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Baseline drug history is also important for interpretation of the electrocardiogram
American Journal of Emergency Medicine (2010) 28, 637–639
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The differential diagnosis includes reversible cerebral vasoconstrictor syndrome To the Editor, The differential diagnosis of reversible leukoencephalopathy should include reversible cerebral vasoconstrictor syndrome. The suggestion that bilateral infarction of the posterior cerebral arteries is the closest differential diagnosis of reversible posterior leukoencephalopathy syndrome (RPLS) probably applies to patients such as the one who featured in a recent report [1], who present without headache, but alternative diagnoses such as reversible cerebral vasoconstrictor syndrome (RCVS) have to be considered in those who present with headache [2]. Notwithstanding that reversible cerebral edema has been the main focus in the imaging of RPLS [3] and reversibility of diffuse cerebral vasoconstriction the main focus in the imaging of RCVS [2], there is considerable overlap in the clinical and radiologic features of the 2 disorders [2,4-7]. Risk factors common to both disorders include the peripartum period and treatment with calcineurin inhibitors, respectively [2,5], and clinical stigmata that the 2 disorders have in common include hypertension, headache, seizures, focal neurologic deficits, and risk of recurrence [2,4]. Furthermore, diffuse multifocal segmental cerebral vasoconstriction, recognized as the hallmark of RCVS [2], may also be a feature of RPLS [6], and 9% of RCVS patients have been reported with “MRI (magnetic resonance imaging) FLAIR hypersignals consistent with RPLS” [2]. The overlap in radiologic stigmata between the 2 disorders is exemplified by the report of a patient presenting with hypertension, headache, and seizures in whom magnetic resonance imaging showed stigmata of RPLS, and angiography demonstrated diffuse reversible vasospasm [7]. Oscar M.P. Jolobe MB, ChB, DPhil Manchester Medical Society C/o John Rylands University Library Manchester M13 9PP, UK E-mail address: [email protected] doi:10.1016/j.ajem.2010.03.030 0735-6757/$ – see front matter © 2010 Elsevier Inc. All rights reserved.
References [1] Mankad K, Hoey E, Yap KS. Reversible leukoencephalopathy syndrome. Am J Emerg Med 2010;28:386.e3-e5. [2] Ducros A, Boukobza M, Porcher R, Sarow M, Valade D, Bousser MG. The clinical and radiological spectrum of reversible cerebral vasoconstrictor syndrome. A prospective series of 67 patients. Brain 2007;130: 3091-101. [3] Bartynski WS. Posterior reversible encephalopathy syndrome, Part 1: fundamental imaging and clinical features. Am J Neuroradiol 2008;29: 1036-42. [4] Lee VH, Wijdicks EFM, Manno EM, Rabinstein AA. Clinical spectrum of reversible posterior leukoencephalopathy syndrome. Arch Neurol 2008;65:205-10. [5] Hinchey J, Chaves C, Appignani B, Breen J, Pao L, Wang A, et al. A reversible posterior leukoencephalopathy syndrome. N Engl J Med 1996;334:494-500. [6] Bartynski WS, Boardman JF. Catheter angiography, MR angiography, and MR perfusion in posterior reversible encephalopathy syndrome. Am J Neuroradiol 2008;29:447-55. [7] Dodick DW, Eross EJ, Drazkowski JF, Ingall TJ. Thundercalap headache associated with reversible vasospasm and posterior leukoencephalopathy syndrome. Cephalalgia 2003;23:994-7.
