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Subclinical atrial fibrillation preceding cardioembolic stroke in a patient with systolic heart failure
International Journal of Cardiology 176 (2014) 1036–1038
Contents lists available at ScienceDirect
International Journal of Cardiology journal homepage: www.elsevier.com/locate/ijcard
Letter to the Editor
Subclinical atrial fibrillation preceding cardioembolic stroke in a patient with systolic heart failure Kihei Yoneyama a, Tomoo Harada a, Hidemichi Ito b, Makoto Takano a, Maya Tsukahara a, Yukio Sato a, Masashi Uchida b, Satoru Nishio a, Yoshihiro J. Akashi a,⁎ a b
Division of Cardiology, Department of Internal Medicine, St. Marianna University School of Medicine, Kawasaki, Japan Department of Neurosurgery, St. Marianna University School of Medicine, Kawasaki, Japan
a r t i c l e
i n f o
Article history: Received 3 June 2014 Accepted 26 July 2014 Available online 13 August 2014 Keywords: Cerebral infarction Atrial flutter Rate control Rhythm control Warfarin Oral anticoagulants
Atrial fibrillation and congestive heart failure are risk factors for cerebral infarction. The most commonly used estimates of stroke risk in patients with atrial fibrillation are cardiac failure, hypertension, age, diabetes mellitus, and stroke (CHADS2 score) [1–4]. Although atrial fibrillation may be recognized by the presence of symptoms, such as palpitations, some patients are occasionally asymptomatic [5–7]. The absence of symptoms results in a delayed diagnosis and may lead to fatal thromboembolic events. We describe an important case of subclinical atrial fibrillation preceding cardioembolic stroke during hospitalization for systolic heart failure. A 42-year-old man with a history of hypertension and diabetes presented to our hospital for congestive heart failure. He was asymptomatic before admission; however, upon admission, his electrocardiogram showed atrial flutter with narrow QRS (Fig. 1). Echocardiography demonstrated a reduced left ventricular ejection fraction of 20%, without critical valvular disease. Anticoagulants (heparin/warfarin) were administered for the arrhythmias as part of conventional heart failure
therapy. The arrhythmia spontaneously changed into atrial fibrillation, but finally reverted to sinus rhythm after intravenous diltiazem infusion. His symptoms and heart failure condition improved and he was moved out of the intensive care unit. Five days after admission, his consciousness suddenly became impaired with right hemiparesis, despite the maintenance of blood pressure and heart rate. An emergent brain computed tomography (CT) image demonstrated subtle findings and CT angiography showed total occlusion of the left intracranial internal carotid artery (ICA), suggesting a broad cerebral infarction (Fig. 2). Although magnetic resonance imaging showed a high intensity area throughout the left hemisphere, tissue plasminogen activator was injected within 2 h after onset because of the acute stroke and his young age. Endovascular thrombectomy was attempted within 6 h of the event. However, reperfusion was not achieved and his neurological status did not improve. Follow-up CT scans revealed a large intracranial hemorrhage and severe edema of the left cerebral hemisphere with a mass effect, which required decompressive craniectomy on the day after the event. The ischemic event due to total occlusion of the left ICA caused functional loss of the right side of his body and speech, requiring a transfer to another hospital. We report a case of cerebral infarction due to subclinical, proximal atrial fibrillation in conjunction with congestive heart failure. Although the CHADS2 score has been used to estimate the thromboembolism risk, it is unclear whether the CHADS2 score components appropriately reflect the thromboembolism risk. Subclinical atrial fibrillation has previously been reported to be associated with an increased risk of ischemic stroke or systemic embolism [8,9]. We believe that the delayed recognition of atrial fibrillation may result in the development of additional left atrial thrombi. Consequently, subclinical atrial fibrillation may be an additional marker of stroke risk, similar to symptomatic atrial fibrillation, and may allow physicians to recognize and appropriately treat asymptomatic atrial fibrillation before the patient experiences a thromboembolic event. Source of funding None.
Abbreviations: CT, computed tomography; ICA, internal carotid artery. ⁎ Corresponding author at: Division of Cardiology, Department of Internal Medicine, St. Marianna University School of Medicine, 2-16-1 Sugao, Miyamae-ku, Kawasaki City, Kanagawa 216-8511, Japan. Tel.: +81 44 977-8111; fax: +81 44 976 7093. E-mail address: [email protected] (Y.J. Akashi).
http://dx.doi.org/10.1016/j.ijcard.2014.07.292 0167-5273/© 2014 Elsevier Ireland Ltd. All rights reserved.
Conflict of interest None.
K. Yoneyama et al. / International Journal of Cardiology 176 (2014) 1036–1038
1037
Fig. 1. Subclinical proximal atrial fibrillation and flutter. (A) Atrial flutter, upon admission. (B) Atrial fibrillation. (C) Spontaneous termination. (D) Subclinical proximal atrial fibrillation and flutter in the heart rate trend.
