Conditions Associated with ST-Segment Elevation
http://www.100md.com
《新英格兰医药杂志》
To the Editor: Wang et al. (Nov. 27 issue)1 review various conditions with ST-segment elevation, but they fail to mention a phenomenon often referred to as tako-tsubo–like left ventricular dysfunction,2 or transient left ventricular apical ballooning.3,4 This disorder is characterized by transient left ventricular dysfunction and a range of electrocardiographic changes that mimic acute myocardial infarction, with no evidence of obstruction in epicardial coronary arteries. Although several mechanisms have been proposed, the pathophysiology of this transient disorder is still not clear. However, given that this left ventricular dysfunction has some similarities to that seen in patients with acute brain injury,5 awareness of this underrecognized phenomenon has clinical importance.
Junya Ako, M.D.
Yasuhiro Honda, M.D.
Peter J. Fitzgerald, M.D., Ph.D.
Stanford University
Stanford, CA 94305
junya-tky@umin.ac.jp
References
Wang K, Asinger RW, Marriott HJL. ST-segment elevation in conditions other than acute myocardial infarction. N Engl J Med 2003;349:2128-2135.
Kurisu S, Sato H, Kawagoe T, et al. Tako-tsubo-like left ventricular dysfunction with ST-segment elevation: a novel cardiac syndrome mimicking acute myocardial infarction. Am Heart J 2002;143:448-455.
Witzke C, Lowe HC, Waldman H, Palacios IF. Transient left ventricular apical ballooning. Circulation 2003;108:2014-2014.
Tsuchihashi K, Ueshima K, Uchida T, et al. Transient left ventricular apical ballooning without coronary artery stenosis: a novel heart syndrome mimicking acute myocardial infarction. J Am Coll Cardiol 2001;38:11-18.
Ako J, Honda Y, Fitzgerald PJ, et al. Tako-tsubo-like left ventricular dysfunction. Circulation 2003;108:e158-e158.
To the Editor: In their excellent review, Wang et al. do not comment on ST-segment elevation changes in intracranial disease states. The reported incidence of ST-segment elevation in patients with subarachnoid hemorrhage has varied from about 7.5 percent to 31.0 percent1,2,3; the ST-segment elevation in these patients probably reflects myocardial stress in a setting of catecholamine flooding or autonomic disturbance. A lower incidence, about 5 percent,3 has been described in patients with ischemic stroke, in whom the ST-segment elevation possibly results from underlying cardiac disease.
In our experience, differentiating secondary electrocardiographic changes from acute ischemia in patients with stroke is a common problem, necessitating serial enzyme analysis and echocardiography. The prognostic value of such changes with respect to outcome has been described.2
Ilias A. Andrianakis, M.D.
Evangelos D. Papadomichelakis, M.D.
Anastasia N. Kotanidou, M.D.
University of Athens Medical School
10675 Athens, Greece
akotanid@med.uoa.gr
References
Sommargren CE, Zaroff JG, Banki N, Drew BJ. Electrocardiographic repolarization abnormalities in subarachnoid hemorrhage. J Electrocardiol 2002;35:Suppl:257-262.
Kawasaki T, Azuma A, Sawada T, et al. Electrocardiographic score as a predictor of mortality after subarachnoid hemorrhage. Circ J 2002;66:567-570.
Khechinashvili G, Asplund K. Electrocardiographic changes in patients with acute stroke: a systematic review. Cerebrovasc Dis 2002;14:67-76.
To the Editor: In Table 1 of their article, Wang et al. list causes of ST-segment elevation. I would like to add to this list the Osborn wave in hypothermia. This phenomenon, first described by Osborn1 in 1953, is a distinctive convex elevation at the junction, or J point, of the ST segment and the QRS complex. This deflection has been attributed to delayed depolarization, a current of "injury," or "early repolarization."2 More recent investigation has indicated that the Osborn wave is the consequence of electrical heterogeneities among the ventricular epicardium, M cells, and endocardium during ventricular repolarization.3
The Osborn wave develops when the body temperature drops to about 30°C.4 In leads facing the left ventricle, the deflection is positive, and the size is inversely related to the body temperature. The Osborn wave is commonly associated with QT prolongation. It has also been reported in hypercalcemia.3
Tsung O. Cheng, M.D.
