Letters to the Editor
consent. The study protocol conforms to the ethical guidelines of the 1975 Declaration of Helsinki as reflected in a priori approval by the Pennsylvania State University IRB. We would like to thank Dr. Mathi Manoj for the assistance in literature review. References [1] McCullough PA, Wolyn R, Rocher LL, Levin RN, O'Neill WW. Acute renal failure after coronary intervention: incidence, risk factors, and relationship to mortality. Am J Med 1997;103:368–75. [2] McCullough PA, Stacul F, Becker CR, et al. Contrast-induced nephropathy (CIN) consensus working panel: executive summary. Rev Cardiovasc Med 2006;7:177–97. [3] Rudnick MR, Goldfarb S, Wexler L, et al. Nephrotoxicity of ionic and nonionic contrast media in 1196 patients: a randomized trial. The Iohexol Cooperative Study. Kidney Int 1995;47:254–61.
597
[4] Mehran R, Aymong ED, Nikolsky E, et al. A simple risk score for prediction of contrast-induced nephropathy after percutaneous coronary intervention: development and initial validation. J Am Coll Cardiol 2004;44:1393–9. [5] Iakovou I, Dangas G, Mehran R, et al. Impact of gender on the incidence and outcome of contrast-induced nephropathy after percutaneous coronary intervention. J Invasive Cardiol 2003;15:18–22. [6] Rao SV, Cohen MG, Kandzari DE, Bertrand OF, Gilchrist IC. The transradial approach to percutaneous coronary intervention: historical perspective, current concepts, and future directions. J Am Coll Cardiol 2010;55:2187–95. [7] Baklanov DV, Kaltenbach LA, Marso SP, et al. The prevalence and outcomes of transradial percutaneous coronary intervention for ST-segment elevation myocardial infarction: analysis from the National Cardiovascular Data Registry (2007 to 2011). J Am Coll Cardiol 2013;61:420–6. [8] Vuurmans T, Byrne J, Fretz E, et al. Chronic kidney injury in patients after cardiac catheterisation or percutaneous coronary intervention: a comparison of radial and femoral approaches (from the British Columbia Cardiac and Renal Registries). Heart 2010;96:1538–42. [9] Scolari F, Ravani P, Gaggi R, et al. The challenge of diagnosing atheroembolic renal disease: clinical features and prognostic factors. Circulation 2007;116:298–304.
http://dx.doi.org/10.1016/j.ijcard.2014.03.092 0167-5273/© 2014 Elsevier Ireland Ltd. All rights reserved.
Parkinsonian tremor-induced electrocardiographic artifacts mimicking atrial flutter/fibrillation or ventricular tachycardia☆ Wen J. Hwang a,⁎, Ju Y. Chen b, Pi S. Sung c, Jen C. Lee d a b c d
Department of Neurology, National Cheng Kung University Hospital, College of Medicine, National Cheng Kung University, Tainan, Taiwan Division of Cardiology, Department of Internal Medicine, National Cheng Kung University Hospital, Tainan, Taiwan Department of Neurology, National Cheng Kung University Hospital, Tainan, Taiwan Department of Internal Medicine, National Cheng Kung University Hospital, Tainan, Taiwan
a r t i c l e
i n f o
Article history: Received 26 January 2014 Accepted 14 March 2014 Available online 20 March 2014 Keywords: Artifacts Electrocardiogram Parkinsonian tremor
Parkinson's disease is the second most common neurodegenerative disorder of the brain; it affects approximately 1–2% of people 65 and older. Typical parkinsonian tremor is present at 4–6 Hz during rest; it has a frequency similar to that of atrial flutter (250–350/min, 4.2–5.8/s) and overlaps with that of ventricular tachycardia (120–250/min, 2–4.2/ s). Parkinsonian tremor can induce electrocardiographic artifacts (hereafter “artifacts”) that mimic atrial flutter/fibrillation [1–5] or ventricular tachycardia [6–10]. Misinterpreting the artifacts can lead to unnecessary and even dangerous treatment or intervention [2,5,8,9]. We assessed the frequency and patterns of tremorinduced artifacts in outpatients in a university hospital, the association between tremor severity and patterns of artifacts, and the misinterpretation rate and their consequences.
