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Bidirectional ventricular tachycardia associated with digoxin toxicity and with normal digoxin levels Michael Chapman, MBChB, MRCP,* Mark Hargreaves, MD, MRCP, CCDS,† Heiko Schneider, MBChB, MRCP,† Martin Royle, MBChB, MRCP, CCDS‡ From the *North Tyneside Hospital, Newcastle-upon-Tyne, United Kingdom, †Rochdale Infirmary, Rochdale, United Kingdom, and ‡Whiston Hospital, St Helen’s, Merseyside, United Kingdom.
Introduction Bidirectional ventricular tachycardia (VT) is a regular tachyarrhythmia of ventricular focus with 2 different QRS morphologies alternating on a beat-to-beat basis.1 The rate typically is between 140 and 180 bpm, with a frontal plane axis varying between –201 to –301 and 1101. Causes of this rare arrhythmia are limited and include catecholaminergic polymorphic VT, digitalis toxicity, myocarditis, left ventricular hypertrophy, myocardial infarction, herbal aconite poisoning, familial hypokalemic periodic paralysis, and Andersen-Tawil syndrome.1–7 Recently, pulmonary embolism8 and pheochromocytoma9 have also been implicated in causing this arrhythmia. We present 2 cases of bidirectional VT attributable to digoxin, one of which had a significantly raised serum digoxin level and 1 within laboratory normal limits.
Case reports Case 1 A 58-year-old woman presented with severe sepsis secondary to community-acquired pneumonia and acute kidney injury approximately 1 year after mechanical aortic and mitral valve replacement for rheumatic heart disease. She previously had been diagnosed with severe mixed mitral valve disease, moderate to severe aortic regurgitation, and pulmonary hypertension with predominantly right-sided heart failure. Coronary angiography was normal, and computed tomography of the chest showed no evidence of thromboembolism. Other past medical history of note was permanent atrial fibrillation and rheumatoid arthritis. Medication on KEYWORDS Bidirectional ventricular tachycardia; Digoxin toxicity; Ventricular tachycardia; Digoxin; Arrhythmia ABBREVIATIONS AVN ¼ atrioventricular node; ECG ¼ electrocardiogram; LBBB ¼ left bundle branch block; RBBB ¼ right bundle branch block; VT ¼ ventricular tachycardia (Heart Rhythm 2014;0:0–4) Address reprint requests and correspondence: Dr. Martin Royle, Department of Cardiology, Whiston Hospital, Warrington Rd, Prescot, Merseyside L35 5DR, United Kingdom. E-mail address: [email protected].
1547-5271/$-see front matter B 2014 Heart Rhythm Society. All rights reserved.
admission included digoxin, warfarin, ramipril, furosemide, spironolactone, and terbutaline. Biochemistry tests on admission revealed a urea level of 106 mg/dL (reference range 7–22.4 mg/dL), creatinine 4.41 mg/dL (0.56–1.0 mg/dL), potassium 5.7 mEq/L (3.5–5.0 mEq/L), magnesium 2.16 mg/dL (1.82–2.31 mg/dL), and adjusted calcium 8.08 mg/dL (8.7–10.3 mg/dL). Routine hematology tests showed a white cell count of 10.0 109/L and prothrombin time of 314.9 seconds (international normalized ratio 28.9). Twelve-lead ECG revealed bidirectional VT with right bundle branch block (RBBB) morphology and alternating frontal plane axis (Figure 1). Serum digoxin level, measured at 8 hours, was significantly elevated at 5.87 ng/mL (0–2.0 ng/mL). Treatment consisted of intravenous fluids, antibiotics, and administration of digoxin-specific antibody fragments. Interestingly, this resulted in cardioversion to sinus bradycardia (Figure 2). The patient’s renal function normalized, and digoxin was discontinued because of the occurrence of this arrhythmia and restoration of normal sinus rhythm.