George Washington University Medical Center
Washington, DC 20037
tcheng@mfa.gwu.edu
References
Osborn JJ. Experimental hypothermia: respiratory and blood pH changes in relation to cardiac function. Am J Physiol 1953;175:389-398.
Santos EM, Kittle CF. Electrocardiographic changes in the dog during hypothermia. Am Heart J 1958;55:415-420.
Yang G-X, Lankipalli RS, Burke JF, Musco S, Kowey PR. Ventricular repolarization components on the electrocardiogram: cellular basis and clinical significance. J Am Coll Cardiol 2003;42:401-409.
Hurst JW. The heart, arteries and veins. 7th ed. New York: McGraw-Hill, 1990:289-90.
To the Editor: Wang and colleagues do not mention dissection of the thoracic aorta, which may cause electrocardiographic changes by affecting coronary flow. We reviewed the electrocardiograms from 14 consecutive patients with type A aortic dissection who were admitted to our university hospital. Only two patients had a normal electrocardiogram, four had clinically significant ST-segment elevation, two had nonsignificant elevation, four had left ventricular hypertrophy, one had previously had inferior infarction, and one had unspecific ST-segment changes. Of the four patients with significant ST-segment elevation, one was given thrombolytic therapy and one was admitted for primary percutaneous coronary intervention. In the latter patient, the right coronary artery was occluded by the dissection, resulting in ST-segment elevation in the inferior electrocardiographic leads.
Eigil Fossum, Ph.D.
Kl?w Nils-Einar, Ph.D.
Arild Mangschau, Ph.D.
Ullevaal University Hospital
0407 Oslo, Norway
eigil.fossum@ioks.uio.no
To the Editor: Wang et al. indicate that the reference for measurement of the ST segment should be the end of the PR segment, not the TP segment, and they cite an article on exercise standards.1 Although the PR segment is used as the reference for the ST segment in exercise testing, at rest it is the end of the TP (isoelectric) segment.2 In fact, Marriott related the ST-segment level to "whether it is elevated or depressed below the TP segment."3 The direction of the PR segment is opposite that of the P wave, so in leads with upright P waves and depressed PR segments, ST-segment elevations will be increased if the PR segment is used as the reference, whereas ST-segment depressions will be diminished. In leads with negative P waves, such as lead V1, the converse will apply. Of course, the clinical context and whether ST-segment findings evolve are as important as the point of reference and the magnitude of deviation. An absence of change argues against an acute process and suggests a benign repolarization variant.
Howard S. Friedman, M.D.
New York University School of Medicine
New York, NY 10016
hsf2727@pol.net
References
Fletcher GF, Balady GJ, Amsterdam EA, et al. Exercise standards for testing and training: a statement for healthcare professionals from the American Heart Association. Circulation 2001;104:1694-1740.
The Criteria Committee of the New York Heart Association. Diseases of the heart and blood vessels: nomenclature and criteria for diagnosis. 6th ed. Boston: Little, Brown, 1964:391.
Marriott HJL. Practical electrocardiography. 6th ed. Baltimore: Williams & Wilkins, 1977:21.
The authors reply: The Osborn wave, which Cheng proposes to include among the causes of ST-segment elevation, can be better described morphologically as a "slurred" downstroke of the QRS complex and is not likely to be confused with the ST-segment elevation of infarction.
In aortic dissection, addressed by Fossum et al., the proximal coronary artery may be compressed by the dissecting hematoma or transected, causing myocardial infarction, in which case the electrocardiogram actually reflects the infarction, not the aortic dissection itself. However, it is important to realize that this infarction is a complication of the aortic dissection, not a primary event, because the treatment approach is different in these two situations.