☆ Authorship: All authors had access to the data and approved the submitted version. Wen-Juh Hwang: conception and design of the study, data analysis, and manuscript preparation; Ju-Yi Chen: data collection, data analysis, and revision of the manuscript; Pi-Shan Sung: data collection and manuscript preparation; Jen-Chieh Lee: data collection and revision of the manuscript. ⁎ Corresponding author at: Department of Neurology, National Cheng Kung University Hospital, College of Medicine, National Cheng Kung University, 138 ShengLi Road, Tainan 704, Taiwan. Tel.: +886 6 276 6187; fax: +886 6 237 4285. E-mail address: [email protected] (W.J. Hwang).
We enrolled a convenience sample of 100 patients (46 men, 54 women [mean age: 67.8 ± 10.5 years]) with Parkinson's disease with rest tremor. Each underwent a 12-lead electrocardiogram (PageWriter Trim III; Philips Healthcare, Andover, MA, USA) and a surface electromyography study (VikingSelect; Nicolet Viasys Biomedical, Madison, WI, USA). The severity of the rest tremor was evaluated on five parts of the body (4 limbs and the face) by neurologists (WJH and PSS) using item 20, “Tremor at rest”, of the Unified Parkinson's Disease Rating Scale (from 0 = absent to 4 = marked in amplitude and present most of the time). The maximum score is 20. One neurologist (PSS) accompanied each patient during the test and checked their consciousness, blood pressure, pulse rate and regularity, and clinical symptoms when the electrocardiogram showed an undulating baseline or suggested probable atrial flutter/fibrillation or ventricular tachycardia. The presence of artifacts and an electrocardiogram pattern simulating an arrhythmia were finally determined by a cardiologist (JYC) and a neurologist (WJH) based on the electrocardiogram changes before and after suppressing the tremor, the surface electromyographic findings, and clinical correlations (consciousness, vital signs, and clinical symptoms). The cardiologist and neurologist reviewed the medical records, checked and determined the abnormalities of each copy of the electrocardiogram, and divided the 100 copies into three groups according to the patterns of artifacts: Group I (patients with no artifacts), Group II (patients with an undulating baseline), and Group III (patients with atrial flutter/fibrillation or ventricular tachycardia mimics). The 100 copies were read by 10 postgraduate year 1 (10 copies each), 5 neurology residents (2 second-year, 3 third-year; 20 copies each), 5 internal medicine residents (3 secondyear, 2 third-year; 20 copies each), and 4 cardiologists (2 chief residents, 2 fellows; 25 copies each). The interpreting doctors were given relevant medical information and a clinical diagnosis of Parkinson's disease and asked to recommend patient management based on their readings of the electrocardiogram. This study was
598
Letters to the Editor
Fig. 1. Electrocardiogram showing tremor-induced artifacts mimicking atrial flutter.
authorized by our hospital's Institutional Review Board. Analysis of variance and Scheffe's method were used to analyze the association between tremor severity and patterns of artifacts. Significance was set at p b 0.05. Patients had a high frequency of artifacts: baseline undulation (78%) and atrial flutter/fibrillation (Fig. 1) or ventricular tachycardia mimics (Fig. 2a) (11%). Those with atrial flutter/fibrillation or ventricular tachycardia mimics had significantly higher tremor score (7.2 ± 3.5) than those with an undulating baseline (4.0 ± 2.7) and those without artifacts (2.5 ± 1.5) (p b 0.001); there was no significant difference between the latter two groups. The electrocardiograph misread the electrocardiograms of 5/89 (5.6%) patients with artifacts: 2/78 (2.6%) patients with an undulating baseline, and 3/11 (27.3%) patients with atrial flutter/fibrillation or ventricular tachycardia mimics. The postgraduate year 1 misread the electrocardiograms of 8/89 (9.0%) patients with artifacts: 3/78 (3.8%) patients with an undulating baseline, and 5/11 (45%) patients with atrial flutter/fibrillation or ventricular tachycardia mimics, and recommended anti-arrhythmic and anticoagulant agents. Neurology residents misread the electrocardiogram of 1/11 (9.1%) patients with atrial flutter/fibrillation or ventricular tachycardia mimics as atrial flutter and recommended an antiarrhythmic agent. Internal medicine residents misread