Correspondence / American Journal of Emergency Medicine 32 (2014) 466–485
showed de Winter sign in Fig. 1. We would like to put emphasis on the ECG in Fig. 2B showing the Wellens syndrome. Wellens syndrome, or left anterior descending artery (LAD) coronary T-wave syndrome, is an acute coronary syndrome characterized by ECG changes of symmetric, deeply inverted T waves or biphasic T waves in the anterior leads with preserved R-wave progression and without pathologic Q waves and ST-segment elevation. Interestingly, pain is usually resolved at the time of these ECG changes and presented with this case presentation. These ECG findings are suggestive of significant LAD stenosis, and patients are at high risk for anterior wall myocardial infarction [2]. The sensitivity, specificity, and positive predictor value of T-wave inversion for significant LAD stenosis are 69%, 89%, and 86%, respectively [3]. Narat Srivali, MD Patompong Ungprasert, MD Lee C. Edmonds, MD Department of Internal Medicine, Bassett Medical Center and Columbia University College of Physicians and Surgeons Cooperstown, NY 13326, USA E-mail address: [email protected] http://dx.doi.org/10.1016/j.ajem.2013.12.054 References [1] Samadov F, Akaslan D, Cincin A, Tigen K, Sarı I. Am J Emerg Med. 2014;32(1):110. e1-3. [2] Rhinehardt J, Brady WJ, Perron AD, et al. Electrocardiographic manifestations of Wellens' syndrome. Am J Emerg Med 2002;20(7):638. [3] Haines DE, Raabe DS, Gundel WD, Wackers FJ. Anatomic and prognostic significance of new T-wave inversion in unstable angina. Am J Cardiol 1983;52 (1):14.
Electrocardiographic criteria of proximal left anterior descending artery occlusion: sign of de Winter or Wellens? To the Editor, We have read with great interest the recently published article by Samadov et al [1] entitled “Acute proximal left anterior descending artery occlusion with de Winter sign.” In that well-described case report, the authors [1] reported a 41-year-old man with an acute thrombotic occlusion of proximal left anterior descending artery (LAD). The authors mentioned that an acute occlusion of coronary arteries could be recognized by ST-segment elevation myocardial infarction equivalents in patients presenting with an atypical electrocardiographic (ECG) manifestation. While this current case report is interesting and provides us exhaustive information, some comments may be of interesting. Precordial ST-segment depression could be regarded as an indicator of concomitant posterior involvement with high specificity (92%) [2]. In acute coronary syndrome patients presenting with precordial ST-segment depression, posterior ECG should be evaluated to detect posterior segment involment or posterior myocardial infarction, thereby avoiding timely intervention [2]. Wellens’ syndrome is characterized by specific T waves (deeply inverted or biphasic) found in precordial leads, thereby suggesting high-grade luminal narrowing of the proximal LAD [3-5]. Wellens’ sign is a predictor of acute anterior wall myocardial infarction within 1 week with high sensitivity and specificity [3,4]. As in this case, ST-segment depression with upright T waves during episodes of pain, biphasic T waves during pain-free periods, no pathologic precordial Q waves, no loss of precordial R waves, absence of ST-segment elevation in lead aVR, dynamic ECG changes, and mildly elevated cardiac enzymes could suggest us Wellens’ syndrome,
469
thereby wandering away from the sign of de Winter, which represents acute proximal LAD occlusion [6]. Nonetheless, whatever the sign is, patients should undergo urgent cardiac catheterization in both conditions. Emre Yalcinkaya, MD Department of Cardiology, Aksaz Military Hospital 48750, Mugla, Turkey E-mail address: [email protected] Murat Celik, MD Department of Cardiology, Gulhane Military Medical Faculty 06018, Ankara, Turkey http://dx.doi.org/10.1016/j.ajem.2013.12.057 References [1] Samadov F, Akaslan D, Cincin A, Tigen K, Sarı I. Acute proximal left anterior descending artery occlusion with de Winter sign. Am J Emerg Med 2014;32(1):110. e1-3. [2] Sugiura T, Iwasaka T, Takehana K, Nagahama Y, Hasegawa T, Inada M. Precordial ST segment depression in patients with Q wave inferior myocardial infarction: role of infarction-associated pericarditis. Am Heart J 1993;125(3):672–5. [3] Ahmed S, Ratanapo S, Srivali N, Ungprasert P, Cheungpasitporn W, Chongnarungsin D. Wellens’ syndrome and clinical significance of T-wave inversion in anterior precordial leads. Am J Emerg Med 2013;31(2):439–40. [4] Mead NE, O'Keefe KP. Wellens’ syndrome: an ominous EKG pattern. J Emerg Trauma Shock 2009;2(3):206–8. [5] Parikh KS, Agarwal R, Mehrotra AK, Swamy RS. Wellens’ syndrome: a life-saving diagnosis. Am J Emerg Med 2012;30(1):255.e3-5. [6] de Winter RJ, Verouden NJW, Wellens HJJ, Wilde AAM. A new ECG sign of proximal LAD occlusion. N Engl J Med 2008;359:2071–3.