The typical electrocardiographic changes of central nervous system events, referred to by Andrianakis et al., are deep, symmetrically inverted T waves with QT prolongation. ST-segment elevation does occur during the early stage, but usually it is not prominent enough to suggest the presence of an infarction from an occluded epicardial coronary artery that requires reperfusion therapy. Even though these electrocardiographic changes were initially described in patients with subarachnoid hemorrhage and hence called neurogenic T-wave changes, the electrocardiographic findings and transient left ventricular regional wall-motion abnormalities are not unique to central nervous system events, since the same phenomena have been observed in a variety of other acute medical conditions.1,2 The report by Tsuchihashi et al. of "transient left ventricular apical ballooning," which Ako et al. cite, may describe the same entity with slightly different manifestations and a different emphasis. The same "apical ballooning" reported by Kurisu et al., also cited by Ako et al., is believed to be due to simultaneous multivessel coronary-artery spasm. If so, it is a variant of Prinzmetal's angina.
Whether the TP segment or the PR segment should be used as a reference point for ST-segment deviation has long been debated, and Friedman raises the question here. We agree with the American College of Cardiology–American Heart Association guidelines stating that the PQ junction (the end of the PR segment) should be used. This issue is best settled by vectorcardiographic analysis. If the QRS-vector loop ends at the point of origin (the beginning of the ventricular depolarization), the loop is closed, and there is no ST-segment deviation; otherwise, the loop is open, and ST-segment deviation is manifested. The point of origin of the QRS-vector loop is the PQ junction on the electrocardiogram. The issue, then, is whether the QRS complex ends at that level or not. The PQ junction may not be at the level of the TP segment because the ventricle depolarizes while the atria are repolarizing, and this can affect the level of the PQ junction. How this atrial-repolarization wave affects the ST segment has been clearly described by Tranchesi et al.3
Kyuhyun Wang, M.D.
Richard W. Asinger, M.D.
Hennepin County Medical Center
Minneapolis, MN 55415
Henry J.L. Marriott, M.D.
University of South Florida, Tampa
Tampa, FL 33620
References
Sharkey SW, Shear W, Hodges M, Herzog CA. Reversible myocardial contraction abnormalities in patients with an acute noncardiac illness. Chest 1998;114:98-105.
Ruiz Bailen M. Reversible myocardial dysfunction in critically ill, noncardiac patients: a review. Crit Care Med 2002;30:1280-1290.
Tranchesi J, Adelardi V, de Oliveira J. Atrial repolarization -- its importance in clinical electrocardiography. Circulation 1960;22:635-644.
Junya Ako, M.D.
Yasuhiro Honda, M.D.
Peter J. Fitzgerald, M.D., Ph.D.
Stanford University
Stanford, CA 94305
junya-tky@umin.ac.jp
References
Wang K, Asinger RW, Marriott HJL. ST-segment elevation in conditions other than acute myocardial infarction. N Engl J Med 2003;349:2128-2135.
Kurisu S, Sato H, Kawagoe T, et al. Tako-tsubo-like left ventricular dysfunction with ST-segment elevation: a novel cardiac syndrome mimicking acute myocardial infarction. Am Heart J 2002;143:448-455.
Witzke C, Lowe HC, Waldman H, Palacios IF. Transient left ventricular apical ballooning. Circulation 2003;108:2014-2014.
Tsuchihashi K, Ueshima K, Uchida T, et al. Transient left ventricular apical ballooning without coronary artery stenosis: a novel heart syndrome mimicking acute myocardial infarction. J Am Coll Cardiol 2001;38:11-18.
Ako J, Honda Y, Fitzgerald PJ, et al. Tako-tsubo-like left ventricular dysfunction. Circulation 2003;108:e158-e158.
To the Editor: In their excellent review, Wang et al. do not comment on ST-segment elevation changes in intracranial disease states. The reported incidence of ST-segment elevation in patients with subarachnoid hemorrhage has varied from about 7.5 percent to 31.0 percent1,2,3; the ST-segment elevation in these patients probably reflects myocardial stress in a setting of catecholamine flooding or autonomic disturbance. A lower incidence, about 5 percent,3 has been described in patients with ischemic stroke, in whom the ST-segment elevation possibly results from underlying cardiac disease.