the electrocardiogram of 1 patient with atrial flutter/fibrillation or ventricular tachycardia mimics as atrial tachycardia with block and recommended antiplatelet treatment. In contrast, cardiology chief residents and fellows correctly identified all artifacts. The results indicated that professional training is associated with better judgment. Parkinsonian tremor has a high probability of causing artifacts. The tremor of patients with atrial flutter/fibrillation or ventricular tachycardia mimics was more severe than that of patients without artifacts or with an undulating baseline. Parkinsonian tremor is present in the limbs and face but not in the trunk. Our finding that tremor-induced artifacts were most prominent in the corresponding limb-leads and less so in the precordial leads is consistent with the distribution of the tremor. Sawtooth flutter waves are most often seen in leads II, III, aVF, and V1 in a 12-lead electrocardiogram. Because left leg tremor also causes atrial flutter/fibrillation mimics in leads II, III, and aVF, the physician
should watch for any movement of the left leg if atrial flutter/ fibrillation is suspected on leads II, III, and aVF in a 12-lead study. Identifying well-preserved P waves in the precordial leads and eliminating “flutter” waves by holding the tremulous limbs suggested tremor-induced artifacts rather than atrial flutter with fixed block. Features that may help differentiate true ventricular tachycardia from mimics include the absence of hemodynamic deterioration during the event and the presence of discrete components of QRS complexes at intervals corresponding to multiples of the baseline rhythm RR interval. Our findings may also have important clinical implications. First, as Parkinson's disease progresses, patients may manifest postural instability with falls, orthostatic hypotension with syncope, and medication-induced sleep attacks. An electrocardiogram done in these situations may cause the physician to mistake tremor-induced atrial flutter/fibrillation or ventricular tachycardia mimics as the cause of the clinical symptoms, which will lead to inadequate treatment or intervention. Second, in a patient with stroke on one side and Parkinson's disease on the other, misinterpreting intermittent and fluctuating parkinsonian tremor-induced artifact as paroxysmal atrial flutter/fibrillation may lead to an unnecessary transesophageal echocardiogram and anticoagulant treatment. This study was supported by grant NSC 97-2314-B-006-024 from the National Science Council Taiwan. We thank professor Hui-ing Ma for reviewing an earlier draft of this manuscript.
References [1] Pallis CA, Calne DB. Parkinsonism and cardiac arrhythmias. Lancet 1970;2:1313. [2] Vanerio G. Tremor as a cause of pseudoatrial flutter. Am J Geriatr Cardiol 2007;16:106–8. [3] Parkin TW, Connolly DC. Muscle-tremor artifact due to Parkinson's syndrome. It simulated atrial flutter and disappeared during sleep. Postgrad Med 1965;37:718–20. [4] Hollendonner WJ. Somatic tremor simulating atrial flutter. Del Med J 1957;29:126–7. [5] Finsterer J, Stollberger C, Gatterer E. Oral anticoagulation for ECG tremor artefact simulating atrial fibrillation. Acta Cardiol 2003;58:425–9. [6] Ortega-Carnicer J. Tremor-related artefact mimicking ventricular tachycardia. Resuscitation 2005;65:243–4.
Letters to the Editor
599
Fig. 2. a. Electrocardiogram showing tremor-induced artifacts mimicking ventricular tachycardia (250/min, 4.2/s). b. Disappearance of tremor-induced artifacts after direct pressure on the tremulous limb (from the patient in panel a). c. A surface electromyography study of the left leg at rest (from the patient in panel a) shows rhythmic alternating bursts of antagonistic muscles at a frequency of 4 Hz.
600
Letters to the Editor
[7] Llinas R, Henderson GV. Images in clinical medicine. Tremor as a cause of pseudo-ventricular tachycardia. N Engl J Med 1999;341:1275. [8] Bhatia L, Turner DR. Parkinson's tremor mimicking ventricular tachycardia. Age Ageing 2005;34:410–1.
[9] Srikureja W, Darbar D, Reeder GS. Tremor-induced ECG artifact mimicking ventricular tachycardia. Circulation 2000;102:1337–8. [10] Chase C, Brady WJ. Artifactual electrocardiographic change mimicking clinical abnormality on the ECG. Am J Emerg Med 2000;18:312–6.
http://dx.doi.org/10.1016/j.ijcard.2014.03.090 0167-5273/© 2014 Elsevier Ireland Ltd. All rights reserved.