Case 2 An 86-year-old man presented with acute onset of palpitations and dyspnea. He had multiple comorbidities including previous lung carcinoma with lobectomy in 1975, chronic obstructive pulmonary disease, permanent atrial fibrillation, congestive cardiac failure with severe left ventricular systolic dysfunction, previous cerebrovascular accident, type 2 diabetes mellitus, peripheral vascular disease with previous femoral–popliteal bypass, and prostate carcinoma. His regular medications were digoxin, perindopril, warfarin, furosemide, amiloride, gliclazide, beclomethasone inhaler, and salbutamol inhaler. There was no family history of arrhythmia or sudden cardiac death, and there had been no recent change to his medication doses. Routine biochemistry testing on admission showed potassium 4.6 mEq/L, urea 16.8 mg/dL, creatinine 0.89 mg/dL, and corrected calcium 9.76 mg/dL. Hematology testing on admission was unremarkable. Serum digoxin level, measured at just over 6 hours, was within normal limits at 0.58 ng/mL. http://dx.doi.org/10.1016/j.hrthm.2014.03.050
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 F1 80 81 82 83 84 F2 85 86 87 88 89 90 91 92 93 94 95 96 97 98 99 100 101 102 103 104 105 106 107 108
2 109 110 111 112 113 114 115 116 117 118 119 120 121 122 123 W 124 E B 125 4 126 C 127 / 128 F 129 P 130 O 131 132 133 134 F3 135Q5 136 137 138 F4 139 140 141 142 143 144 145 146 147 148 149 150 151 152 153 154 155 156 157 W 158 E 159 B 160 4 161 C 162 / 163 F P 164 O 165
Heart Rhythm, Vol 0, No 0, Month 2014
Figure 1
Twelve-lead ECG showing bidirectional ventricular tachycardia in a patient with acute kidney injury and elevated serum digoxin
The patient was noted to be hypotensive with a blood pressure of 85/62 mmHg and tachycardic. His admission ECG (Figure 3) confirmed bidirectional VT that, as in case 1, had an RBBB morphology and alternating frontal plane axis. Immediate direct current cardioversion resulted in atrial fibrillation with partial left bundle branch block (LBBB) and left-axis deviation (Figure 4). Digoxin was discontinued because it was the only recognized trigger of bidirectional VT in this patient. Diltiazem was later commenced for rate control.
Figure 2
Discussion Digitalis toxicity can produce a diverse set of arrhythmias because of its effect on intracellular calcium leading to delayed afterdepolarizations and enhancement of vagal tone on the atrioventricular node (AVN). These arrhythmias can include premature atrial or ventricular contractions, varying degrees of AVN block, accelerated junctional rhythms, paroxysmal atrial tachycardia with block, and bidirectional VT. When digitalis toxicity is suspected, the serum glycoside
Twelve-lead ECG post-treatment with digoxin-specific antibody fragments.
166 167 168 169 170 171 172 173 174 175 176 177 178 179 180 181 182 183 184 185 186 187 188 189 190 191 192 193 194 195 196 197 198 199 200 201 202 203 204 205 206 207 208 209 210 211 212 213 214 215 216 217 218 219 220 221 222
Chapman et al 223 224 225 226 227 228 229 230 231 232 233 234 235 236 237 238 239 240 241 242 243 244 245 246 247 248 249 250 251 252 253 254 255 256 257 258 259 260 261 262 263 264 265 266 267 268 269 270 271 272 273 274 275 276 277 278 279
Bidirectional Ventricular Tachycardia with Digoxin
Figure 3
3
Twelve-lead ECG showing bidirectional ventricular tachycardia in a patient receiving digoxin treatment.
level is of considerable value, especially when it is assayed 6 hours post dose. Levels 42 ng/mL are generally considered toxic; however, there is considerable overlap. Toxic manifestations can seen with levels o2.0 ng/mL but can be absent in others cases with levels 43 ng/mL.10 Observational studies have evaluated the clinical characteristics of patients with arrhythmias attributable to digoxin.10–12 Other than serum digoxin level, statistically significant differences have been found with regard to age, elevated blood urea nitrogen
Figure 4
level, presence of coronary artery disease, and acute or chronic pulmonary disease.10,11 Retrospective analysis of 73 patients presenting with arrhythmias attributable to digoxin also found serum digoxin levels to be significantly lower in those patients who were hypokalemic compared to those who were normokalemic.12 During bidirectional VT, the surface ECG most often shows a tachycardia with RBBB morphology and alternating QRS axis best seen in the inferior limb leads. However, there
Twelve-lead ECG after direct current cardioversion.