Determining the etiology of hypotension: associated with reperfusion injury?☆ To the Editor, We read the recently published article by Zarar et al [1] entitled “Anaphylactic shock associated with intravenous thrombolytics” with great interest. In that well-described case report, the authors [1] presented a case of an anaphylactic reaction directly attributable to intravenous recombinant tissue plasminogen activator (r-tPA). Although we commend the authors for their valuable article, some comments may be beneficial. Type I hypersensitivity is an allergic reaction provoked by reexposure to a specific antigen [2]. Anaphylactic shock, a systemic form of type I hypersensitivity, is associated with systemic vasodilation that could cause low blood pressure. Given that the late-phase type 1 hypersensitivity reaction could occur 1 to 4 hours after the exposure to an antigen [2,3], omnipaque iodinated contrast agent could not be excluded to be a potential antigen. Ischemia-reperfusion–induced cerebral or cardiac injury could result in systemic hypotension. Reperfusion-induced cerebral injury could result in hypotension due to cerebral reactive hyperemia as a consequence of repressurization in hypotensive vascularity [4]. Reflex hypotension and bradycardia could be observed after cardiac reperfusion therapy associated with the Bezold-Jarisch reflex, which maintains the arterial pressure constant [5,6]. Consequently, hypersensitivity to recombinant tissue plasminogen activator or omnipaque iodinated contrast agent could have been determined before administration. The lack of accompanying symptoms of anaphylactic reaction causes us to question the diagnosis of anaphylactic shock. Hypotension could be associated with either anaphylactic reaction or reperfusion-induced cerebral injury. ☆ Conflict of interest: None declared.
showed de Winter sign in Fig. 1. We would like to put emphasis on the ECG in Fig. 2B showing the Wellens syndrome. Wellens syndrome, or left anterior descending artery (LAD) coronary T-wave syndrome, is an acute coronary syndrome characterized by ECG changes of symmetric, deeply inverted T waves or biphasic T waves in the anterior leads with preserved R-wave progression and without pathologic Q waves and ST-segment elevation. Interestingly, pain is usually resolved at the time of these ECG changes and presented with this case presentation. These ECG findings are suggestive of significant LAD stenosis, and patients are at high risk for anterior wall myocardial infarction [2]. The sensitivity, specificity, and positive predictor value of T-wave inversion for significant LAD stenosis are 69%, 89%, and 86%, respectively [3]. Narat Srivali, MD Patompong Ungprasert, MD Lee C. Edmonds, MD Department of Internal Medicine, Bassett Medical Center and Columbia University College of Physicians and Surgeons Cooperstown, NY 13326, USA E-mail address: [email protected] http://dx.doi.org/10.1016/j.ajem.2013.12.054 References [1] Samadov F, Akaslan D, Cincin A, Tigen K, Sarı I. Am J Emerg Med. 2014;32(1):110. e1-3. [2] Rhinehardt J, Brady WJ, Perron AD, et al. Electrocardiographic manifestations of Wellens' syndrome. Am J Emerg Med 2002;20(7):638. [3] Haines DE, Raabe DS, Gundel WD, Wackers FJ. Anatomic and prognostic significance of new T-wave inversion in unstable angina. Am J Cardiol 1983;52 (1):14.