The link between sleep duration and inflammation: Effects on cardiovascular disease Alberto Dominguez-Rodriguez a,b,⁎, Pedro Abreu-Gonzalez b,c a b c
Hospital Universitario de Canarias, Servicio de Cardiología, Tenerife, Spain Instituto Universitario de Tecnologías Biomédicas, Tenerife, Spain Universidad de La Laguna, Departamento de Fisiología, Tenerife, Spain
a r t i c l e
i n f o
Article history: Received 27 January 2014 Accepted 14 March 2014 Available online 19 March 2014 Keywords: Sleep duration Inflammation Cardiovascular disease
To the Editor: We read with great interest the article of Cheng et al., about whether long working hours and short sleep duration, are associated with an increased risk of acute myocardial infarction or severe coronary heart diseases, independent of established psychosocial work-related factors [1]. They must be congratulated by your article. However, in the discussion the authors do not discuss the relationship that exists between the inflammation, sleep duration and cardiovascular disease. Inflammation is well established as a key mechanism in the development of cardiovascular disease [2–4]. Libby describes how the inflammatory process contributes to all stages of cardiovascular disease, from the development of atherosclerotic plaques in the vascular wall to end stage thrombotic complications [5]. Inflammation is a plausible mechanism linking sleep duration and cardiovascular disease. There is evidence that sleep loss is associated with inflammation [6–8] and negative cardiovascular outcomes [6–9]. Recently, observational and experimental sleep deprivation studies have shown an association between sleep loss and proinflammatory processes that promote the development of atherosclerotic plaques [6]. A study by van Leeuwen et al. assessed 13 healthy young men who were restricted to 4 h in bed for five nights, followed by two nights of recovery sleep. This study assessed Creactive protein at baseline, after sleep restriction, and after recovery. Following sleep restriction, C-reactive protein was increased when compared to baseline, and continued to increase during recovery. These studies suggest that shortened sleep produces an acute increase in C-reactive protein that is not immediately ameliorated by recovery [10]. Moreover, sex differences were reported for sleep duration and C-reactive protein among 4600
⁎ Corresponding author at: Hospital Universitario de Canarias, Department of Cardiology, Ofra s/n La Cuesta E-38320, Tenerife, Spain. Tel.: +34 922679040; fax: +34 922 678460. E-mail address: [email protected] (A. Dominguez-Rodriguez).
adults in the Whitehall II Study [11]. The authors reported a null association between short and long sleep duration and C-reactive protein among men in that cohort after adjusting for covariates. Among women, however, long sleep (≥ 9 h) was associated with a 35% increase in C-reactive protein levels after adjusting for covariates. A recent study utilizing the 2007–2008 National Health and Nutrition Examination Survey cohort had its goal to discern relationships between sleep duration and C-reactive protein in the American population (N = 5587). In a nationally representative sample of U.S. adults, a J-shaped relationship between C-reactive protein and sleep duration was demonstrated, such that those with very short or very long sleep duration were more likely to show elevated C-reactive protein. In addition, this pattern was only partially explained by sleep disorders and other medical comorbidities. Thus, the role of sleep duration in proinflammatory processes, as marked by C-reactive protein levels, is complex, but the current data suggest that extremes of sleep duration increase proinflammatory risk [12]. In summary, important bi-directional effects between inflammation and sleep exist and short and long term sleep deprivation may have different effects on markers of inflammation and cardiovascular outcomes. Therefore, in the article of Cheng et al. [1], the omission of this aspect important in the discussion would deprive at the medical community of potentially useful information. The authors of this manuscript have certified that they comply with the Principles of Ethical Publishing in the International Journal of Cardiology. References [1] Cheng Y, Du CL, Hwang JJ, Chen IS, Chen MF, Su TC. Working hours, sleep duration and the risk of acute coronary heart disease: a case–control study of middle-aged men in Taiwan. Int J Cardiol 2014;171:419–22. [2] Dominguez-Rodriguez A, Abreu-Gonzalez P, Kaski JC. Inflammatory systemic biomarkers in setting acute coronary syndromes—effects of the diurnal variation. Curr Drug Targets 2009;10:1001–8. [3] Battistoni A, Rubattu S, Volpe M. Circulating biomarkers with preventive, diagnostic and prognostic implications in cardiovascular diseases. Int J Cardiol 2012;157:160–8. [4] Aldous SJ. Cardiac biomarkers in acute myocardial infarction. Int J Cardiol 2013;164:282–94. [5] Libby P. Inflammation and cardiovascular disease mechanisms. Am J Clin Nutr 2006;83:456S–60S. [6] Grandner MA, Sands-Lincoln MR, Pak VM, Garland SN. Sleep duration, cardiovascular disease, and proinflammatory biomarkers. Nat Sci Sleep 2013;5:93–107. [7] Matthews KA, Zheng H, Kravitz HM, et al. Are inflammatory and coagulation biomarkers related to sleep characteristics in mid-life women?: study of women's health across the nation sleep study. Sleep 2010;33:1649–55. [8] Mullington JM, Haack M, Toth M, Serrador JM, Meier-Ewert HK. Cardiovascular, inflammatory, and metabolic consequences of sleep deprivation. Prog Cardiovasc Dis 2009;51:294–302.