Baseline drug history is also important for interpretation of the electrocardiogram To the Editor, Given the increasing recognition of the risk of narrow QRS complex proarrhythmia after “as required” selfadministration of flecainide in patients with paroxysmal atrial fibrillation (AF) [1], it seems prudent that over and above the documentation of age, sex, chief complaint, specific indication for the test, history of the present illness, medical history, and baseline electrocardiogram, the static algorithm [2] ought also to document cardiovascular drug history. In particular, the phenomenon of atrial flutter, with 1:1 conduction, but at a ventricular rate of 200 beats/min, or 2:1 atrioventricular block with a ventricular rate of 100 beats/ min, seems to be almost unique to narrow QRS complex proarrhythmia attributable to class 1 drugs such as flecainide which, in the process of organizing AF into atrial flutter,
638
Correspondence
slow down the atrial flutter rate from the typical rate of 300 beats/min to 200 beats/min [1]. To quote a recent report citing examples of flecainide-related atrial flutter with ventricular rate 100/min, “this recognition can be a useful clue to interpreting tachycardia on electrocardiograms in primary care and emergency departments” [1]. Propafenone is another class 1 drug recognized as being responsible for atrial proarrhythmia leading to conversion of AF to atrial flutter with 1:1 conduction [3]. According to one study, a short P-R interval during sinus rhythm seems to be a risk factor for conversion of AF to atrial flutter with 1:1 conduction [4]. For that reason, the authors of that study recommended avoiding class 1c drugs in patients manifesting short P-R interval during sinus rhythm. In the presence of apparently normal P-R interval during sinus rhythm, the appearance of continuity between the P wave and the QRS complex (indicative of rapid atrioventricular conduction) on signal-averaged electrocardiogram also constitutes a risk factor for this atrial proarrhythmia [4]. A counsel of safety is also to prescribe “as required”(so-called pill-in-the-pocket) self-administration of class 1 drugs “only if the administration of a loading oral dose of flecainide or propafenone has been proved safe in hospital” [5]. Even after that has become universal good practice, it would still be prudent to record cardiovascular drug history in the “static” algorithm. Oscar M.P. Jolobe MB, ChB, DPhil Manchester Medical Society C/o John Rylands University Library M13 9PP Manchester, UK E-mail address: [email protected] doi:10.1016/j.ajem.2010.04.009
References [1] Taylor R, Gandhi MM, Lloyd G. Tachycardia due to atrial flutter with rapid 1:1 conduction following treatment of atrial fibrillation with flecainide. BMJ 2010;340:595-6. [2] Borloz MP, Mark DG, Pines J, Brady WJ. Electrocardiographic differential diagnosis of narrow QRS complex tachycardia: an EDoriented algorithmic approach. Am J Emerg Med 2010;28:278-81. [3] Murdock CJ, Kyles AE, Yeung-Lai-Wah JA, Vorderbrugge S, Kerr CR. Atrial flutter in patients treated for atrial fibrillation with propafenone. Am J Cardiol 2009;66:755-7. [4] Bremlin-Perrot B, Houriez P, Beurrier D, Claudon O, de la Terrier A, Louis P. Predictors of atrial flutter with 1:1 conduction in patients treated with class 1 drugs for atrial tacharrhythmias. Int J Cardiol 2001;80:7-15. [5] Alboni P, Botto G, Boriani G, Russo G, Pacchioni F, Iori M, et al. Intravenous administration of flecainide or propafenone in patients with recent-onset atrial fibrillation does not predict adverse effect during “pill-in-the-pocket” treatment. HEART 2010;96:546-9.
More rigorous risk profiling of prospective candidates for plasminogen activator therapy To the Editor, Given the fact that the use of plasminogen activator in elderly subjects with ischemic stroke is one characterized by a precarious balance between risk and benefit [1], more rigorous profiling of prospective candidates for this treatment modality ought to be undertaken to reduce the risk of treatment-related intracerebral hemorrhage (ICH). Cerebral amyloid angiopathy (CAA), already identified as a risk factor for warfarin-related ICH [2], is the most obvious candidate risk factor for plasminogen activator–related ICH. Although no in vivo imaging techniques exist to visualize CAA, indirect evidence of CAA can be obtained from documentation of lobar cerebral microbleeds by nuclear magnetic resonance imaging, based on the inference that CAA typically results in microhemorrhages around the vessel wall [3]. On the basis of a case control study, cerebral microbleeds, in turn, also appear to be significantly (P b .001) associated with increased risk of warfarin-related intracerebral hemorrhage [4] and, by