American Journal of Internal Medicine
Volume 4, Issue 6, November 2016, Pages: 117-119
Received: Oct. 21, 2016;
Accepted: Nov. 1, 2016;
Published: Nov. 25, 2016
Views 2658 Downloads 68
Ali Areef Fadhlullah, Faculty of Medicine, University of Omar El mukhtar, Albayda, Libya; Department of Internal Medicine, University of Omar El mukhtar, Albayda, Libya
Asgad A. Abdalgbar, Faculty of Medicine, University of Omar El mukhtar, Albayda, Libya; Department of Internal Medicine, University of Omar El mukhtar, Albayda, Libya
Hanan K. Altalhi, Faculty of Medicine, University of Omar El mukhtar, Albayda, Libya; Department of Internal Medicine, University of Omar El mukhtar, Albayda, Libya
Atrial fibrillation (AF) is one of the main risk factor for ischemic stroke. The reason for an increased stroke risk in AF has always been claimed to be the occurrence of left atrial thrombosis causing arterial embolism. In patients with Rheumatic heart disease especially mitral valve stenosis with AF, the frequency of atrial thrombosis has found to be 30 - 42% (Keren G et al. 1987), and the prevalence of left atrial thrombosis in NRAF are higher than in control 13-27% (Petersen P et al. 1988). Objectives: We investigated if there are any differences in risk factors or atherosclerotic manifestations between ischemic brain infarction patients with and without AF? Are the brain lesions characteristics in these patients similar?Patients and Methods: This is a case- control study of 26 patients with acute ischemic stroke and NRAF (case subjects) a and 26 patients with acute ischemic stroke and sinus rhythm. (control subjects). The patients admitted to the hospital; the diagnosis of cerebral infarction was confirmed by new CT of the brain. All the participants underwent the standard examination and testing as well as ECG and ECHO. Result: Patient with NRAF had higher mortality 30% than in control (SR) 7% (P<0.001). NRAF patients had positive brain CT finding 68% compared to 23% of the SR Patients (P<0.001). Conclusion: Brain infarction in non-Rheumatic AF group are more serious than other and therefor make up a (high risk) group for which acute treatment would be specially indicated and primary prophylaxis with anticoagulants might therefore be considered.
Ali Areef Fadhlullah,
Asgad A. Abdalgbar,
Hanan K. Altalhi,
Non Rheumatic Atrial Fibrillation as Risk of Stroke, American Journal of Internal Medicine.
Vol. 4, No. 6,
2016, pp. 117-119.
Copyright © 2016 Authors retain the copyright of this article.
This article is an open access article distributed under the Creative Commons Attribution License (http://creativecommons.org/licenses/by/4.0/
) which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.
Britton M, Gustafsson C, Non-rheumatic atrial fibrillation as a risk factor for stroke. 1985; 16: 182-188.
Cai H, Li Z, Goette A, Mera F, Honeycutt C, Feterik K, et al. Down regulation of endocardial nitric oxide synthase expression and nitric oxide production in atrial fibrillation: potential mechanisms for atrial thrombosis and stroke. Circulation. 2002: 106: 2854-2858.
Easton JD, Sherman DG: Management of cerebral embolism of cardiac origin. Stroke11: 433-442, 1980.
Frustaci A, Chimenti C, Bellocci F. Morgante E, Russo MA, Maseri A. Histological substrate of atrial biopsies in patients with lone atrial fibrillation. Circulation. 1997; 96: 1180-1184.
Heijman J, Voiget N, Nattel S, Dobrev D. Cellular and molecular electrophysiology of atrial fibrillation initiation maintenance and progression Circ Res. 2014; 114: 1483-1499. Doi: 10.1161/ CIRCRESAHA.114.302226.
Kannel WB, Abbott RD, Savage DD, McNamara PM, Epidemiologic features of chronic atrial fibrillation: the Framingham study N Engl J. Med. 1982; 306: 1018-1022.
Kannel WB, Wolf PA, Verter J: manifestations of coronary disease predisposing to stroke: The Framingham Study. JAMA 1983; 250: 2942-2946.
Keren G, Etzion T, Sherez J, Zelcer A, Megidish R, Miller H, Laniado S. Atrial fibrillation and atrial enlargement in patients with mitral stenosis. Am Heart J. 1987; 114: 1146-1155.
Lodder J, Bamford JM, Sandercock PA, Jones LN, Warlow CP. Are hypertension or cardiac embolism likely causes of lacunar infarction? Stroke. 1990; 21: 375-381.
Mihm MJ, Yu F, Carnes CA, Reiser PJ, McCarthy, PM, Van Wagoner DR, et al. Impaired myofrillar energetics and oxidative injury during human atrial fibrillation. Circulation. 2001; 104: 174-180.
Peterson P, Godtfredsen J: Risk factor for stroke in chronic atrial fibrillation. Eur Heart J 1988; 9: 291-294.
Roden A, Britton M: Progression of stroke after arrival at hospital. Acta Neurol Scand 66 (suppl 91): 43, 1982.
The Scandinavian Committee on ECG Classification: The Minnesota code for ECG Classification. Adaption to Cr leads and modification of the code for ECG recording during and after exercise. Acta Med Scand (suppl): 481, 1967.
Jorgensen L, Torvic A: Ischemic cerebrovascular diseases in an autopsy series. Part 2. Prevalence, location, pathogenesis, and clinical course of cerebral infarcts. J Neurol Sci 9: 285-320, 1969.
Warraich HJ, Gandhavadi M, Manning WJ. Mechanical discordance of the left atrium and appendage: a novel mechanism of stroke in paroxysmal atrial fibrillation, Stroke. 2014; 45: 1481-1484, doi: 10.1161/STROKEAHA.114.004800.
Weyman AE. Principles and practice of echocardiography, Lea and Febiger Publ. 194; 606.
Wolf PA, Abbott RD, Kannel WB: Atrial fibrillation: A major contributor to stroke in the elderly. Am Heart J 1986; 112: 1039-1043.
Zimetbaum P, Waks JW, Ellis ER, Glotzer TV, Passman RS. Role of atrial fibrillation burden in assessing thromboembolic risk. Circ. Arrhythm Electrophysiology 2014; 7: 1223-1229.