consent. The study protocol conforms to the ethical guidelines of the 1975 Declaration of Helsinki as reflected in a priori approval by the Pennsylvania State University IRB. We would like to thank Dr. Mathi Manoj for the assistance in literature review. References [1] McCullough PA, Wolyn R, Rocher LL, Levin RN, O'Neill WW. Acute renal failure after coronary intervention: incidence, risk factors, and relationship to mortality. Am J Med 1997;103:368–75. [2] McCullough PA, Stacul F, Becker CR, et al. Contrast-induced nephropathy (CIN) consensus working panel: executive summary. Rev Cardiovasc Med 2006;7:177–97. [3] Rudnick MR, Goldfarb S, Wexler L, et al. Nephrotoxicity of ionic and nonionic contrast media in 1196 patients: a randomized trial. The Iohexol Cooperative Study. Kidney Int 1995;47:254–61.
597
[4] Mehran R, Aymong ED, Nikolsky E, et al. A simple risk score for prediction of contrast-induced nephropathy after percutaneous coronary intervention: development and initial validation. J Am Coll Cardiol 2004;44:1393–9. [5] Iakovou I, Dangas G, Mehran R, et al. Impact of gender on the incidence and outcome of contrast-induced nephropathy after percutaneous coronary intervention. J Invasive Cardiol 2003;15:18–22. [6] Rao SV, Cohen MG, Kandzari DE, Bertrand OF, Gilchrist IC. The transradial approach to percutaneous coronary intervention: historical perspective, current concepts, and future directions. J Am Coll Cardiol 2010;55:2187–95. [7] Baklanov DV, Kaltenbach LA, Marso SP, et al. The prevalence and outcomes of transradial percutaneous coronary intervention for ST-segment elevation myocardial infarction: analysis from the National Cardiovascular Data Registry (2007 to 2011). J Am Coll Cardiol 2013;61:420–6. [8] Vuurmans T, Byrne J, Fretz E, et al. Chronic kidney injury in patients after cardiac catheterisation or percutaneous coronary intervention: a comparison of radial and femoral approaches (from the British Columbia Cardiac and Renal Registries). Heart 2010;96:1538–42. [9] Scolari F, Ravani P, Gaggi R, et al. The challenge of diagnosing atheroembolic renal disease: clinical features and prognostic factors. Circulation 2007;116:298–304.
http://dx.doi.org/10.1016/j.ijcard.2014.03.092 0167-5273/© 2014 Elsevier Ireland Ltd. All rights reserved.
Parkinsonian tremor-induced electrocardiographic artifacts mimicking atrial flutter/fibrillation or ventricular tachycardia☆ Wen J. Hwang a,⁎, Ju Y. Chen b, Pi S. Sung c, Jen C. Lee d a b c d
Department of Neurology, National Cheng Kung University Hospital, College of Medicine, National Cheng Kung University, Tainan, Taiwan Division of Cardiology, Department of Internal Medicine, National Cheng Kung University Hospital, Tainan, Taiwan Department of Neurology, National Cheng Kung University Hospital, Tainan, Taiwan Department of Internal Medicine, National Cheng Kung University Hospital, Tainan, Taiwan
a r t i c l e
i n f o
Article history: Received 26 January 2014 Accepted 14 March 2014 Available online 20 March 2014 Keywords: Artifacts Electrocardiogram Parkinsonian tremor
Parkinson's disease is the second most common neurodegenerative disorder of the brain; it affects approximately 1–2% of people 65 and older. Typical parkinsonian tremor is present at 4–6 Hz during rest; it has a frequency similar to that of atrial flutter (250–350/min, 4.2–5.8/s) and overlaps with that of ventricular tachycardia (120–250/min, 2–4.2/ s). Parkinsonian tremor can induce electrocardiographic artifacts (hereafter “artifacts”) that mimic atrial flutter/fibrillation [1–5] or ventricular tachycardia [6–10]. Misinterpreting the artifacts can lead to unnecessary and even dangerous treatment or intervention [2,5,8,9]. We assessed the frequency and patterns of tremorinduced artifacts in outpatients in a university hospital, the association between tremor severity and patterns of artifacts, and the misinterpretation rate and their consequences.