inference, might also be associated with thrombolysis-related ICH. The prevalence of cerebral microbleeds is age related, as shown by a study comprising 1062 subjects with a mean age of 69.6 years in which the prevalence of cerebral microbleeds was 38.3% among 120 subjects aged 80 to 79 years as opposed to 17.1% among 670 subjects aged 60 to 69 years [5]. Accordingly, instead of the usual practice whereby “acute stroke patients seldom have an urgent MR (magnetic resonance) but rather a CT (computerised tomography) scan” [6], elderly subjects who are prospective candidates for plasminogen activator therapy ought to have nuclear magnetic resonance imaging, both for validation of ischemic stroke and for documentation of extent and localization of cerebral microbleeds, given the fact that multiple cortical and subcortical microbleeds located in the frontal and parietal lobes are the ones most likely to be associated with the genotype for CAA [5]. However, in view of the fact “that there has been no systematic neuropathological validation of thrombolysis-related intracerebral haemorrhage, despite detailed clinicoradiological descriptions” [7], case control studies analogous to the one suggesting an association between cerebral microbleeds and warfarin-related ICH [4] might have to suffice to establish the link between CAA, cerebral microbleeds, and thrombolysis. Oscar M.P. Jolobe MB, ChB, DPhil Manchester Medical Society C/o John Rylands University Library M13 9PP Manchester, UK E-mail address: [email protected] doi:10.1016/j.ajem.2010.04.010
www.elsevier.com/locate/ajem
Correspondence
The differential diagnosis includes reversible cerebral vasoconstrictor syndrome To the Editor, The differential diagnosis of reversible leukoencephalopathy should include reversible cerebral vasoconstrictor syndrome. The suggestion that bilateral infarction of the posterior cerebral arteries is the closest differential diagnosis of reversible posterior leukoencephalopathy syndrome (RPLS) probably applies to patients such as the one who featured in a recent report [1], who present without headache, but alternative diagnoses such as reversible cerebral vasoconstrictor syndrome (RCVS) have to be considered in those who present with headache [2]. Notwithstanding that reversible cerebral edema has been the main focus in the imaging of RPLS [3] and reversibility of diffuse cerebral vasoconstriction the main focus in the imaging of RCVS [2], there is considerable overlap in the clinical and radiologic features of the 2 disorders [2,4-7]. Risk factors common to both disorders include the peripartum period and treatment with calcineurin inhibitors, respectively [2,5], and clinical stigmata that the 2 disorders have in common include hypertension, headache, seizures, focal neurologic deficits, and risk of recurrence [2,4]. Furthermore, diffuse multifocal segmental cerebral vasoconstriction, recognized as the hallmark of RCVS [2], may also be a feature of RPLS [6], and 9% of RCVS patients have been reported with “MRI (magnetic resonance imaging) FLAIR hypersignals consistent with RPLS” [2]. The overlap in radiologic stigmata between the 2 disorders is exemplified by the report of a patient presenting with hypertension, headache, and seizures in whom magnetic resonance imaging showed stigmata of RPLS, and angiography demonstrated diffuse reversible vasospasm [7]. Oscar M.P. Jolobe MB, ChB, DPhil Manchester Medical Society C/o John Rylands University Library Manchester M13 9PP, UK E-mail address: [email protected] doi:10.1016/j.ajem.2010.03.030 0735-6757/$ – see front matter © 2010 Elsevier Inc. All rights reserved.
References [1] Mankad K, Hoey E, Yap KS. Reversible leukoencephalopathy syndrome. Am J Emerg Med 2010;28:386.e3-e5. [2] Ducros A, Boukobza M, Porcher R, Sarow M, Valade D, Bousser MG. The clinical and radiological spectrum of reversible cerebral vasoconstrictor syndrome. A prospective series of 67 patients. Brain 2007;130: 3091-101. [3] Bartynski WS. Posterior reversible encephalopathy syndrome, Part 1: fundamental imaging and clinical features. Am J Neuroradiol 2008;29: 1036-42. [4] Lee VH, Wijdicks EFM, Manno EM, Rabinstein AA. Clinical spectrum of reversible posterior leukoencephalopathy syndrome. Arch Neurol 2008;65:205-10. [5] Hinchey J, Chaves C, Appignani B, Breen J, Pao L, Wang A, et al. A reversible posterior leukoencephalopathy syndrome. N Engl J Med 1996;334:494-500. [6] Bartynski WS, Boardman JF. Catheter angiography, MR angiography, and MR perfusion in posterior reversible encephalopathy syndrome. Am J Neuroradiol 2008;29:447-55. [7] Dodick DW, Eross EJ, Drazkowski JF, Ingall TJ. Thundercalap headache associated with reversible vasospasm and posterior leukoencephalopathy syndrome. Cephalalgia 2003;23:994-7.
