E CG Challenges. The ST segment on an electrocardiogram (ECG) correlates to the plateau. Wellens Syndrome

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1 AACN Advanced Critical Care Volume 29, Number 3, pp AACN E CG Challenges Karen M. Marzlin, DNP, RN, CCNS, ACNPC-AG, CCRN-CMC, CHFN Department Editor Wellens Syndrome Karen M. Marzlin, DNP, RN, CCNS, ACNPC-AG, CCRN-CMC, CHFN The ST segment on an electrocardiogram (ECG) correlates to the plateau phase of ventricular repolarization; the T wave is associated with rapid ventricular repolarization in phase 3 of the cardiac action potential. Patients can develop repolarization (ST-T wave) changes, called secondary changes, because of abnormal depolarization. Secondary ST-T wave changes occur when the QRS complex is abnormal, such as in ventricular hypertrophy, bundle-branch blocks, or Wolff-Parkinson-White syndrome. 1,2 When an ST-T wave abnormality is unrelated to a QRS abnormality, such as in injury or ischemia, it is considered a primary repolarization abnormality. 1 This column of ECG Challenges highlights the primary repolarization abnormality of T-wave inversion seen in Wellens syndrome. Initial Discovery De Zwaan et al 3 found that T-wave inversion occurring in leads V 2 and V 3 (with or without other ST-T wave changes in the other precordial leads) was associated with recent injury or ischemia caused by a left anterior descending coronary artery (LAD) lesion and placed the patient at risk for anterior wall myocardial infarction in the absence of coronary revascularization. In their 1982 study of 145 patients presenting to the hospital with symptoms (recentonset crescendo angina, worsening of stable angina, or postinfarction angina) and no or minimal elevation in cardiac enzymes, de Zwaan et al 3 found that 26 (18%) had T-wave inversion in leads V 2 and V 3 on admission or within 24 hours of admission. The prognostic significance of ST-T wave changes in leads V 2 and V 3 was not known for the first 9 of these 26 patients, and of those 9, 8 developed myocardial infarctions despite symptom resolution with medical management. Patients 10 through 26 were treated based on the suspected prognostic significance of these changes, and many underwent planned angiography and subsequent revascularization. Thirteen of the 26 total patients received coronary angiography, and 12 of these 13 had coronary artery disease (CAD). All patients with CAD had a 90% or greater stenosis of the LAD, and most had stenosis proximal to the first septal perforator. 3 Seventy-five percent of the 16 patients who did not receive early angiography developed a substantial anterior wall myocardial infarction. Of those 12 patients, Karen M. Marzlin is an APRN, Aultman Hospital; Adjunct Faculty, Malone University; and Owner/Author/ Educator/Consultant, Key Choice/Cardiovascular Nursing Education Associates, 4565 Venus Rd, Uniontown, OH (Karen@cardionursing.com). The author declares no conflicts of interest. DOI: 360

2 VOLUME 29 NUMBER 3 FALL 2018 ECG Challenges Table 1: Electrocardiogram Changes in Wellens Syndrome Leads V 2 and V 3 V 4 (sometimes V 5 and V 6 ) Expected Electrocardiogram Changes An isoelectric or minimally elevated J point, a concave or straight ST segment that transitions into a negative T wave at an angle of 60 to 90, and a symmetrically inverted T wave An isoelectric or minimally elevated J point and a concave or straight ST segment passing into the first part of the T wave at 135, followed by T-wave inversion A J point below baseline with a convex ST segment passing into a negative T wave at an angle of approximately 120 with a deeply symmetrical, inverted T wave 11 had myocardial infarction occur within a few weeks (mean, 8.5 days) after discharge. Three of the 12 patients died because of the myocardial infarction. 