1 2 Q43Q3 4 5Q1 6 7 8 9 10 11 12 13 14 15 16 P 17 R 18 I 19 N T 20 & 21 W 22 E 23 B 24 4 25 C 26 / F 27 P 28 O 29 30 31 32 33 34 35 36 F1 37 38 39 40 41 42 43 44 45 46 47 48 49 50 51 52 53 54
JOSEPHSON AND WELLENS ECG LESSONS: A Monthly Visit to the 12 Lead ECG
Young woman with a stroke and palpitations Mark E. Josephson, MD,*† Hein J.J. Wellens, MD† From the *Division of Cardiology, Beth Israel Deaconess Medical Center, Boston, Massachusetts, and † Cardiovascular Research Institute, Maastricht, The Netherlands.
Figure 1 Sinus rhythm and spontaneous initiation of supraventricular tachycardia. In sinus rhythm (left panel), preexcitation with an appearance of a right atrioventricular posteroseptal pathway is present. The P wave is completed before the delta wave. Spontaneous supraventricular tachycardia with a right bundle branch block pattern is initiated by an atrial premature complex. The P wave is negative in the inferior leads and has a relatively long RP interval of 150 ms.
A 28-year-old woman with a history of palpitations presented with a stroke. Palpitations were documented to be secondary to supraventricular tachycardia (SVT) with a longest RP interval (150 ms) and inverted P waves in leads II, III, and aVF and preexcitation in sinus rhythm (Figure 1).
interval of only 150 ms, which is a little shorter than the PR interval during the tachycardia and has a different P-wave configuration. The initiation of the tachycardia was always block in the AP associated with only modest prolongation of the PR interval. This suggests but does not
Question What is the likely cause of the tachycardia, and where is the accessory pathway (AP) located?
Discussion The SVT has an RP interval that is longer than most rapidly conducting APs. Such RP intervals may be seen in atypical atrioventricular nodal reentrant pathways sometimes referred to as “slow-slow” variants. Atrial tachycardia can also have such an RP/PR ratio. However, as seen in Figure 1 the tachycardia is initiated by block in the AP by an atrial premature complex that is conducted with a PR Address reprint requests and correspondence: Dr Mark E. Josephson, Division of Cardiology, Beth Israel Deaconess Medical Center, 185 Pilgrim Rd, Baker 4, Boston, MA 02215. E-mail address: mjoseph2@bidmc. harvard.edu.
Figure 2 Echocardiogram demonstrating Ebstein anomaly of the tricuspid valve. The arrow shows displacement of the septal leaflet of the tricuspid valve (TV) from the tricuspid annulus (dashed line).
1547-5271/$-see front matter B 2015 Published by Elsevier Inc. on behalf of Heart Rhythm Society.
http://dx.doi.org/10.1016/j.hrthm.2015.04.023
55 56 57 58 59 60 61 62 63 64 65 66 67 68 69 70 71 72 73 74 75 76 77 78 79 80 81 82 83 84 85 86 87 Q5 88 89 90 91 92 93 94 95 P 96 R 97 I 98 N 99 T 100 & W101 E 102 B 103 4 104 C 105 / 106 F 107 P O 108
109 110 111 112 113 114 115 116 117 118 119 120 121 122 123 124 125
prove that this is a circus movement tachycardia. Why is the RP interval so long? The electrocardiogram in sinus rhythm (Figure 1) suggests preexcitation over a right posteroseptal pathway with a ventricular insertion near 6 o’clock on the tricuspid annulus. The P wave is completed before the onset of the delta wave, suggesting either a decremental AP or one with a long conduction time. The marked slurring on the downstroke in lead V1 suggests the presence of an atrioventricular AP and not an atriofascicular AP, which typically shows minimal preexcitation in sinus rhythm and, when present, looks like a typical left bundle branch block with rapid initial forces. The presence of a long RP tachycardia with right bundle branch block and preexcitation over a posteroseptal pathway with a long anterograde conduction time suggests the presence of Ebstein anomaly. The physical
examination demonstrated a loud systolic sail sound and tricuspid regurgitation. An echocardiogram (Figure 2) confirmed the diagnosis of Ebstein anomaly. She also had an atrial septal defect through which a paradoxical embolus theoretically could have produced the stroke. Venous studies showed normal venous flow. She was not on birth control pills and did not have factor V Leiden or a lupus anticoagulant. She did have transient atrial fibrillation initiated by her SVT, which was the most likely cause of her stroke. She underwent a cone procedure and repair of her atrial septal defect. At surgery, the AP was a broad band (1.5 cm) and required extensive cryoablation to eliminate it. The patient is doing well with no preexcitation or SVT, but still has mild tricuspid regurgitation.
