Thromboembolism in Patients With Atrial Fibrillation

Sherman, D G; Goldman, L. Elizabeth; Whiting, Richard B.; Jurgensen, K; Kaste, Markku; Easton, J. Donald

doi:10.1001/archneur.1984.04050180030011

Cited by 130 publications

(33 citation statements)

References 22 publications

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“…In our sample, one-third of the subjects with atrial fibrillation had paroxysmal versus persistent atrial fibrillation. Paroxysmal atrial fibrillation is postulated to be less likely to be associated with structural heart disease, more likely to occur in younger persons, and paroxysmal atrial fibrillation episodes tend to be preceded by fluctuations in autonomic tone, which is consistent with dynamic changes occurring in SDB (19)(20)(21)(22).…”

Section: Discussion Principal Findingsmentioning

confidence: 76%

Association of Nocturnal Arrhythmias with Sleep-disordered Breathing

Mehra

Benjamin

Shahar

et al. 2006

Am J Respir Crit Care Med

1,115

610

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Rationale: Sleep-disordered breathing recurrent intermittent hypoxia and sympathetic nervous system activity surges provide the milieu for cardiac arrhythmia development. Objective: We postulate that the prevalence of nocturnal cardiac arrhythmias is higher among subjects with than without sleepdisordered breathing. Methods: The prevalence of arrhythmias was compared in two samples of participants from the Sleep Heart Health Study frequencymatched on age, sex, race/ethnicity, and body mass index: (1 ) 228 subjects with sleep-disordered breathing (respiratory disturbance index у 30) and (2 ) 338 subjects without sleep-disordered breathing (respiratory disturbance index Ͻ 5). Supported by National Heart, Lung and Blood Institute cooperative agreements U01HL53940 (University of Washington), U01HL53941 (Boston University), U01HL53938 (University of Arizona), U01HL53916 (University of California, Davis), U01HL53934 (University of Minnesota), U01HL53931 (New York University), U01HL53937 and U01HL64360 (Johns Hopkins University), U01HL63463 (Case Western Reserve University), and U01HL63429 (Missouri Breaks Research).The opinions expressed in this paper are those of the authors and do not necessarily reflect the views of the Indian Health Service.Correspondence and requests for reprints should be addressed to Reena Mehra, M.D., M.S., Case Western Reserve University, University Hospitals of Cleveland, 11100 Euclid Avenue, Cleveland, OH 44106. E-mail: mehrar@ameritech.net This article has an online supplement, which is accessible from this issue's table of contents at www.atsjournals.org Patients with sleep-disordered breathing (SDB) may be predisposed to arrhythmias because of alterations in sympathetic and parasympathetic nervous system activity occurring with SDBassociated hypoxemia, acidosis, apneas, and arousal (1-3). Mechanisms of arrhythmogenesis involve abnormal automaticity, triggered automaticity, and reentry mechanisms. Abnormal automaticity involves spontaneous cardiac impulse formation and may occur in SDB due to hypoxemia and respiratory acidosis accompanying apneic events (4). Triggered automaticity, pacemaker activity due to a stimulated action potential, may arise in SDB due to enhanced sympathetic nervous system activity associated with respiratory event-related hypoxemia and arousal (5). Reentry mechanisms may occur through the vagal stimulation that results from respiration against a partially occluded airway, which may lead to bradycardia-dependent increased dispersion of atrial repolarization predisposing to intraatrial entry (5-7). Also, SDB-related mechanical effects of negative intrathoracic pressure on the atrial and ventricular free walls promote cardiac stretch, which may predispose to arrhythmias via mechanicalelectrical feedback mechanisms (8).Despite the biological plausibility for SDB-associated hypoxemia, arousals, and autonomic nervous system dysregulation causing generation of abnormal cardiac electrophysiologic impulses, only limited research has rigorously characterized the association...

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Section: Discussion Principal Findingsmentioning

confidence: 76%

Association of Nocturnal Arrhythmias with Sleep-disordered Breathing

Mehra

Benjamin

Shahar

et al. 2006

Am J Respir Crit Care Med

1,115

610

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“…The most common cause of early death in patients with AF was neurological damage from the initial stroke, as might be anticipated, since they had more severe strokes with a predominantly cortical localization. 11,17,19,21,28 …”

Section: Discussionmentioning

confidence: 99%

“…6,10,11,14 One explanation for the different estimates might be different selection of patients. However, approximately one sixth of the patients in IST were in AF, which is very similar to that found in community-based incidence studies of stroke.…”

Section: Absolute Risk Of Early Recurrent Stroke In Afmentioning

confidence: 99%

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Risk of Early Death and Recurrent Stroke and Effect of Heparin in 3169 Patients With Acute Ischemic Stroke and Atrial Fibrillation in the International Stroke Trial

Saxena

Lewis

Berge

et al. 2001

Stroke

249

113

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Background and Purpose — We sought to investigate the apparently high risk of early death after an ischemic stroke among patients with atrial fibrillation (AF), identify the main factors associated with early death, and assess the effect of treatment with different doses of subcutaneous unfractionated heparin (UFH) given within 48 hours. Methods — We studied the occurrence of major clinical events within 14 days among 18 451 patients from the International Stroke Trial, first for all treatment groups combined. Then, among patients with AF, we examined the effects of treatment with subcutaneous UFH started within 48 hours and continued until 14 days after stroke onset. Results — A total of 3169 patients (17%) had AF. Seven hundred eighty-four patients were allocated to UFH 12 500 IU SC BID, 773 to UFH 5000 IU SC BID, and 1612 to no heparin. Within each of these groups, half of the patients were randomly assigned to aspirin 300 mg once daily. Compared with patients without AF, patients with AF were more likely to be female (56% versus 45%), to be old (mean age, 78 versus 71 years), to have an infarct on prerandomization CT (57% versus 47%), and to have impaired consciousness (37% versus 20%). The initial ischemic stroke type was more often a large-artery infarct (36% versus 21%). A lacunar stroke syndrome was less common (13% versus 26%). Death within 14 days was more common in patients with AF (17% versus 8%) and more often attributed to neurological damage from the initial stroke (10% versus 4%). The frequency of recurrent ischemic or undefined stroke was not significantly different (3.9% versus 3.3%). The proportion of AF patients with further events within 14 days allocated to UFH 12 500 IU (n=784), UFH 5000 IU (n=773), and to no-heparin (n=1612) groups were as follows: ischemic stroke, 2.3%, 3.4%, 4.9% ( P =0.001); hemorrhagic stroke, 2.8%, 1.3%, 0.4% ( P <0.0001); and any stroke or death, 18.8%, 19.4% and 20.7% ( P =0.3), respectively. No effect of heparin on the proportion of patients dead or dependent at 6 months was apparent. Conclusions — Acute ischemic stroke patients with AF have a higher risk of early death, which can be explained by older age and larger infarcts but not by a higher risk of early recurrent ischemic stroke, although slightly more patients with AF died from a fatal recurrent stroke of ischemic or unknown type (1.3% versus 0.9%). In patients with AF the absolute risk of early recurrent stroke is low, and there is no net advantage to treatment with heparin. These data do not support the widespread use of intensive heparin regimens in the acute phase of ischemic stroke associated with AF.

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“…[1][2][3][4][5][6] Identifying PAF in ischemic stroke patients can be challenging because intermittent AF might not be detected on electrocardiograms. Holter monitoring (HM) has been increasingly utilized in stroke and TIA patients as a routine investigation to search for occult PAF, but its clinical utility remains a matter of debate for a number of reasons.…”

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confidence: 99%