In our experience, differentiating secondary electrocardiographic changes from acute ischemia in patients with stroke is a common problem, necessitating serial enzyme analysis and echocardiography. The prognostic value of such changes with respect to outcome has been described.2
Ilias A. Andrianakis, M.D.
Evangelos D. Papadomichelakis, M.D.
Anastasia N. Kotanidou, M.D.
University of Athens Medical School
10675 Athens, Greece
akotanid@med.uoa.gr
References
Sommargren CE, Zaroff JG, Banki N, Drew BJ. Electrocardiographic repolarization abnormalities in subarachnoid hemorrhage. J Electrocardiol 2002;35:Suppl:257-262.
Kawasaki T, Azuma A, Sawada T, et al. Electrocardiographic score as a predictor of mortality after subarachnoid hemorrhage. Circ J 2002;66:567-570.
Khechinashvili G, Asplund K. Electrocardiographic changes in patients with acute stroke: a systematic review. Cerebrovasc Dis 2002;14:67-76.
To the Editor: In Table 1 of their article, Wang et al. list causes of ST-segment elevation. I would like to add to this list the Osborn wave in hypothermia. This phenomenon, first described by Osborn1 in 1953, is a distinctive convex elevation at the junction, or J point, of the ST segment and the QRS complex. This deflection has been attributed to delayed depolarization, a current of "injury," or "early repolarization."2 More recent investigation has indicated that the Osborn wave is the consequence of electrical heterogeneities among the ventricular epicardium, M cells, and endocardium during ventricular repolarization.3
The Osborn wave develops when the body temperature drops to about 30°C.4 In leads facing the left ventricle, the deflection is positive, and the size is inversely related to the body temperature. The Osborn wave is commonly associated with QT prolongation. It has also been reported in hypercalcemia.3
Tsung O. Cheng, M.D.
George Washington University Medical Center
Washington, DC 20037
tcheng@mfa.gwu.edu
References
Osborn JJ. Experimental hypothermia: respiratory and blood pH changes in relation to cardiac function. Am J Physiol 1953;175:389-398.
Santos EM, Kittle CF. Electrocardiographic changes in the dog during hypothermia. Am Heart J 1958;55:415-420.
Yang G-X, Lankipalli RS, Burke JF, Musco S, Kowey PR. Ventricular repolarization components on the electrocardiogram: cellular basis and clinical significance. J Am Coll Cardiol 2003;42:401-409.
Hurst JW. The heart, arteries and veins. 7th ed. New York: McGraw-Hill, 1990:289-90.
To the Editor: Wang and colleagues do not mention dissection of the thoracic aorta, which may cause electrocardiographic changes by affecting coronary flow. We reviewed the electrocardiograms from 14 consecutive patients with type A aortic dissection who were admitted to our university hospital. Only two patients had a normal electrocardiogram, four had clinically significant ST-segment elevation, two had nonsignificant elevation, four had left ventricular hypertrophy, one had previously had inferior infarction, and one had unspecific ST-segment changes. Of the four patients with significant ST-segment elevation, one was given thrombolytic therapy and one was admitted for primary percutaneous coronary intervention. In the latter patient, the right coronary artery was occluded by the dissection, resulting in ST-segment elevation in the inferior electrocardiographic leads.
Eigil Fossum, Ph.D.
Kl?w Nils-Einar, Ph.D.
Arild Mangschau, Ph.D.
Ullevaal University Hospital
0407 Oslo, Norway
eigil.fossum@ioks.uio.no
To the Editor: Wang et al. indicate that the reference for measurement of the ST segment should be the end of the PR segment, not the TP segment, and they cite an article on exercise standards.1 Although the PR segment is used as the reference for the ST segment in exercise testing, at rest it is the end of the TP (isoelectric) segment.2 In fact, Marriott related the ST-segment level to "whether it is elevated or depressed below the TP segment."3 The direction of the PR segment is opposite that of the P wave, so in leads with upright P waves and depressed PR segments, ST-segment elevations will be increased if the PR segment is used as the reference, whereas ST-segment depressions will be diminished. In leads with negative P waves, such as lead V1, the converse will apply. Of course, the clinical context and whether ST-segment findings evolve are as important as the point of reference and the magnitude of deviation. An absence of change argues against an acute process and suggests a benign repolarization variant.