3 As a result of the study, the ECG finding of T-wave inversion in leads V 2 and V 3 (usually during a pain-free period) in patients with a history of intermittent symptoms consistent with unstable angina became known as Wellens syndrome. This ECG finding was considered a warning of a proximal LAD lesion associated with poor outcomes in patients not receiving coronary angiography and revascularization. Moreover, these findings resulted in important clinical practice changes. Previously, the standard of care in unstable angina had been medical management with nitrates and β-adrenergic blocking agents. Coronary angiography was previously considered only in patients whose symptoms did not resolve in response to medications. 3 In a subsequent larger study by de Zwaan et al, 4 14% of 1260 patients presenting with unstable angina had similar T-wave abnormalities in leads V 2 and V 3 as found in the original de Zwaan study. 3 Angiography of those with T-wave inversions revealed a 50% or greater narrowing of the LAD in all patients, with the culprit lesion proximal to the second septal perforator in 83% of patients. The mean degree of narrowing was 79% to 85%, with 18% of patients having a total occlusion. Among the patients with infarction, the incidence of collateral circulation to the LAD was low. 4 Because of the association between T-wave inversion in leads V 2 and V 3 and disease of the LAD, Wellens syndrome has also been referred to as LAD coronary T-wave syndrome. 5 Specific ECG Findings The ECG pattern of T-wave inversion in leads V 2 and V 3 reported in patients with 361 Wellens syndrome can be a deeper, more symmetrical T-wave inversion or a positivenegative biphasic T wave (in which only the second component of the T wave is inverted). Most patients (76%) present with deeper, more symmetrical T-wave inversion, and 24% present with a positive-negative biphasic T wave. 3,4 The specific ST-T wave changes in leads V 2 and V 3 are outlined in Table 1. 3,4 Most patients have a typical pattern of ST-T wave abnormalities in leads and V 4 and sometimes in V 5 and V 6 (Table 1). 3,4 An occlusion proximal to the second septal perforator produces T-wave changes in leads V 2 and V 3. If the lesion is more proximal, T-wave changes will be seen in more precordial leads. 4 QTc prolongation often accompanies T-wave inversion. 4 T-wave inversion is commonly seen in pain-free periods but also can be present during episodes of pain. T-wave inversion may be present only for a limited time. 4 Changes in the ECG usually are persistent and typically remain present for hours to weeks or months; the changes may normalize with medical management or revascularization. 3,5 Neither specific ST-T wave morphology variations nor the duration of ECG changes adds prognostic significance. 3 The described ST-T wave changes in leads V 2 and V 3 and potentially other precordial leads do not provide information regarding the presence or absence of disease in other coronary arteries. 3,4 Electrocardiographic findings of T-wave inversion in leads V 2 and V 3 should not be assessed in isolation but rather should be evaluated in context of the ECG exclusion criteria and clinical presentation features associated with Wellens syndrome (Table 2). 3,4 Mechanisms and Variation of ECG Changes The T-wave inversion of Wellens syndrome is thought to be caused by brief periods of severe ischemia not associated with significant

3 ECG Challenges Table 2: Characteristics of Wellens Syndrome Clinical Presentation ECG Exclusion Criteria Admitted for symptoms consistent with the spectrum of unstable angina Normal or only slight rise in cardiac biomarkers Pathological Q wave or QS pattern in precordial leads Loss of initial R wave in lead or loss of Q wave in lead V 5 or V 6 Complete RBBB or incomplete LBBB Probable or definite right or left ventricular hypertrophy Abbreviations: ECG, electrocardiogram; LBBB, left bundle-branch block; RBBB, right bundle-branch block. necrosis. 3 Electrocardiograms in most patients normalize, suggesting stunning or hibernation of myocardium as the mechanism. 4 Deeper, more symmetrical T-wave inversion may follow terminal T-wave inversion, including after revascularization, and may be associated with reperfusion. 6 Reperfusion may be due to resolution of spasm of the LAD. 7 In patients with ECG changes consistent with Wellens syndrome with no CAD but with another cause of reversible left ventricular dysfunction, magnetic resonance imaging suggests myocardial edema as the mechanism of the T-wave inversions. 