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4 337 338 339 340 341 342 343 344 345 346 347 348 349 350 351 352 353 354 355 356 357 358 359 360 361 362 363 364 365 Q6 366 367 368 369
are cases of LBBB morphology bidirectional VT8 as well as alternating LBBB and RBBB morphology,2 leading to some debate regarding the exact mechanism. Current understanding is thought to be related to elevated intracellular calcium causing delayed afterdepolarization in anatomically separate parts of the conducting system.13 In 2011, a model by Baher et al13 based on rabbit ventricles was able to produce the ECG characteristics of bidirectional VT. They proposed that for this arrhythmia to initiate, 2 separate foci with different rate thresholds for delayed afterdepolarization–induced ventricular bigeminy needed to be present. Because the ventricular rate exceeded the lower threshold, ventricular bigeminy would develop. This would effectively double the heart rate, taking the overall ventricular rate above the second threshold. Once this had developed, the 2 competing sites would simply alternate on a beat-to-beat basis. The authors proposed that this mechanism would explain why the rhythm is often of RBBB morphology with alternating frontal axis (where the 2 foci are in the anterior and posterior fascicles of the left bundle branch). It also explains why cases have been reported with alternating LBBB and RBBB morphology (with foci in the left and right bundles) and why this arrhythmia may progress to polymorphic VT (where Z3 foci develop). Both of our cases were attributable to digoxin and remarkably were admitted within 2 weeks of each other. The finding of this arrhythmia in the presence of a therapeutic serum digoxin level serves to further highlight the arrhythmic properties of digoxin within normal laboratory limits. Our patient was elderly with severe left ventricular systolic dysfunction, both of which have been shown
Heart Rhythm, Vol 0, No 0, Month 2014 to lead to increased risk of digoxin toxicity.10,11 This may explain the occurrence of this arrhythmia with a normal digoxin level.
References 1. Grimard C, De Labroille A, Charbonnier B, Babuty D. Bidirectional ventricular tachycardia resulting from digoxin toxicity. J Cardiovasc Electrophysiol 2005;16: 807–808. 2. Tai YT, Lau CP, But PP, Fong PC, Li JP. Bidirectional tachycardia induced by herbal aconite poisoning. Pacing Clin Electrophysiol 1992;15:831–839. 3. Chin A, Nair V, Healey JS. Bidirectional ventricular tachycardia secondary to subacute myocarditis. Can J Cardiol 2013;29:254. 4. Stubbs WA. Bidirectional ventricular tachycardia in familial hypokalaemic periodic paralysis. Proc R Soc Med 1976;69:223–224. 5. Sonmez O, Gul EE, Duman C, Düzenli MA, Tokaç M, Cooper J. Type II bidirectional ventricular tachycardia in a patient with myocardial infarction. J Electrocardiol 2009;42:631–632. 6. Bonnemeier H, Barantke M. It is not always digitalis: bidirectional ventricular tachycardia in left ventricular hypertrophy. Ann Noninvasive Electrocardiol 2008;13:208–210. 7. Sumitomo N, Shimizu W, Taniguchi K, Hiraoka M. Calcium channel blocker and adenosine triphosphate terminate bidirectional ventricular tachycardia in a patient with Andersen-Tawil syndrome. Heart Rhythm 2008;5:498–499. 8. Tatli E, Aktoz M, Barutcu A, Altun A. Bidirectional tachycardia in a patient with pulmonary embolism. Cardiol J 2010;17:194–195. 9. Traykov VB, Kotirkov KI, Petrov IS. Pheochromocytoma presenting with bidirectional ventricular tachycardia. Heart 2013;99:509. 10. Smith TW, Haber E. Digoxin intoxication: the relationship of clinical presentation to serum digoxin concentration. J Clin Invest 1970;49:2377. 11. Beller GA, Smith TW, Abelmann WH, Haber E, Hood WB Jr. Digitalis intoxication: a prospective clinical study with serum level correlations. N Engl J Med 1971;284:989–997. 12. Shapiro W. Correlative studies of serum digitalis levels and the arrhythmias of digitalis intoxication. Am J Cardiol 1978;41:852–859. 13. Baher AA, Uy M, Xie F, Garfinkel A, Qu Z, Weiss JN. Bidirectional ventricular tachycardia: ping pong in the His-Purkinje system. Heart Rhythm 2011;8: 599–605.