☆ Authorship: All authors had access to the data and approved the submitted version. Wen-Juh Hwang: conception and design of the study, data analysis, and manuscript preparation; Ju-Yi Chen: data collection, data analysis, and revision of the manuscript; Pi-Shan Sung: data collection and manuscript preparation; Jen-Chieh Lee: data collection and revision of the manuscript. ⁎ Corresponding author at: Department of Neurology, National Cheng Kung University Hospital, College of Medicine, National Cheng Kung University, 138 ShengLi Road, Tainan 704, Taiwan. Tel.: +886 6 276 6187; fax: +886 6 237 4285. E-mail address: [email protected] (W.J. Hwang).
We enrolled a convenience sample of 100 patients (46 men, 54 women [mean age: 67.8 ± 10.5 years]) with Parkinson's disease with rest tremor. Each underwent a 12-lead electrocardiogram (PageWriter Trim III; Philips Healthcare, Andover, MA, USA) and a surface electromyography study (VikingSelect; Nicolet Viasys Biomedical, Madison, WI, USA). The severity of the rest tremor was evaluated on five parts of the body (4 limbs and the face) by neurologists (WJH and PSS) using item 20, “Tremor at rest”, of the Unified Parkinson's Disease Rating Scale (from 0 = absent to 4 = marked in amplitude and present most of the time). The maximum score is 20. One neurologist (PSS) accompanied each patient during the test and checked their consciousness, blood pressure, pulse rate and regularity, and clinical symptoms when the electrocardiogram showed an undulating baseline or suggested probable atrial flutter/fibrillation or ventricular tachycardia. The presence of artifacts and an electrocardiogram pattern simulating an arrhythmia were finally determined by a cardiologist (JYC) and a neurologist (WJH) based on the electrocardiogram changes before and after suppressing the tremor, the surface electromyographic findings, and clinical correlations (consciousness, vital signs, and clinical symptoms). The cardiologist and neurologist reviewed the medical records, checked and determined the abnormalities of each copy of the electrocardiogram, and divided the 100 copies into three groups according to the patterns of artifacts: Group I (patients with no artifacts), Group II (patients with an undulating baseline), and Group III (patients with atrial flutter/fibrillation or ventricular tachycardia mimics). The 100 copies were read by 10 postgraduate year 1 (10 copies each), 5 neurology residents (2 second-year, 3 third-year; 20 copies each), 5 internal medicine residents (3 secondyear, 2 third-year; 20 copies each), and 4 cardiologists (2 chief residents, 2 fellows; 25 copies each). The interpreting doctors were given relevant medical information and a clinical diagnosis of Parkinson's disease and asked to recommend patient management based on their readings of the electrocardiogram. This study was
598
Letters to the Editor
Fig. 1. Electrocardiogram showing tremor-induced artifacts mimicking atrial flutter.
authorized by our hospital's Institutional Review Board. Analysis of variance and Scheffe's method were used to analyze the association between tremor severity and patterns of artifacts. Significance was set at p b 0.05. Patients had a high frequency of artifacts: baseline undulation (78%) and atrial flutter/fibrillation (Fig. 1) or ventricular tachycardia mimics (Fig. 2a) (11%). Those with atrial flutter/fibrillation or ventricular tachycardia mimics had significantly higher tremor score (7.2 ± 3.5) than those with an undulating baseline (4.0 ± 2.7) and those without artifacts (2.5 ± 1.5) (p b 0.001); there was no significant difference between the latter two groups. The electrocardiograph misread the electrocardiograms of 5/89 (5.6%) patients with artifacts: 2/78 (2.6%) patients with an undulating baseline, and 3/11 (27.3%) patients with atrial flutter/fibrillation or ventricular tachycardia mimics. The postgraduate year 1 misread the electrocardiograms of 8/89 (9.0%) patients with artifacts: 3/78 (3.8%) patients with an undulating baseline, and 5/11 (45%) patients with atrial flutter/fibrillation or ventricular tachycardia mimics, and recommended anti-arrhythmic and anticoagulant agents. Neurology residents misread the electrocardiogram of 1/11 (9.1%) patients with atrial flutter/fibrillation or ventricular tachycardia mimics as atrial flutter and recommended an antiarrhythmic agent. Internal medicine residents misread