American Journal of Emergency Medicine 34 (2016) 338.e3–338.e5
Contents lists available at ScienceDirect
American Journal of Emergency Medicine journal homepage: www.elsevier.com/locate/ajem
Case Report
Late diagnosis of Wellens syndrome in a patient presenting with an atypical acute coronary syndrome☆,☆☆,★,★★ Atypical myocardial infarctions (MIs) are one of the more feared diagnoses among cardiologists, emergency department physicians, and internists for patients presenting with presumed noncardiac chest pain. Delays in care for patients presenting with atypical MIs can lead to increases in morbidity and mortality. This is also true in the case of Wellens syndrome, where delays in coronary revascularization can also lead to left ventricular dysfunction and death. Here, we report the case of a 48-year-old man with no known risk factors for coronary disease who presents with atypical symptoms, a very late rise in serum troponin, and electrocardiogram changes consistent with Wellens syndrome as part of an acute non–ST elevation MI. Mr S is a 48-year-old white man with no medical history who presented to the emergency department (ED) for pain, described as a burning sensation in the epigastrium that radiated up to the center of the chest and to both shoulders and down to both arms. Symptoms had been intermittent for 3 weeks prior to presentation in the ED. He noted that the pain was incited and exacerbated by meals, lying in the supine position, and relieved with proton pump inhibitor therapy. Pain was rated anywhere from a 4/10 to 8/10; however, it became acutely worse shortly prior to presentation in the ED. He was given antacid therapy in the ED with resolution of the pain and no significant recurrence for the remainder of his hospital course. There was no associated shortness of breath, diaphoresis, nausea, or vomiting. He had not experienced pain like this in the past. He was a nonsmoker and did not use any other types of tobacco. He denied any family history of cardiac disease. Physical examination was noncontributory. Chest x-ray showed clear lungs and no cardiomegaly. Initial electrocardiogram (ECG) obtained at the time of chest pain showed normal findings (Fig. 1). Findings from blood counts and chemistries were normal, as well. Serial cardiac biomarkers, including troponin I, were negative over a 12-hour time span. The patient was then admitted to our institution's chest pain unit to proceed with stress echocardiography. However, during the resting portion of the test, 2-dimensional echocardiography revealed hypokinesis of the left ventricular anterior wall, septum, and apex, with a decreased ejection fraction of 40% to 45%. Cardiology consultation was obtained at this point, and the decision was made to cancel the stress portion and pursue coronary
☆ Each author listed contributed sufficiently to the creation of this manuscript. ☆☆ Financial support: No financial support was provided to any of the authors for the creation/writing of this manuscript. ★ Conflicts of interest: There are no potential conflicts of interest with any of the authors on the creation/writing of this manuscript. ★★ Informed consent: Informed consent was obtained from all involved patients. All identifying information has been removed in the manuscript.
0735-6757/© 2015 Elsevier Inc. All rights reserved.
angiography. Given this resting wall motion abnormality, we also continued to trend the patient's cardiac biomarkers. Interestingly, after 3 negative sets, the fourth set (drawn about 36 hours after the initial set) revealed a troponin I of 0.146, which was elevated by our institution's reference laboratory value. In addition, the patient's ECG obtained during a chest pain–free period developed new, T-wave inversions in the precordial leads (Fig. 2). The left heart catheterization revealed a 99% stenosis in the proximal-middle portion of the left anterior descending (LAD) coronary artery. Percutaneous coronary intervention was performed, and a drug-eluting stent was placed in the LAD (Figs. 3 and 4). He tolerated the procedure well and had no recurrence of symptoms. Final diagnosis was non–ST elevation myocardial infarction (MI) with near total LAD occlusion. He was discharged on clopidogrel, aspirin, metoprolol, enalapril, and atorvastatin. Patients with atypical symptoms of an acute MI on average take longer to present to the hospital and have higher in-hospital mortality rates [1]. This should not come as a surprise given the already wellestablished association between an increase in morbidity/mortality and a delay in treatment in acute MI [2]. Certain patient populations have a higher rate of atypical MI compared with the general population. These include patients older than 70 years, female patients, diabetic patients, and patients with stroke and heart failure. Studies have shown that women are 1.36 times more likely to have an atypical presentation of MI when compared with men [1]. Our case illustrates an example of a patient who can present in an atypical manner without these risk factors. Echocardiography can be very helpful in patients who present with atypical chest pain. In the case of our patient, his cardiac biomarkers were negative times 3 sets initially. Current guidelines support either discharge of low-risk patients at this point if outpatient stress testing can be scheduled within 72 hours or admission to chest pain units for stress testing consideration [3]. Discharge could have been a hazardous decision given our patient's cardiac catheterization findings. In our patient, it was the resting transthoracic echocardiogram that revealed a wall motion abnormality alerting us to this patient having possible myocardial ischemia prior to any elevation in the cardiac biomarkers. Studies have demonstrated resting wall motion abnormality on echo to be more sensitive than serum troponin I in predicting major cardiac events in patients with unstable angina, and the sensitivity of echo detecting an acute MI is close to 100% [4,5]. The superiority of echocardiography in this case is of particular significance because of the late rise in serum troponin. This phenomenon of a late rise in troponin has not been well described but has been thought to occur in patients with certain risk factors, which again were largely absent from our patient [6]. It is also important to realize the value of obtaining serial ECGs along with cardiac biomarkers in the evaluation of possible acute coronary
338.e4
R. Venkatesan et al. / American Journal of Emergency Medicine 34 (2016) 338.e3–338.e5
Fig. 1. Normal ECG finding on admission.