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Bidirectional ventricular tachycardia associated with digoxin toxicity and with normal digoxin levels Michael Chapman, MBChB, MRCP,* Mark Hargreaves, MD, MRCP, CCDS,† Heiko Schneider, MBChB, MRCP,† Martin Royle, MBChB, MRCP, CCDS‡ From the *North Tyneside Hospital, Newcastle-upon-Tyne, United Kingdom, †Rochdale Infirmary, Rochdale, United Kingdom, and ‡Whiston Hospital, St Helen’s, Merseyside, United Kingdom.
Introduction Bidirectional ventricular tachycardia (VT) is a regular tachyarrhythmia of ventricular focus with 2 different QRS morphologies alternating on a beat-to-beat basis.1 The rate typically is between 140 and 180 bpm, with a frontal plane axis varying between –201 to –301 and 1101. Causes of this rare arrhythmia are limited and include catecholaminergic polymorphic VT, digitalis toxicity, myocarditis, left ventricular hypertrophy, myocardial infarction, herbal aconite poisoning, familial hypokalemic periodic paralysis, and Andersen-Tawil syndrome.1–7 Recently, pulmonary embolism8 and pheochromocytoma9 have also been implicated in causing this arrhythmia. We present 2 cases of bidirectional VT attributable to digoxin, one of which had a significantly raised serum digoxin level and 1 within laboratory normal limits.
Case reports Case 1 A 58-year-old woman presented with severe sepsis secondary to community-acquired pneumonia and acute kidney injury approximately 1 year after mechanical aortic and mitral valve replacement for rheumatic heart disease. She previously had been diagnosed with severe mixed mitral valve disease, moderate to severe aortic regurgitation, and pulmonary hypertension with predominantly right-sided heart failure. Coronary angiography was normal, and computed tomography of the chest showed no evidence of thromboembolism. Other past medical history of note was permanent atrial fibrillation and rheumatoid arthritis. Medication on KEYWORDS Bidirectional ventricular tachycardia; Digoxin toxicity; Ventricular tachycardia; Digoxin; Arrhythmia ABBREVIATIONS AVN ¼ atrioventricular node; ECG ¼ electrocardiogram; LBBB ¼ left bundle branch block; RBBB ¼ right bundle branch block; VT ¼ ventricular tachycardia (Heart Rhythm 2014;0:0–4) Address reprint requests and correspondence: Dr. Martin Royle, Department of Cardiology, Whiston Hospital, Warrington Rd, Prescot, Merseyside L35 5DR, United Kingdom. E-mail address: [email protected].
1547-5271/$-see front matter B 2014 Heart Rhythm Society. All rights reserved.
admission included digoxin, warfarin, ramipril, furosemide, spironolactone, and terbutaline. Biochemistry tests on admission revealed a urea level of 106 mg/dL (reference range 7–22.4 mg/dL), creatinine 4.41 mg/dL (0.56–1.0 mg/dL), potassium 5.7 mEq/L (3.5–5.0 mEq/L), magnesium 2.16 mg/dL (1.82–2.31 mg/dL), and adjusted calcium 8.08 mg/dL (8.7–10.3 mg/dL). Routine hematology tests showed a white cell count of 10.0 109/L and prothrombin time of 314.9 seconds (international normalized ratio 28.9). Twelve-lead ECG revealed bidirectional VT with right bundle branch block (RBBB) morphology and alternating frontal plane axis (Figure 1). Serum digoxin level, measured at 8 hours, was significantly elevated at 5.87 ng/mL (0–2.0 ng/mL). Treatment consisted of intravenous fluids, antibiotics, and administration of digoxin-specific antibody fragments. Interestingly, this resulted in cardioversion to sinus bradycardia (Figure 2). The patient’s renal function normalized, and digoxin was discontinued because of the occurrence of this arrhythmia and restoration of normal sinus rhythm.