References [1] January CT, Wann LS, Alpert JS, et al. AHA/ACC/HRS guideline for the management of patients with atrial fibrillation: executive summary: a report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines and the Heart Rhythm Society. Circulation 2014;2014. [2] Providencia R. Is there a need for adjusting the results of the recent meta-analysis on the novel oral anticoagulants in atrial fibrillation to the baseline CHADS(2)score? Int J Cardiol 2012;159:161–2. [3] Capodanno D, Capranzano P, Giacchi G, Calvi V, Tamburino C. Increasing CHADS(2) scores may attenuate the benefit of novel oral anticoagulants versus warfarin in reducing intracranial bleeding. Int J Cardiol 2012;161:176–7. [4] Schwammenthal Y, Bornstein NM, Goldbourt U, et al. Anticoagulation remains underused in prevention of stroke associated with atrial fibrillation: insights from two consecutive national surveys. Int J Cardiol 2011;152:356–61.
[5] Rienstra M, Vermond RA, Crijns HJ, Tijssen JG, Van Gelder IC. Asymptomatic persistent atrial fibrillation and outcome: results of the RACE study. Heart Rhythm 2014;11: 939–45. [6] Turagam MK. Silent atrial fibrillation: a clinical conundrum. Int J Cardiol 2013;168: 2953. [7] Forleo GB, De Martino G, Mantica M, et al. Clinical impact of catheter ablation in patients with asymptomatic atrial fibrillation: the IRON-AF (Italian registry on NavX atrial fibrillation ablation procedures) study. Int J Cardiol 2013;168:3968–70. [8] Healey JS, Connolly SJ, Gold MR, et al. Subclinical atrial fibrillation and the risk of stroke. N Engl J Med 2012;366:120–9. [9] Brambatti M, Connolly SJ, Gold MR, et al. Temporal relationship between subclinical atrial fibrillation and embolic events. Circulation 2014;129:2094–9.
1038
K. Yoneyama et al. / International Journal of Cardiology 176 (2014) 1036–1038
Fig. 2. Cerebral infarction, corresponding with the left internal carotid artery territory. (A) Emergent computed tomography (CT) image demonstrated very subtle findings. (B) Diffusionweighted magnetic resonance imaging showed a high-intensity area throughout the left hemisphere, suggesting cerebral infarction in the left internal carotid artery (ICA) territory. (C) Angiography revealed left intracranial ICA occlusion (white arrow). Reperfusion was not achieved by endovascular thrombectomy. (D) Hemispherectomy was required on the day after the event.
Contents lists available at ScienceDirect
International Journal of Cardiology journal homepage: www.elsevier.com/locate/ijcard
Letter to the Editor
Subclinical atrial fibrillation preceding cardioembolic stroke in a patient with systolic heart failure Kihei Yoneyama a, Tomoo Harada a, Hidemichi Ito b, Makoto Takano a, Maya Tsukahara a, Yukio Sato a, Masashi Uchida b, Satoru Nishio a, Yoshihiro J. Akashi a,⁎ a b
Division of Cardiology, Department of Internal Medicine, St. Marianna University School of Medicine, Kawasaki, Japan Department of Neurosurgery, St. Marianna University School of Medicine, Kawasaki, Japan
a r t i c l e
i n f o
Article history: Received 3 June 2014 Accepted 26 July 2014 Available online 13 August 2014 Keywords: Cerebral infarction Atrial flutter Rate control Rhythm control Warfarin Oral anticoagulants
Atrial fibrillation and congestive heart failure are risk factors for cerebral infarction. The most commonly used estimates of stroke risk in patients with atrial fibrillation are cardiac failure, hypertension, age, diabetes mellitus, and stroke (CHADS2 score) [1–4]. Although atrial fibrillation may be recognized by the presence of symptoms, such as palpitations, some patients are occasionally asymptomatic [5–7]. The absence of symptoms results in a delayed diagnosis and may lead to fatal thromboembolic events. We describe an important case of subclinical atrial fibrillation preceding cardioembolic stroke during hospitalization for systolic heart failure. A 42-year-old man with a history of hypertension and diabetes presented to our hospital for congestive heart failure. He was asymptomatic before admission; however, upon admission, his electrocardiogram showed atrial flutter with narrow QRS (Fig. 1). Echocardiography demonstrated a reduced left ventricular ejection fraction of 20%, without critical valvular disease. Anticoagulants (heparin/warfarin) were administered for the arrhythmias as part of conventional heart failure
therapy. The arrhythmia spontaneously changed into atrial fibrillation, but finally reverted to sinus rhythm after intravenous diltiazem infusion. His symptoms and heart failure condition improved and he was moved out of the intensive care unit. Five days after admission, his consciousness suddenly became impaired with right hemiparesis, despite the maintenance of blood pressure and heart rate. An emergent brain computed tomography (CT) image demonstrated subtle findings and CT angiography showed total occlusion of the left intracranial internal carotid artery (ICA), suggesting a broad cerebral infarction (Fig. 2). Although magnetic resonance imaging showed a high intensity area throughout the left hemisphere, tissue plasminogen activator was injected within 2 h after onset because of the acute stroke and his young age. Endovascular thrombectomy was attempted within 6 h of the event. However, reperfusion was not achieved and his neurological status did not improve. Follow-up CT scans revealed a large intracranial hemorrhage and severe edema of the left cerebral hemisphere with a mass effect, which required decompressive craniectomy on the day after the event. The ischemic event due to total occlusion of the left ICA caused functional loss of the right side of his body and speech, requiring a transfer to another hospital. We report a case of cerebral infarction due to subclinical, proximal atrial fibrillation in conjunction with congestive heart failure. Although the CHADS2 score has been used to estimate the thromboembolism risk, it is unclear whether the CHADS2 score components appropriately reflect the thromboembolism risk. Subclinical atrial fibrillation has previously been reported to be associated with an increased risk of ischemic stroke or systemic embolism [8,9]. We believe that the delayed recognition of atrial fibrillation may result in the development of additional left atrial thrombi. Consequently, subclinical atrial fibrillation may be an additional marker of stroke risk, similar to symptomatic atrial fibrillation, and may allow physicians to recognize and appropriately treat asymptomatic atrial fibrillation before the patient experiences a thromboembolic event. Source of funding None.
