Case Report and Brief Review

Simultaneous Spontaneous Coronary and Vertebral Artery Dissection in a Postpartum Woman

Aditya M Sharma, MD1, Brenda Herrera, MD1, Herbert D. Aronow, MD, MPH1,2

Aditya M Sharma, MD1, Brenda Herrera, MD1, Herbert D. Aronow, MD, MPH1,2

ABSTRACT: Spontaneous coronary and vertebral artery dissection are rare but life-threatening conditions. They are more prevalent in pregnant and postpartum women with few atherosclerotic risk factors than in the general population. The pathophysiology of spontaneous arterial dissections remains ambiguous and the management may be challenging. We present a case of simultaneous spontaneous coronary and vertebral artery dissection in a postpartum woman. We review the presentation, diagnosis, clinical course and management and place this in context with the existing literature.
J INVASIVE CARDIOL 2010;22:E229–E232
————————————————————
Case Report. A 28-year-old, g2p2 woman with two uncomplicated term pregnancies presented 10 days postpartum with a 2-day history of substernal chest pain and headache. The chest pain was described as sharp, 10/10 in intensity, intermittent, non-exertional, associated with left arm numbness and without aggravating or relieving factors. She had 8 such episodes over a 2-day period, each resolving spontaneously within 20 minutes. She denied symptoms of heart failure such as dyspnea, orthopnea or paroxysmal nocturnal dyspnea and did not have symptoms of dysrrhythmia such as palpitations, presyncope or syncope. She experienced similar chest pain shortly following her first pregnancy, but did not bring this to medical attention. Her episodes of headache were described as intermittent, bi-frontal and posterior cervical, each spontaneously resolving within 30 minutes. These were unlike her typical migraine headaches. There were no aggravating or relieving factors. She denied any chiropractic manipulations, neck or chest trauma. There was no relation between the onset and duration of headache and chest pain episodes. At the time of presentation, she was free of chest pain and headache symptoms. Her past medical history is as noted above. In addition, she had no history of diabetes, hypertension or dyslipidemia, nor did she have a history of fibromuscular dysplasia, immune or inflammatory disease, Marfan syndrome or any other connective tissue disorder. There was no history of prior surgery. She was on no medications at home and had no drug allergies. She was a lifetime non-smoker and denied cocaine or other illicit drug use. Her family history was notable for premature coronary artery disease in her mother who suffered a myocardial infarction at the age of 40 and also suffered a stroke at a young age. On physical examination, respiratory rate was 16 breaths per minute, pulse was 80 beats per minute (bpm) and blood pressure was 146/84 mmHg. There was no jugular venous distension or cervical bruits. Lungs were clear without rales or wheezing and cardiac exam was unremarkable. Abdomen was soft, non-tender, non-distended with no organomegaly and bowel sounds were normal. Hepatojugular reflux was absent. Lower extremity pulses were normal and there was no lower extremity edema. Her detailed neurological exam (including cognitive, cranial nerve, sensory and motor functions as well as cerebellar function) was normal. Electrocardiogram (ECG) revealed normal sinus rhythm, at 76 bpm with no ST-T wave or conduction abnormalities. Laboratory evaluation on presentation revealed CK, CK-MB and troponin-I levels of 1131 IU/L, 80 ng/ml and 17 ng/ml, respectively. Complete blood count, electrolyes and renal function were normal. She was treated with aspirin 325 mg once daily and metoprolol 25 mg twice daily. She developed recurrent chest pain within 1 hour of admission to the hospital. ECG demonstrated sinus rhythm with a right bundle branch block at a rate of 83 bpm with ST elevation in leads V1 and V2 and frequent premature ventricular contractions (Figure 1). Intravenous nitroglycerin and heparin were initiated. Her pain resolved within 20 minutes of onset and her ST segments normalized. An echocardiogram obtained within an hour of chest pain onset showed no regional wall motion abnormalities and normal left ventricular systolic function with no pericardial effusion or valvular abnormalities. She was transferred to the cardiac intensive care unit. Eight hours later, CK, CK-MB and Troponin I were 1055 IU/L, 71 ng/ml and 16 ng/ml, respectively.
Given her young age, that her chest pain was non-exertional, intermittent, nitrate responsive, and not relieved by rest with relative absence of atherosclerotic risk factors and history of migraine headaches, coronary vasospasm was suspected. Coronary computed tomography angiography suggested soft plaque in the left anterior descending artery (LAD) and her other coronary vessels appeared normal. An invasive coronary angiogram revealed a 90% eccentric stenosis in the ostial LAD extending beyond the first septal perforator (Figure 2A). A dissection with pooling of contrast was seen in the proximal left circumflex artery (LCx) (Figure 3). These findings were not altered by injection of intracoronary nitroglycerin. Intravascular ultrasound (IVUS) demonstrated a dissection flap in the LAD with flow present only within the true lumen beginning at the ostium and extending up to the first septal perforator (Figure 2B). In the LCx, IVUS revealed an intraluminal filling defect extending along its entire course through the atrio-ventricular groove. She underwent coronary artery bypass grafting (CABG) involving a left internal mammary artery graft to the LAD and a saphenous vein bypass graft to the first obtuse marginal. Healed and fresh coronary artery dissections were confirmed intraoperatively in the LCx and LAD, respectively. Her post-operative course was unremarkable. Following her CABG, to evaluate the etiology of her headaches, magnetic resonance imaging with gadolinium of the brain was performed and was normal. However, a magnetic resonance angiogram (MRA) of the cervicocephalic vessels revealed 50% stenosis with a double lumen in the mid-cervical left vertebral artery, consistent with a dissection (Figure 4). The patient was treated with aspirin 325 mg daily, metoprolol 25 mg daily, simvastatin 40 mg daily and was anticoagulated with coumadin. She was also encouraged to avoid further pregnancies. A cervical MRA performed 6 weeks later showed a normal appearing left vertebral artery with complete luminal recanalization, consistent with a healed vertebral artery dissection. Anticoagulation therapy was then discontinued. She has remained free of recurrent neurological or cardiac symptoms at follow-up. Discussion. Spontaneous coronary artery dissection is a rare phenomenon, with fewer than 400 cases reported in the literature. It accounts for 0.2–0.3% of acute coronary syndromes (ACS) in the general population; however, it may account for 1/4 of ACS in pregnant and postpartum woman.1–4 The Western Denmark Heart registry reported spontaneous coronary artery dissection in 22 of the 11,175 patients presenting with ACS; 77% of those with spontaneous coronary artery dissection were women.2 In 2 case series comprised of 83 patients with pregnancy-related spontaneous coronary artery dissection presenting between 1952 and 2008, the mean age was approximately 33 years and 72% occurred postpartum (most commonly in the first 2 weeks).5,6 The LAD was the most commonly affected vessel, seen in 76% of cases; 26% of cases had multi-vessel involvement.5,6 The exact etiology and pathogenesis of pregnancy-related spontaneous coronary artery dissection is uncertain. However, arterial dissection likely results from a multi-factorial process involving hormonal and hemodynamic changes. Excessive progesterone production during pregnancy may weaken the tunica media.7 Total cardiac output (CO) and blood volume increase by 50% during pregnancy8 and during labor, CO further increases by 50–80%, leading to increases in shear stress.9 In addition to her current presentation, our patient also developed chest pain during the postpartum period after her first pregnancy. We suspect the healed LCx dissection noted on coronary angiography may have occurred during her first postpartum period. In a series of 152 cases of spontaneous coronary artery dissection, Kamineni et al estimated recurrence in 50% of the cases within 2 months.10 Another review of 42 cases of pregnancy-associated spontaneous coronary artery dissection reported recurrent dissection in 20.8% of patients.11 Management of pregnancy-related spontaneous coronary artery dissection remains challenging and is based upon the clinical presentation, coronary anatomy and response to medical therapy. Fibrinolytic therapy has been used, but may lead to intramural hematoma, extension of the dissection and compression of the true lumen.3,5 Primary angioplasty with stent placement has been successful for focal dissections.4,6 CABG has traditionally been reserved for patients with multi-vessel or left main involvement or with long lesions.2–6 Cardiac transplantation was successfully performed in 4 patients with severely depressed left ventricular systolic function.5 Coronary dissection may be missed on invasive angiography and IVUS should be considered in high-risk individuals such as pregnant and postpartum women if any doubt remains.12,13 IVUS may facilitate both the diagnosis and endovascular treatment of this condition.12,13 Postpartum vertebral artery dissection is an even rarer phenomenon, with only 8 published cases.14–16,20 Presumed etiologies are similar to those described for pregnancy-related spontaneous coronary artery dissection. 80% of patients with cervicocephalic dissection present with head and neck pain, only 56% present with cerebral ischemia, and one-third of these patients have history of migraine headaches.17 Antiplatelet or anticoagulation therapies have been recommended in the acute phase to prevent primary or recurrent ischemic neurological events. No comparative studies have been performed for treatment of vertebral artery dissection. A meta-analysis of non-randomized studies of carotid artery dissections reported no difference in the rates of death or disability between anticoagulation and antiplatelet therapies.18 Antiplatelet drugs are preferred in the setting of a large infarct.19 The optimal duration of therapy is unclear and is often guided by follow-up imaging to evaluate for recanalization of the arterial lumen or to a maximum duration of 6 months if complete recanalization is not achieved.17–19 To our knowledge, our case is the second reported case of simultaneous spontaneous coronary and vertebral artery dissection.20 Conclusion. A high index of suspicion for spontaneous coronary artery dissection is essential in pregnant and postpartum women presenting with angina, in order to allow for timely diagnosis and initiation of appropriate therapies. Similarly, pregnant and postpartum women presenting with headache or neck pain should be evaluated for cervicocephalic dissection, as these symptoms may precede ischemic neurological events.