Case 2 An 86-year-old man presented with acute onset of palpitations and dyspnea. He had multiple comorbidities including previous lung carcinoma with lobectomy in 1975, chronic obstructive pulmonary disease, permanent atrial fibrillation, congestive cardiac failure with severe left ventricular systolic dysfunction, previous cerebrovascular accident, type 2 diabetes mellitus, peripheral vascular disease with previous femoral–popliteal bypass, and prostate carcinoma. His regular medications were digoxin, perindopril, warfarin, furosemide, amiloride, gliclazide, beclomethasone inhaler, and salbutamol inhaler. There was no family history of arrhythmia or sudden cardiac death, and there had been no recent change to his medication doses. Routine biochemistry testing on admission showed potassium 4.6 mEq/L, urea 16.8 mg/dL, creatinine 0.89 mg/dL, and corrected calcium 9.76 mg/dL. Hematology testing on admission was unremarkable. Serum digoxin level, measured at just over 6 hours, was within normal limits at 0.58 ng/mL. http://dx.doi.org/10.1016/j.hrthm.2014.03.050
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 F1 80 81 82 83 84 F2 85 86 87 88 89 90 91 92 93 94 95 96 97 98 99 100 101 102 103 104 105 106 107 108
2 109 110 111 112 113 114 115 116 117 118 119 120 121 122 123 W 124 E B 125 4 126 C 127 / 128 F 129 P 130 O 131 132 133 134 F3 135Q5 136 137 138 F4 139 140 141 142 143 144 145 146 147 148 149 150 151 152 153 154 155 156 157 W 158 E 159 B 160 4 161 C 162 / 163 F P 164 O 165
Heart Rhythm, Vol 0, No 0, Month 2014
Figure 1
Twelve-lead ECG showing bidirectional ventricular tachycardia in a patient with acute kidney injury and elevated serum digoxin
The patient was noted to be hypotensive with a blood pressure of 85/62 mmHg and tachycardic. His admission ECG (Figure 3) confirmed bidirectional VT that, as in case 1, had an RBBB morphology and alternating frontal plane axis. Immediate direct current cardioversion resulted in atrial fibrillation with partial left bundle branch block (LBBB) and left-axis deviation (Figure 4). Digoxin was discontinued because it was the only recognized trigger of bidirectional VT in this patient. Diltiazem was later commenced for rate control.
Figure 2
Discussion Digitalis toxicity can produce a diverse set of arrhythmias because of its effect on intracellular calcium leading to delayed afterdepolarizations and enhancement of vagal tone on the atrioventricular node (AVN). These arrhythmias can include premature atrial or ventricular contractions, varying degrees of AVN block, accelerated junctional rhythms, paroxysmal atrial tachycardia with block, and bidirectional VT. When digitalis toxicity is suspected, the serum glycoside
Twelve-lead ECG post-treatment with digoxin-specific antibody fragments.
166 167 168 169 170 171 172 173 174 175 176 177 178 179 180 181 182 183 184 185 186 187 188 189 190 191 192 193 194 195 196 197 198 199 200 201 202 203 204 205 206 207 208 209 210 211 212 213 214 215 216 217 218 219 220 221 222
Chapman et al 223 224 225 226 227 228 229 230 231 232 233 234 235 236 237 238 239 240 241 242 243 244 245 246 247 248 249 250 251 252 253 254 255 256 257 258 259 260 261 262 263 264 265 266 267 268 269 270 271 272 273 274 275 276 277 278 279
Bidirectional Ventricular Tachycardia with Digoxin
Figure 3
3
Twelve-lead ECG showing bidirectional ventricular tachycardia in a patient receiving digoxin treatment.
level is of considerable value, especially when it is assayed 6 hours post dose. Levels 42 ng/mL are generally considered toxic; however, there is considerable overlap. Toxic manifestations can seen with levels o2.0 ng/mL but can be absent in others cases with levels 43 ng/mL.10 Observational studies have evaluated the clinical characteristics of patients with arrhythmias attributable to digoxin.10–12 Other than serum digoxin level, statistically significant differences have been found with regard to age, elevated blood urea nitrogen
Figure 4
level, presence of coronary artery disease, and acute or chronic pulmonary disease.10,11 Retrospective analysis of 73 patients presenting with arrhythmias attributable to digoxin also found serum digoxin levels to be significantly lower in those patients who were hypokalemic compared to those who were normokalemic.12 During bidirectional VT, the surface ECG most often shows a tachycardia with RBBB morphology and alternating QRS axis best seen in the inferior limb leads. However, there
Twelve-lead ECG after direct current cardioversion.