Abbreviations: CT, computed tomography; ICA, internal carotid artery. ⁎ Corresponding author at: Division of Cardiology, Department of Internal Medicine, St. Marianna University School of Medicine, 2-16-1 Sugao, Miyamae-ku, Kawasaki City, Kanagawa 216-8511, Japan. Tel.: +81 44 977-8111; fax: +81 44 976 7093. E-mail address: [email protected] (Y.J. Akashi).
http://dx.doi.org/10.1016/j.ijcard.2014.07.292 0167-5273/© 2014 Elsevier Ireland Ltd. All rights reserved.
Conflict of interest None.
K. Yoneyama et al. / International Journal of Cardiology 176 (2014) 1036–1038
1037
Fig. 1. Subclinical proximal atrial fibrillation and flutter. (A) Atrial flutter, upon admission. (B) Atrial fibrillation. (C) Spontaneous termination. (D) Subclinical proximal atrial fibrillation and flutter in the heart rate trend.
References [1] January CT, Wann LS, Alpert JS, et al. AHA/ACC/HRS guideline for the management of patients with atrial fibrillation: executive summary: a report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines and the Heart Rhythm Society. Circulation 2014;2014. [2] Providencia R. Is there a need for adjusting the results of the recent meta-analysis on the novel oral anticoagulants in atrial fibrillation to the baseline CHADS(2)score? Int J Cardiol 2012;159:161–2. [3] Capodanno D, Capranzano P, Giacchi G, Calvi V, Tamburino C. Increasing CHADS(2) scores may attenuate the benefit of novel oral anticoagulants versus warfarin in reducing intracranial bleeding. Int J Cardiol 2012;161:176–7. [4] Schwammenthal Y, Bornstein NM, Goldbourt U, et al. Anticoagulation remains underused in prevention of stroke associated with atrial fibrillation: insights from two consecutive national surveys. Int J Cardiol 2011;152:356–61.
[5] Rienstra M, Vermond RA, Crijns HJ, Tijssen JG, Van Gelder IC. Asymptomatic persistent atrial fibrillation and outcome: results of the RACE study. Heart Rhythm 2014;11: 939–45. [6] Turagam MK. Silent atrial fibrillation: a clinical conundrum. Int J Cardiol 2013;168: 2953. [7] Forleo GB, De Martino G, Mantica M, et al. Clinical impact of catheter ablation in patients with asymptomatic atrial fibrillation: the IRON-AF (Italian registry on NavX atrial fibrillation ablation procedures) study. Int J Cardiol 2013;168:3968–70. [8] Healey JS, Connolly SJ, Gold MR, et al. Subclinical atrial fibrillation and the risk of stroke. N Engl J Med 2012;366:120–9. [9] Brambatti M, Connolly SJ, Gold MR, et al. Temporal relationship between subclinical atrial fibrillation and embolic events. Circulation 2014;129:2094–9.
1038
K. Yoneyama et al. / International Journal of Cardiology 176 (2014) 1036–1038
Fig. 2. Cerebral infarction, corresponding with the left internal carotid artery territory. (A) Emergent computed tomography (CT) image demonstrated very subtle findings. (B) Diffusionweighted magnetic resonance imaging showed a high-intensity area throughout the left hemisphere, suggesting cerebral infarction in the left internal carotid artery (ICA) territory. (C) Angiography revealed left intracranial ICA occlusion (white arrow). Reperfusion was not achieved by endovascular thrombectomy. (D) Hemispherectomy was required on the day after the event.