Howard S. Friedman, M.D.
New York University School of Medicine
New York, NY 10016
hsf2727@pol.net
References
Fletcher GF, Balady GJ, Amsterdam EA, et al. Exercise standards for testing and training: a statement for healthcare professionals from the American Heart Association. Circulation 2001;104:1694-1740.
The Criteria Committee of the New York Heart Association. Diseases of the heart and blood vessels: nomenclature and criteria for diagnosis. 6th ed. Boston: Little, Brown, 1964:391.
Marriott HJL. Practical electrocardiography. 6th ed. Baltimore: Williams & Wilkins, 1977:21.
The authors reply: The Osborn wave, which Cheng proposes to include among the causes of ST-segment elevation, can be better described morphologically as a "slurred" downstroke of the QRS complex and is not likely to be confused with the ST-segment elevation of infarction.
In aortic dissection, addressed by Fossum et al., the proximal coronary artery may be compressed by the dissecting hematoma or transected, causing myocardial infarction, in which case the electrocardiogram actually reflects the infarction, not the aortic dissection itself. However, it is important to realize that this infarction is a complication of the aortic dissection, not a primary event, because the treatment approach is different in these two situations.
The typical electrocardiographic changes of central nervous system events, referred to by Andrianakis et al., are deep, symmetrically inverted T waves with QT prolongation. ST-segment elevation does occur during the early stage, but usually it is not prominent enough to suggest the presence of an infarction from an occluded epicardial coronary artery that requires reperfusion therapy. Even though these electrocardiographic changes were initially described in patients with subarachnoid hemorrhage and hence called neurogenic T-wave changes, the electrocardiographic findings and transient left ventricular regional wall-motion abnormalities are not unique to central nervous system events, since the same phenomena have been observed in a variety of other acute medical conditions.1,2 The report by Tsuchihashi et al. of "transient left ventricular apical ballooning," which Ako et al. cite, may describe the same entity with slightly different manifestations and a different emphasis. The same "apical ballooning" reported by Kurisu et al., also cited by Ako et al., is believed to be due to simultaneous multivessel coronary-artery spasm. If so, it is a variant of Prinzmetal's angina.
Whether the TP segment or the PR segment should be used as a reference point for ST-segment deviation has long been debated, and Friedman raises the question here. We agree with the American College of Cardiology–American Heart Association guidelines stating that the PQ junction (the end of the PR segment) should be used. This issue is best settled by vectorcardiographic analysis. If the QRS-vector loop ends at the point of origin (the beginning of the ventricular depolarization), the loop is closed, and there is no ST-segment deviation; otherwise, the loop is open, and ST-segment deviation is manifested. The point of origin of the QRS-vector loop is the PQ junction on the electrocardiogram. The issue, then, is whether the QRS complex ends at that level or not. The PQ junction may not be at the level of the TP segment because the ventricle depolarizes while the atria are repolarizing, and this can affect the level of the PQ junction. How this atrial-repolarization wave affects the ST segment has been clearly described by Tranchesi et al.3
Kyuhyun Wang, M.D.
Richard W. Asinger, M.D.
Hennepin County Medical Center
Minneapolis, MN 55415
Henry J.L. Marriott, M.D.
University of South Florida, Tampa
Tampa, FL 33620
References
Sharkey SW, Shear W, Hodges M, Herzog CA. Reversible myocardial contraction abnormalities in patients with an acute noncardiac illness. Chest 1998;114:98-105.
Ruiz Bailen M. Reversible myocardial dysfunction in critically ill, noncardiac patients: a review. Crit Care Med 2002;30:1280-1290.
Tranchesi J, Adelardi V, de Oliveira J. Atrial repolarization -- its importance in clinical electrocardiography. Circulation 1960;22:635-644.