syndrome. Wellens syndrome is not a rare presentation, reported to occur in 14% to 18% of patients presenting with unstable angina [7,8]. Wellens syndrome criteria include the development of deep symmetric T-wave inversions or biphasic T waves in the anterior chest leads without Q waves or ST elevation. This ECG pattern occurs during a chest pain–free state with normal or slightly elevated cardiac biomarkers. The ST segments either normalize or become elevated during chest pain [9]. Our patient's symptoms and ECG patterns met these criteria. However, it is also interesting to note that our patient's symptoms seemed to be initially consistent with gastroesophageal reflux disease and not with unstable angina, as was the case in Wellens original series [7]. In addition, significant narrowing is present in the proximal portion
of the LAD in patients with Wellens syndrome, as was the case in our patient [8]. In conclusion, in addition to presenting a case of an unusual and atypical MI, the present report highlights that there still exists a patient population that needs to be further risk stratified beyond serial cardiac biomarkers before being allowed to either be discharged safely from the ED or proceed to stress testing in a chest pain unit setting. It is cases such as this that emphasize the need to obtain serial ECGs in all patients undergoing evaluation for possible acute coronary syndrome as the ECG changes that occur in Wellens syndrome happen without a significant rise in troponin or during periods of chest pain. Finally, noninvasive cardiac imaging with echocardiography can provide further and
Fig. 2. Electrocardiogram showing new T-wave inversions in precordial leads.
R. Venkatesan et al. / American Journal of Emergency Medicine 34 (2016) 338.e3–338.e5
338.e5
Umamahesh Rangasetty, MD1 Department of Internal Medicine, Division of Cardiology University of Texas Medical Branch, Galveston, TX E-mail address:
[email protected] Rafic F. Berbarie, MD *,1 Department of Internal Medicine, Division of Cardiology University of Texas Medical Branch, Galveston, TX *Corresponding author. Department of Internal Medicine, Division of Cardiology, University of Texas Medical Branch, 301 University Blvd John Sealy Annex 5.106, Galveston, TX 77555-0553 Tel.: +1 4097721533; fax: +1 4097724982 E-mail address:
[email protected] 1
Tel.: +1 409 772 1533; fax: +1 409 772 4982
2
Tel.: +1 409 772 4182; fax: +1 409 772 6507
http://dx.doi.org/10.1016/j.ajem.2015.06.018 Fig. 3. Severe 99% stenosis at the proximal LAD.
even superior risk stratification over serial cardiac biomarkers in the evaluation of chest pain patients presenting to the ED. Rohit Venkatesan, MD Department of Internal Medicine Residency Program University of Texas Medical Branch, Galveston, TX E-mail address:
[email protected] Nilubon Methachittiphan, MD1 Department of Cardiology, University of Texas Medical Branch Galveston, TX E-mail address:
[email protected] Emily Aaron, MD2 Department of Internal Medicine Residency Program University of Texas Medical Branch, Galveston, TX E-mail address:
[email protected] Zehra Jaffery, MD1 Department of Cardiology, University of Texas Medical Branch Galveston, TX E-mail address:
[email protected]
Fig. 4. Proximal LAD lesion after PCI.
References [1] Hyun K, Jeong M. Atypical presentation in patients with acute coronary syndrome. Acute Coron Syndr 2012:109–13. [2] Berger PB, Ellis SG, Holmes Jr DR, Granger CB, Criger DA, Betriu A, et al. Relationship between delay in performing direct coronary angioplasty and early clinical outcome in patients with acute myocardial infarction: results from the global use of strategies to open occluded arteries in Acute Coronary Syndromes (GUSTO-IIB) trial. Circulation 1999;100:14–20. [3] Amsterdam EA, Wenger NK, Brindis RG, Casey Jr DE, Ganiats TG, Holmes Jr DR, et al. 2014 AHA/ACC guideline for the management of patients with non–ST-elevation acute coronary syndromes: executive summary: a report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines. J Am Coll Cardiol 2014;64:2645–87. [4] Olatidoye A, Ford L, Feng Y, Wu AHB, Gilliam LD, Waters D, et al. Echocardiographic wall motion abnormality or serum troponin I for predicting prognosis in patients with unstable angina. 1998;31(Supplement 1):122. [5] Nanuwa K, Chambers J, Senior R. Echocardiography for chest pain in the emergency department. Int J Clin Pract 2005;59:1374–6. [6] Januzzi JL, Newby LK, Murphy SA, Pieper K, Antman EM, Morrow DA, et al. Predicting a late positive serum troponin in initially troponin-negative patients with non–STelevation acute coronary syndrome: clinical predictors and validated risk score results from the TIMI IIIB and GUSTO IIA studies. Am Heart J 2006;151:360–6. [7] de Zwaan C, Bär FW, Wellens HJ. Characteristic electrocardiographic pattern indicating a critical stenosis high in left anterior descending coronary artery in patients admitted because of impending myocardial infarction. Am Heart J 1982;103:730–6. [8] de Zwaan C, Ba FW, Janssen JH, Cheriex EC, Dassen WR, Brugada P, et al. Angiographic and clinical characteristics of patients with unstable angina showing an ECG pattern indicating critical narrowing of the proximal LAD coronary artery. Am Heart J 1989;117:657–65. [9] Rhinehardt J, Brady WJ, Perron AD, Mattu A. Electrocardiographic manifestations of Wellens' syndrome. Am J Emerg Med 2002;20:638–43.