8 Symmetrical T-wave inversion in leads through V 4 has also been seen in cocaineinduced vasospasm of the LAD. 9 T-wave inversion of Wellens syndrome in leads V 2 and V 3 can be seen in restenosis of a stent in the proximal LAD. 10 Patients can present with repeat Wellens syndrome, and the morphology of the T-wave inversion may be different at each presentation. 10 Variations exist in how patients present with Wellens syndrome. For example, Figure 1 shows a positivenegative biphasic T wave recorded in a patient 3 hours after hospital presentation during a pain-free period. The patient presented to the emergency department with new-onset unstable angina, and the ECG changes shown in Figure 1 were not present on arrival. Approximately 2 hours after the ECG was recorded, the patient had a symptomatic episode at rest. At this time, the ECG in Figure 2 was recorded and showed deeper symmetrical T waves in most of the precordial leads. Another case report describes a patient with symmetrical T-wave inversion on arrival to the emergency department during an episode of pain. This patient s ECG evolved into a positive-negative biphasic T wave, recorded at day 10 during a pain-free period. 11 Differential Diagnoses T-wave inversion in the precordial leads occurs in conditions other than ischemia, including persistent juvenile T-wave inversion, evolving stages of pericarditis or myocarditis, and acute neurological conditions. 2 I avr V 4 avl V 2 V 5 I avf V 3 V 6 Dev: Speed: 25 mm/sec Limb: 10 mm/mv Chest: 10.0 mm/mv 60~ Hz PH080A P? Figure 1: Electrocardiogram of a patient admitted with new-onset unstable angina, recorded during a pain-free period approximately 3 hours after presentation. T-wave inversion is just beginning in the terminal part of the T wave in lead V 2. A biphasic positive-negative T wave is seen in lead V 3. A symmetrical but not deep T-wave inversion is seen in lead V

4 VOLUME 29 NUMBER 3 FALL 2018 ECG Challenges I avr V 4 avl V 2 V 5 I avf V 3 V 6 Dev: Speed: 25 mm/sec Limb: 10 mm/mv Chest: 10.0 mm/mv 60~ Hz PH080A P? Figure 2: Electrocardiogram recorded approximately 2 hours after Figure 1 during a symptomatic episode in the same patient. Deeper, more symmetrical T-wave inversion is seen in leads V 2 through V 5, and smaller T-wave inversions are present in leads and V 6. In the first study by de Zwaan et al, 3 one patient with T-wave inversion in leads V 2 and V 3 had normal coronary arteries but a prolapsed mitral valve. In a study of patients with confirmed pulmonary embolus, precordial T-wave inversion was the most common ECG finding (68% of patients); precordial T-wave inversion presence correlated with increased severity of the pulmonary embolus. 12 Additionally, T-wave inversion in leads through V 3 is considered one of the diagnostic features of arrhythmogenic cardiomyopathy. 13,14 Precordial T-wave inversion after pacing or tachyarrhythmias, called T-wave memory or cardiac memory, 15 has been seen in patients with intermittent left bundle-branch block during periods of conduction without the left bundle-branch block. 16 Precordial T-wave inversion must always be correlated to the patient s clinical condition. The T-wave inversion of Wellens syndrome is observed in patients presenting with unstable angina. Chest pain, however, also may be present in other nonacute coronary syndrome conditions. The morphology of the ST segment and T-wave inversion provide insight in patients presenting with both chest pain and precordial T-wave inversion. T-wave inversions associated with ischemia most often have a classic narrow and symmetric quality. 2 Conclusion T-wave inversion in leads V 2 and V 3 often is seen in a pain-free period; 40% to 50% of patients who develop T-wave inversions in leads V 2 and V 3 do so after admission to the hospital. 3,4 Patients with ECG changes on admission likely have a history of unstable angina approximately 2 days longer than that of patients who developed changes after admission. 