Baseline drug history is also important for interpretation of the electrocardiogram To the Editor, Given the increasing recognition of the risk of narrow QRS complex proarrhythmia after “as required” selfadministration of flecainide in patients with paroxysmal atrial fibrillation (AF) [1], it seems prudent that over and above the documentation of age, sex, chief complaint, specific indication for the test, history of the present illness, medical history, and baseline electrocardiogram, the static algorithm [2] ought also to document cardiovascular drug history. In particular, the phenomenon of atrial flutter, with 1:1 conduction, but at a ventricular rate of 200 beats/min, or 2:1 atrioventricular block with a ventricular rate of 100 beats/ min, seems to be almost unique to narrow QRS complex proarrhythmia attributable to class 1 drugs such as flecainide which, in the process of organizing AF into atrial flutter,
638
Correspondence
slow down the atrial flutter rate from the typical rate of 300 beats/min to 200 beats/min [1]. To quote a recent report citing examples of flecainide-related atrial flutter with ventricular rate 100/min, “this recognition can be a useful clue to interpreting tachycardia on electrocardiograms in primary care and emergency departments” [1]. Propafenone is another class 1 drug recognized as being responsible for atrial proarrhythmia leading to conversion of AF to atrial flutter with 1:1 conduction [3]. According to one study, a short P-R interval during sinus rhythm seems to be a risk factor for conversion of AF to atrial flutter with 1:1 conduction [4]. For that reason, the authors of that study recommended avoiding class 1c drugs in patients manifesting short P-R interval during sinus rhythm. In the presence of apparently normal P-R interval during sinus rhythm, the appearance of continuity between the P wave and the QRS complex (indicative of rapid atrioventricular conduction) on signal-averaged electrocardiogram also constitutes a risk factor for this atrial proarrhythmia [4]. A counsel of safety is also to prescribe “as required”(so-called pill-in-the-pocket) self-administration of class 1 drugs “only if the administration of a loading oral dose of flecainide or propafenone has been proved safe in hospital” [5]. Even after that has become universal good practice, it would still be prudent to record cardiovascular drug history in the “static” algorithm. Oscar M.P. Jolobe MB, ChB, DPhil Manchester Medical Society C/o John Rylands University Library M13 9PP Manchester, UK E-mail address: [email protected] doi:10.1016/j.ajem.2010.04.009
References [1] Taylor R, Gandhi MM, Lloyd G. Tachycardia due to atrial flutter with rapid 1:1 conduction following treatment of atrial fibrillation with flecainide. BMJ 2010;340:595-6. [2] Borloz MP, Mark DG, Pines J, Brady WJ. Electrocardiographic differential diagnosis of narrow QRS complex tachycardia: an EDoriented algorithmic approach. Am J Emerg Med 2010;28:278-81. [3] Murdock CJ, Kyles AE, Yeung-Lai-Wah JA, Vorderbrugge S, Kerr CR. Atrial flutter in patients treated for atrial fibrillation with propafenone. Am J Cardiol 2009;66:755-7. [4] Bremlin-Perrot B, Houriez P, Beurrier D, Claudon O, de la Terrier A, Louis P. Predictors of atrial flutter with 1:1 conduction in patients treated with class 1 drugs for atrial tacharrhythmias. Int J Cardiol 2001;80:7-15. [5] Alboni P, Botto G, Boriani G, Russo G, Pacchioni F, Iori M, et al. Intravenous administration of flecainide or propafenone in patients with recent-onset atrial fibrillation does not predict adverse effect during “pill-in-the-pocket” treatment. HEART 2010;96:546-9.
More rigorous risk profiling of prospective candidates for plasminogen activator therapy To the Editor, Given the fact that the use of plasminogen activator in elderly subjects with ischemic stroke is one characterized by a precarious balance between risk and benefit [1], more rigorous profiling of prospective candidates for this treatment modality ought to be undertaken to reduce the risk of treatment-related intracerebral hemorrhage (ICH). Cerebral amyloid angiopathy (CAA), already identified as a risk factor for warfarin-related ICH [2], is the most obvious candidate risk factor for plasminogen activator–related ICH. Although no in vivo imaging techniques exist to visualize CAA, indirect evidence of CAA can be obtained from documentation of lobar cerebral microbleeds by nuclear magnetic resonance imaging, based on the inference that CAA typically results in microhemorrhages around the vessel wall [3]. On the basis of a case control study, cerebral microbleeds, in turn, also appear to be significantly (P b .001) associated with increased risk of warfarin-related intracerebral hemorrhage [4] and, by inference, might also be associated with thrombolysis-related ICH. The prevalence of cerebral microbleeds is age related, as shown by a study comprising 1062 subjects with a mean age of 69.6 years in which the prevalence of cerebral microbleeds was 38.3% among 120 subjects aged 80 to 79 years as opposed to 17.1% among 670 subjects aged 60 to 69 years [5]. Accordingly, instead of the usual practice whereby “acute stroke patients seldom have an urgent MR (magnetic resonance) but rather a CT (computerised tomography) scan” [6], elderly subjects who are prospective candidates for plasminogen activator therapy ought to have nuclear magnetic resonance imaging, both for validation of ischemic stroke and for documentation of extent and localization of cerebral microbleeds, given the fact that multiple cortical and subcortical microbleeds located in the frontal and parietal lobes are the ones most likely to be associated with the genotype for CAA [5]. However, in view of the fact “that there has been no systematic neuropathological validation of thrombolysis-related intracerebral haemorrhage, despite detailed clinicoradiological descriptions” [7], case control studies analogous to the one suggesting an association between cerebral microbleeds and warfarin-related ICH [4] might have to suffice to establish the link between CAA, cerebral microbleeds, and thrombolysis. Oscar M.P. Jolobe MB, ChB, DPhil Manchester Medical Society C/o John Rylands University Library M13 9PP Manchester, UK E-mail address: [email protected] doi:10.1016/j.ajem.2010.04.010