References

1. Nishikawa H, Nakanishi S, Nishiyama S, et al. Primary coronary artery dissection observed at coronary angiography. Am J Cardiol 1988;61:645–648. 2. Mortensen KH, Thuesen L, Kristensen IB, Christiansen EH. Spontaneous coronary artery dissection: A Western Denmark Heart Registry Study. Catheter Cardiovasc Interv 2009;74:710–717. 3. Roth A, Elkayam U. Acute myocardial infarction associated with pregnancy — An update. Ann Intern Med 1996;125:751–762. 4. Roth A, Elkayam U. Acute myocardial infarction associated with pregnancy. J Am Coll Cardiol 2008;52:171–180. 5. Koul AK, Hollander G, Moskovits N, et al. Coronary artery dissection during pregnancy and the postpartum period: Two case reports and review of literature. Catheter Cardiovasc Interv 2001;52:88–94. 6. Appleby CE, Barolet A, Ing D, et al. Contemporary management of pregnancy-related coronary artery dissection: A single-centre experience and literature review. Exp Clin Cardiol 2009;14:E8–E16. 7. Manalo-Estrella P, Barker AE. Histopathologic findings in human aortic media associated with pregnancy. Arch Pathol 1967;83:336–341. 8. Robson SC, Hunter S, Boys RJ, et al. Serial study of factors influencing changes in cardiac output during human pregnancy. Am J Physiol 1989;256:H1060–H1065. 9. Veland K, Hansen JM. Maternal cardiovascular dynamics–II. Posture and uterine contractions. Am J Obstet Gynecol 1969;103:1–7. 10. Kamineni R, Sadhu S, Alpert JS. Spontaneous coronary artery dissection: Report of two cases and a 50-year review of the literature. Cardiol Rev 2002;10:279–284. 11. Koller PT, Cliffe CM, Ridley DJ. Immunosuppressive therapy for peripartum-type spontaneous coronary artery dissection: Case report and review. Clin Cardiol 1998;21:40–46.
12. Maehara A, Mintz GS, Castagna MT, et al. Intravascular ultrasound assessment of spontaneous coronary artery dissection. Am J Cardiol 2002;89:466–468. 13. Arnold JR, West NE, van Gaal WJ, et al. The role of intravascular ultrasound in the management of spontaneous coronary artery dissection. Cardiovasc Ultrasound 2008;6:24. 14. Sharshar T, Lamy C, Mas JL. Incidence and causes of strokes associated with pregnancy and puerperium. A study in public hospitals of Ile de France. Stroke in Pregnancy Study Group. Stroke 1995;26:930–936. 15. Arnold M, Camus-Jacqmin M, Stapf C, et al. Postpartum cervicocephalic artery dissection. Stroke 2008;39:2377–2379. E-published June 5, 2008. 16. Gasecki AP, Kwiecinski H, Lyrer PA, et al. Dissections after childbirth. J Neurol 1999;246:712–715. 17. Lee VH, Brown RD Jr., Mandrekar JN, Mokri B. Incidence and outcome of cervical artery dissection: A population-based study. Neurology 2006;67:1809–1812. 18. Lyrer P, Engelter S. Antithrombotic drugs for carotid artery dissection. Cochrane Database Syst Rev 2003;4:CD000255. 19. Debette S, Leys D. Cervical-artery dissections: Predisposing factors, diagnosis, and outcome. Lancet Neurol 2009;8:668–678. 20. Motreff P, Souteyrand G, Dauphin C, et al. Management of spontaneous coronary artery dissection: Review of the literature and discussion based on a series of 12 young women with acute coronary syndrome. Cardiology 2009;115:10–18.
————————————————————
From 1the Department of Internal Medicine, Saint Joseph Mercy Hospital, Ann Arbor, Michigan, and 2Michigan Heart, P.C., Ypsilanti, Michigan. The authors report no conflicts of interest regarding the content herein. Manuscript submitted March 2, 2010, provisional acceptance given March 10, 2010, final version accepted April 12, 2010. Address for correspondence: Herbert D. Aronow, MD, MPH, Michigan Heart, P.C., 5325 Elliott Dr., Ste. #202, Ypsilanti, MI 48197. E-mail: haronow@michiganheart.com