280 281 282 283 284 285 286 287 288 289 290 291 292 293 294 295 296 297 298 299 300 301 302 303 304 305 306 307 308 309 310 311 312 313 314 315 316 317 318 319 320 321 322 323 324 325 326 327 328 329 330 331 332 333 334 335 336
4 337 338 339 340 341 342 343 344 345 346 347 348 349 350 351 352 353 354 355 356 357 358 359 360 361 362 363 364 365 Q6 366 367 368 369
are cases of LBBB morphology bidirectional VT8 as well as alternating LBBB and RBBB morphology,2 leading to some debate regarding the exact mechanism. Current understanding is thought to be related to elevated intracellular calcium causing delayed afterdepolarization in anatomically separate parts of the conducting system.13 In 2011, a model by Baher et al13 based on rabbit ventricles was able to produce the ECG characteristics of bidirectional VT. They proposed that for this arrhythmia to initiate, 2 separate foci with different rate thresholds for delayed afterdepolarization–induced ventricular bigeminy needed to be present. Because the ventricular rate exceeded the lower threshold, ventricular bigeminy would develop. This would effectively double the heart rate, taking the overall ventricular rate above the second threshold. Once this had developed, the 2 competing sites would simply alternate on a beat-to-beat basis. The authors proposed that this mechanism would explain why the rhythm is often of RBBB morphology with alternating frontal axis (where the 2 foci are in the anterior and posterior fascicles of the left bundle branch). It also explains why cases have been reported with alternating LBBB and RBBB morphology (with foci in the left and right bundles) and why this arrhythmia may progress to polymorphic VT (where Z3 foci develop). Both of our cases were attributable to digoxin and remarkably were admitted within 2 weeks of each other. The finding of this arrhythmia in the presence of a therapeutic serum digoxin level serves to further highlight the arrhythmic properties of digoxin within normal laboratory limits. Our patient was elderly with severe left ventricular systolic dysfunction, both of which have been shown
Heart Rhythm, Vol 0, No 0, Month 2014 to lead to increased risk of digoxin toxicity.10,11 This may explain the occurrence of this arrhythmia with a normal digoxin level.
References 1. Grimard C, De Labroille A, Charbonnier B, Babuty D. Bidirectional ventricular tachycardia resulting from digoxin toxicity. J Cardiovasc Electrophysiol 2005;16: 807–808. 2. Tai YT, Lau CP, But PP, Fong PC, Li JP. Bidirectional tachycardia induced by herbal aconite poisoning. Pacing Clin Electrophysiol 1992;15:831–839. 3. Chin A, Nair V, Healey JS. Bidirectional ventricular tachycardia secondary to subacute myocarditis. Can J Cardiol 2013;29:254. 4. Stubbs WA. Bidirectional ventricular tachycardia in familial hypokalaemic periodic paralysis. Proc R Soc Med 1976;69:223–224. 5. Sonmez O, Gul EE, Duman C, Düzenli MA, Tokaç M, Cooper J. Type II bidirectional ventricular tachycardia in a patient with myocardial infarction. J Electrocardiol 2009;42:631–632. 6. Bonnemeier H, Barantke M. It is not always digitalis: bidirectional ventricular tachycardia in left ventricular hypertrophy. Ann Noninvasive Electrocardiol 2008;13:208–210. 7. Sumitomo N, Shimizu W, Taniguchi K, Hiraoka M. Calcium channel blocker and adenosine triphosphate terminate bidirectional ventricular tachycardia in a patient with Andersen-Tawil syndrome. Heart Rhythm 2008;5:498–499. 8. Tatli E, Aktoz M, Barutcu A, Altun A. Bidirectional tachycardia in a patient with pulmonary embolism. Cardiol J 2010;17:194–195. 9. Traykov VB, Kotirkov KI, Petrov IS. Pheochromocytoma presenting with bidirectional ventricular tachycardia. Heart 2013;99:509. 10. Smith TW, Haber E. Digoxin intoxication: the relationship of clinical presentation to serum digoxin concentration. J Clin Invest 1970;49:2377. 11. Beller GA, Smith TW, Abelmann WH, Haber E, Hood WB Jr. Digitalis intoxication: a prospective clinical study with serum level correlations. N Engl J Med 1971;284:989–997. 12. Shapiro W. Correlative studies of serum digitalis levels and the arrhythmias of digitalis intoxication. Am J Cardiol 1978;41:852–859. 13. Baher AA, Uy M, Xie F, Garfinkel A, Qu Z, Weiss JN. Bidirectional ventricular tachycardia: ping pong in the His-Purkinje system. Heart Rhythm 2011;8: 599–605.
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