the electrocardiogram of 1 patient with atrial flutter/fibrillation or ventricular tachycardia mimics as atrial tachycardia with block and recommended antiplatelet treatment. In contrast, cardiology chief residents and fellows correctly identified all artifacts. The results indicated that professional training is associated with better judgment. Parkinsonian tremor has a high probability of causing artifacts. The tremor of patients with atrial flutter/fibrillation or ventricular tachycardia mimics was more severe than that of patients without artifacts or with an undulating baseline. Parkinsonian tremor is present in the limbs and face but not in the trunk. Our finding that tremor-induced artifacts were most prominent in the corresponding limb-leads and less so in the precordial leads is consistent with the distribution of the tremor. Sawtooth flutter waves are most often seen in leads II, III, aVF, and V1 in a 12-lead electrocardiogram. Because left leg tremor also causes atrial flutter/fibrillation mimics in leads II, III, and aVF, the physician
should watch for any movement of the left leg if atrial flutter/ fibrillation is suspected on leads II, III, and aVF in a 12-lead study. Identifying well-preserved P waves in the precordial leads and eliminating “flutter” waves by holding the tremulous limbs suggested tremor-induced artifacts rather than atrial flutter with fixed block. Features that may help differentiate true ventricular tachycardia from mimics include the absence of hemodynamic deterioration during the event and the presence of discrete components of QRS complexes at intervals corresponding to multiples of the baseline rhythm RR interval. Our findings may also have important clinical implications. First, as Parkinson's disease progresses, patients may manifest postural instability with falls, orthostatic hypotension with syncope, and medication-induced sleep attacks. An electrocardiogram done in these situations may cause the physician to mistake tremor-induced atrial flutter/fibrillation or ventricular tachycardia mimics as the cause of the clinical symptoms, which will lead to inadequate treatment or intervention. Second, in a patient with stroke on one side and Parkinson's disease on the other, misinterpreting intermittent and fluctuating parkinsonian tremor-induced artifact as paroxysmal atrial flutter/fibrillation may lead to an unnecessary transesophageal echocardiogram and anticoagulant treatment. This study was supported by grant NSC 97-2314-B-006-024 from the National Science Council Taiwan. We thank professor Hui-ing Ma for reviewing an earlier draft of this manuscript.
References [1] Pallis CA, Calne DB. Parkinsonism and cardiac arrhythmias. Lancet 1970;2:1313. [2] Vanerio G. Tremor as a cause of pseudoatrial flutter. Am J Geriatr Cardiol 2007;16:106–8. [3] Parkin TW, Connolly DC. Muscle-tremor artifact due to Parkinson's syndrome. It simulated atrial flutter and disappeared during sleep. Postgrad Med 1965;37:718–20. [4] Hollendonner WJ. Somatic tremor simulating atrial flutter. Del Med J 1957;29:126–7. [5] Finsterer J, Stollberger C, Gatterer E. Oral anticoagulation for ECG tremor artefact simulating atrial fibrillation. Acta Cardiol 2003;58:425–9. [6] Ortega-Carnicer J. Tremor-related artefact mimicking ventricular tachycardia. Resuscitation 2005;65:243–4.
Letters to the Editor
599
Fig. 2. a. Electrocardiogram showing tremor-induced artifacts mimicking ventricular tachycardia (250/min, 4.2/s). b. Disappearance of tremor-induced artifacts after direct pressure on the tremulous limb (from the patient in panel a). c. A surface electromyography study of the left leg at rest (from the patient in panel a) shows rhythmic alternating bursts of antagonistic muscles at a frequency of 4 Hz.
600
Letters to the Editor
[7] Llinas R, Henderson GV. Images in clinical medicine. Tremor as a cause of pseudo-ventricular tachycardia. N Engl J Med 1999;341:1275. [8] Bhatia L, Turner DR. Parkinson's tremor mimicking ventricular tachycardia. Age Ageing 2005;34:410–1.
[9] Srikureja W, Darbar D, Reeder GS. Tremor-induced ECG artifact mimicking ventricular tachycardia. Circulation 2000;102:1337–8. [10] Chase C, Brady WJ. Artifactual electrocardiographic change mimicking clinical abnormality on the ECG. Am J Emerg Med 2000;18:312–6.
http://dx.doi.org/10.1016/j.ijcard.2014.03.090 0167-5273/© 2014 Elsevier Ireland Ltd. All rights reserved.