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JOSEPHSON AND WELLENS ECG LESSONS: A Monthly Visit to the 12 Lead ECG
Young woman with a stroke and palpitations Mark E. Josephson, MD,*† Hein J.J. Wellens, MD† From the *Division of Cardiology, Beth Israel Deaconess Medical Center, Boston, Massachusetts, and † Cardiovascular Research Institute, Maastricht, The Netherlands.
Figure 1 Sinus rhythm and spontaneous initiation of supraventricular tachycardia. In sinus rhythm (left panel), preexcitation with an appearance of a right atrioventricular posteroseptal pathway is present. The P wave is completed before the delta wave. Spontaneous supraventricular tachycardia with a right bundle branch block pattern is initiated by an atrial premature complex. The P wave is negative in the inferior leads and has a relatively long RP interval of 150 ms.
A 28-year-old woman with a history of palpitations presented with a stroke. Palpitations were documented to be secondary to supraventricular tachycardia (SVT) with a longest RP interval (150 ms) and inverted P waves in leads II, III, and aVF and preexcitation in sinus rhythm (Figure 1).
interval of only 150 ms, which is a little shorter than the PR interval during the tachycardia and has a different P-wave configuration. The initiation of the tachycardia was always block in the AP associated with only modest prolongation of the PR interval. This suggests but does not
Question What is the likely cause of the tachycardia, and where is the accessory pathway (AP) located?
Discussion The SVT has an RP interval that is longer than most rapidly conducting APs. Such RP intervals may be seen in atypical atrioventricular nodal reentrant pathways sometimes referred to as “slow-slow” variants. Atrial tachycardia can also have such an RP/PR ratio. However, as seen in Figure 1 the tachycardia is initiated by block in the AP by an atrial premature complex that is conducted with a PR Address reprint requests and correspondence: Dr Mark E. Josephson, Division of Cardiology, Beth Israel Deaconess Medical Center, 185 Pilgrim Rd, Baker 4, Boston, MA 02215. E-mail address: mjoseph2@bidmc. harvard.edu.
Figure 2 Echocardiogram demonstrating Ebstein anomaly of the tricuspid valve. The arrow shows displacement of the septal leaflet of the tricuspid valve (TV) from the tricuspid annulus (dashed line).
1547-5271/$-see front matter B 2015 Published by Elsevier Inc. on behalf of Heart Rhythm Society.
http://dx.doi.org/10.1016/j.hrthm.2015.04.023
55 56 57 58 59 60 61 62 63 64 65 66 67 68 69 70 71 72 73 74 75 76 77 78 79 80 81 82 83 84 85 86 87 Q5 88 89 90 91 92 93 94 95 P 96 R 97 I 98 N 99 T 100 & W101 E 102 B 103 4 104 C 105 / 106 F 107 P O 108
109 110 111 112 113 114 115 116 117 118 119 120 121 122 123 124 125
prove that this is a circus movement tachycardia. Why is the RP interval so long? The electrocardiogram in sinus rhythm (Figure 1) suggests preexcitation over a right posteroseptal pathway with a ventricular insertion near 6 o’clock on the tricuspid annulus. The P wave is completed before the onset of the delta wave, suggesting either a decremental AP or one with a long conduction time. The marked slurring on the downstroke in lead V1 suggests the presence of an atrioventricular AP and not an atriofascicular AP, which typically shows minimal preexcitation in sinus rhythm and, when present, looks like a typical left bundle branch block with rapid initial forces. The presence of a long RP tachycardia with right bundle branch block and preexcitation over a posteroseptal pathway with a long anterograde conduction time suggests the presence of Ebstein anomaly. The physical
examination demonstrated a loud systolic sail sound and tricuspid regurgitation. An echocardiogram (Figure 2) confirmed the diagnosis of Ebstein anomaly. She also had an atrial septal defect through which a paradoxical embolus theoretically could have produced the stroke. Venous studies showed normal venous flow. She was not on birth control pills and did not have factor V Leiden or a lupus anticoagulant. She did have transient atrial fibrillation initiated by her SVT, which was the most likely cause of her stroke. She underwent a cone procedure and repair of her atrial septal defect. At surgery, the AP was a broad band (1.5 cm) and required extensive cryoablation to eliminate it. The patient is doing well with no preexcitation or SVT, but still has mild tricuspid regurgitation.
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