary artery dissection. Interact Cardiovasc Thorac Surg. 2008;7(5):943-944.

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From the Henry Ford Hospital, Departments of 1Internal Medicine and 2Division of Cardiovascular Disease, Detroit, Michigan.
Disclosure: The authors have completed and returned the ICMJE Form for Disclosure of Potential Conflicts of Interest. The authors report no conflicts of interest regarding the content herein.
Manuscript submitted March 21, 2012 and accepted April 10, 2012.
Address for correspondence: Eric H Yang, Henry Ford Hospital, Division of Cardiovascular Disease, 2799 W. Grand Blvd, Detroit, MI 48202, USA. Email: eyang1@hfhs.org