4 Most patients who develop T-wave inversions after admission do so within the first 24 hours, but changes have been reported as late as 5 days after admission. 4 Monitoring the ST segment in lead V 3 may identify this ECG change and result in treatment and improved outcomes in high-risk patients. T-wave inversion in leads V 2 and V 3 in patients presenting with unstable angina is associated with a proximal occlusion of the LAD and represents a risk for impending anterior wall myocardial infarction in patients who do not undergo revascularization. 1 Nurses must recognize this important ECG feature in patients presenting with cardiac symptoms to ensure that patients are appropriately risk stratified to undergo angiography and, when appropriate, coronary revascularization. Appropriate treatment aimed at improving clinical outcomes has been initiated in multiple reported cases based on recognition of T-wave inversions in leads V 2 and V 3 associated with Wellens 363

5 ECG Challenges syndrome. 10,11,17 Stress testing is absolutely contraindicated in these patients because a proximal LAD lesion may be the culprit. Patients warrant revascularization because medical management alone has been associated with risk for a large anterior wall myocardial infarction. 6,18,19 REFERENCES 1. Hanna EB, Glancy DL. ST-segment depression and T-wave inversion: classification, differential diagnosis, and caveats. Cleve Clin J Med. 2011;78(6): Hayden GE, Brady WJ, Perron AD, Somers MP, Mattu A. Electrocardiographic T-wave inversion: differential diagnosis in the chest pain patient. Am J Emerg Med. 2002;20(3): 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(4 Pt 2): de Zwaan C, Bär FW, Janssen JH, 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(3): Rhinehardt J, Brady WJ, Perron AD, Mattu A. Electrocardiographic manifestations of Wellens syndrome. Am J Emerg Med. 2002;20(7): Win Htut Oo SZ, Khalighi K, Kodali A, May C, Aung TT, Snyder R. Ominous T-wave inversions: Wellens syndrome revisited. J Community Hosp Intern Med Perspect. 2016;6(4): doi: /jchimp.v Sheng FQ, He MR, Zhang ML, Shen GY. Wellens syndrome caused by spasm of the proximal left anterior descending coronary artery. J Electrocardiol. 2015;48(3): Migliore F, Zorzi A, Marra MP, et al. Myocardial edema underlies dynamic T-wave inversion (Wellens ECG pattern) in patients with reversible left ventricular dysfunction. Heart Rhythm. 2011;8(10): Dhawan SS. Pseudo-Wellens syndrome after crack cocaine use. Can J Cardiol. 2008;24(5): Nisbet BC, Zlupko G. Repeat Wellens syndrome: case report of critical proximal left anterior descending artery restenosis. J Emerg Med. 2010;39(3): Kardesoglu E, Celik T, Cebeci BS, Cingozbay BY, Dincturk M, Demiralp E. Wellens syndrome: a case report. J Int Med Res. 2003;31(6): Ferrari E, Imbert A, Chevalier T, Mihoubi A, Morand P, Baudouy M. The ECG in pulmonary embolism. Predictive value of negative T waves in precordial leads-80 case reports. Chest. 1997;111(3): Marcus FI. Prevalence of T-wave inversion beyond in young normal individuals and usefulness for the diagnosis of arrhythmogenic right ventricular cardiomyopathy/dysplasia. Am J Cardiol. 2005;95(9): Morin DP, Mauer AC, Gear K, et al. Usefulness of precordial T-wave inversion to distinguish arrhythmogenic right ventricular cardiomyopathy from idiopathic ventricular tachycardia arising from the right ventricular outflow tract. Am J Cardiol. 2010;105(12): Shvilkin A, Ho KK, Rosen MR, Josephson ME. T-vector direction differentiates postpacing from ischemic T-wave inversion in precordial leads. Circulation. 2005;111(8): Denes PA, Pick A, Miller RH, Pietras RJ, Rosen KM. A characteristic precordial repolarization abnormality with intermittent left bundle-branch block. Ann Intern Med. 1978;89(1): Parikh KS, Agarwal R, Mehrotra AK, Swamy RS. Wellens syndrome: a life-saving diagnosis. Am J Emerg Med. 2012;30(1):255.e3-255.e5. doi: /j.ajem Mead NE, OʼKeefe KP. Wellen s syndrome: an ominous EKG pattern. J Emerg Trauma Shock. 2009;2(3): Tandy TK, Bottomy DP, Lewis JG. Wellens syndrome. Ann Emerg Med. 1999;33(3):