The link between sleep duration and inflammation: Effects on cardiovascular disease Alberto Dominguez-Rodriguez a,b,⁎, Pedro Abreu-Gonzalez b,c a b c
Hospital Universitario de Canarias, Servicio de Cardiología, Tenerife, Spain Instituto Universitario de Tecnologías Biomédicas, Tenerife, Spain Universidad de La Laguna, Departamento de Fisiología, Tenerife, Spain
a r t i c l e
i n f o
Article history: Received 27 January 2014 Accepted 14 March 2014 Available online 19 March 2014 Keywords: Sleep duration Inflammation Cardiovascular disease
To the Editor: We read with great interest the article of Cheng et al., about whether long working hours and short sleep duration, are associated with an increased risk of acute myocardial infarction or severe coronary heart diseases, independent of established psychosocial work-related factors [1]. They must be congratulated by your article. However, in the discussion the authors do not discuss the relationship that exists between the inflammation, sleep duration and cardiovascular disease. Inflammation is well established as a key mechanism in the development of cardiovascular disease [2–4]. Libby describes how the inflammatory process contributes to all stages of cardiovascular disease, from the development of atherosclerotic plaques in the vascular wall to end stage thrombotic complications [5]. Inflammation is a plausible mechanism linking sleep duration and cardiovascular disease. There is evidence that sleep loss is associated with inflammation [6–8] and negative cardiovascular outcomes [6–9]. Recently, observational and experimental sleep deprivation studies have shown an association between sleep loss and proinflammatory processes that promote the development of atherosclerotic plaques [6]. A study by van Leeuwen et al. assessed 13 healthy young men who were restricted to 4 h in bed for five nights, followed by two nights of recovery sleep. This study assessed Creactive protein at baseline, after sleep restriction, and after recovery. Following sleep restriction, C-reactive protein was increased when compared to baseline, and continued to increase during recovery. These studies suggest that shortened sleep produces an acute increase in C-reactive protein that is not immediately ameliorated by recovery [10]. Moreover, sex differences were reported for sleep duration and C-reactive protein among 4600
⁎ Corresponding author at: Hospital Universitario de Canarias, Department of Cardiology, Ofra s/n La Cuesta E-38320, Tenerife, Spain. Tel.: +34 922679040; fax: +34 922 678460. E-mail address: [email protected] (A. Dominguez-Rodriguez).
adults in the Whitehall II Study [11]. The authors reported a null association between short and long sleep duration and C-reactive protein among men in that cohort after adjusting for covariates. Among women, however, long sleep (≥ 9 h) was associated with a 35% increase in C-reactive protein levels after adjusting for covariates. A recent study utilizing the 2007–2008 National Health and Nutrition Examination Survey cohort had its goal to discern relationships between sleep duration and C-reactive protein in the American population (N = 5587). In a nationally representative sample of U.S. adults, a J-shaped relationship between C-reactive protein and sleep duration was demonstrated, such that those with very short or very long sleep duration were more likely to show elevated C-reactive protein. In addition, this pattern was only partially explained by sleep disorders and other medical comorbidities. Thus, the role of sleep duration in proinflammatory processes, as marked by C-reactive protein levels, is complex, but the current data suggest that extremes of sleep duration increase proinflammatory risk [12]. In summary, important bi-directional effects between inflammation and sleep exist and short and long term sleep deprivation may have different effects on markers of inflammation and cardiovascular outcomes. Therefore, in the article of Cheng et al. [1], the omission of this aspect important in the discussion would deprive at the medical community of potentially useful information. The authors of this manuscript have certified that they comply with the Principles of Ethical Publishing in the International Journal of Cardiology. References [1] Cheng Y, Du CL, Hwang JJ, Chen IS, Chen MF, Su TC. Working hours, sleep duration and the risk of acute coronary heart disease: a case–control study of middle-aged men in Taiwan. Int J Cardiol 2014;171:419–22. [2] Dominguez-Rodriguez A, Abreu-Gonzalez P, Kaski JC. Inflammatory systemic biomarkers in setting acute coronary syndromes—effects of the diurnal variation. Curr Drug Targets 2009;10:1001–8. [3] Battistoni A, Rubattu S, Volpe M. Circulating biomarkers with preventive, diagnostic and prognostic implications in cardiovascular diseases. Int J Cardiol 2012;157:160–8. [4] Aldous SJ. Cardiac biomarkers in acute myocardial infarction. Int J Cardiol 2013;164:282–94. [5] Libby P. Inflammation and cardiovascular disease mechanisms. Am J Clin Nutr 2006;83:456S–60S. [6] Grandner MA, Sands-Lincoln MR, Pak VM, Garland SN. Sleep duration, cardiovascular disease, and proinflammatory biomarkers. Nat Sci Sleep 2013;5:93–107. [7] Matthews KA, Zheng H, Kravitz HM, et al. Are inflammatory and coagulation biomarkers related to sleep characteristics in mid-life women?: study of women's health across the nation sleep study. Sleep 2010;33:1649–55. [8] Mullington JM, Haack M, Toth M, Serrador JM, Meier-Ewert HK. Cardiovascular, inflammatory, and metabolic consequences of sleep deprivation. Prog Cardiovasc Dis 2009;51:294–302.