Electrocardiographic criteria of proximal left anterior descending artery occlusion: sign of de Winter or Wellens? To the Editor, We have read with great interest the recently published article by Samadov et al [1] entitled “Acute proximal left anterior descending artery occlusion with de Winter sign.” In that well-described case report, the authors [1] reported a 41-year-old man with an acute thrombotic occlusion of proximal left anterior descending artery (LAD). The authors mentioned that an acute occlusion of coronary arteries could be recognized by ST-segment elevation myocardial infarction equivalents in patients presenting with an atypical electrocardiographic (ECG) manifestation. While this current case report is interesting and provides us exhaustive information, some comments may be of interesting. Precordial ST-segment depression could be regarded as an indicator of concomitant posterior involvement with high specificity (92%) [2]. In acute coronary syndrome patients presenting with precordial ST-segment depression, posterior ECG should be evaluated to detect posterior segment involment or posterior myocardial infarction, thereby avoiding timely intervention [2]. Wellens’ syndrome is characterized by specific T waves (deeply inverted or biphasic) found in precordial leads, thereby suggesting high-grade luminal narrowing of the proximal LAD [3-5]. Wellens’ sign is a predictor of acute anterior wall myocardial infarction within 1 week with high sensitivity and specificity [3,4]. As in this case, ST-segment depression with upright T waves during episodes of pain, biphasic T waves during pain-free periods, no pathologic precordial Q waves, no loss of precordial R waves, absence of ST-segment elevation in lead aVR, dynamic ECG changes, and mildly elevated cardiac enzymes could suggest us Wellens’ syndrome,
469
thereby wandering away from the sign of de Winter, which represents acute proximal LAD occlusion [6]. Nonetheless, whatever the sign is, patients should undergo urgent cardiac catheterization in both conditions. Emre Yalcinkaya, MD Department of Cardiology, Aksaz Military Hospital 48750, Mugla, Turkey E-mail address: [email protected] Murat Celik, MD Department of Cardiology, Gulhane Military Medical Faculty 06018, Ankara, Turkey http://dx.doi.org/10.1016/j.ajem.2013.12.057 References [1] Samadov F, Akaslan D, Cincin A, Tigen K, Sarı I. Acute proximal left anterior descending artery occlusion with de Winter sign. Am J Emerg Med 2014;32(1):110. e1-3. [2] Sugiura T, Iwasaka T, Takehana K, Nagahama Y, Hasegawa T, Inada M. Precordial ST segment depression in patients with Q wave inferior myocardial infarction: role of infarction-associated pericarditis. Am Heart J 1993;125(3):672–5. [3] Ahmed S, Ratanapo S, Srivali N, Ungprasert P, Cheungpasitporn W, Chongnarungsin D. Wellens’ syndrome and clinical significance of T-wave inversion in anterior precordial leads. Am J Emerg Med 2013;31(2):439–40. [4] Mead NE, O'Keefe KP. Wellens’ syndrome: an ominous EKG pattern. J Emerg Trauma Shock 2009;2(3):206–8. [5] Parikh KS, Agarwal R, Mehrotra AK, Swamy RS. Wellens’ syndrome: a life-saving diagnosis. Am J Emerg Med 2012;30(1):255.e3-5. [6] de Winter RJ, Verouden NJW, Wellens HJJ, Wilde AAM. A new ECG sign of proximal LAD occlusion. N Engl J Med 2008;359:2071–3.
Determining the etiology of hypotension: associated with reperfusion injury?☆ To the Editor, We read the recently published article by Zarar et al [1] entitled “Anaphylactic shock associated with intravenous thrombolytics” with great interest. In that well-described case report, the authors [1] presented a case of an anaphylactic reaction directly attributable to intravenous recombinant tissue plasminogen activator (r-tPA). Although we commend the authors for their valuable article, some comments may be beneficial. Type I hypersensitivity is an allergic reaction provoked by reexposure to a specific antigen [2]. Anaphylactic shock, a systemic form of type I hypersensitivity, is associated with systemic vasodilation that could cause low blood pressure. Given that the late-phase type 1 hypersensitivity reaction could occur 1 to 4 hours after the exposure to an antigen [2,3], omnipaque iodinated contrast agent could not be excluded to be a potential antigen. Ischemia-reperfusion–induced cerebral or cardiac injury could result in systemic hypotension. Reperfusion-induced cerebral injury could result in hypotension due to cerebral reactive hyperemia as a consequence of repressurization in hypotensive vascularity [4]. Reflex hypotension and bradycardia could be observed after cardiac reperfusion therapy associated with the Bezold-Jarisch reflex, which maintains the arterial pressure constant [5,6]. Consequently, hypersensitivity to recombinant tissue plasminogen activator or omnipaque iodinated contrast agent could have been determined before administration. The lack of accompanying symptoms of anaphylactic reaction causes us to question the diagnosis of anaphylactic shock. Hypotension could be associated with either anaphylactic reaction or reperfusion-induced cerebral injury. ☆ Conflict of interest: None declared.
