Randomized trial of atrial arrhythmia monitoring to guide anticoagulation in patients with implanted defibrillator and cardiac resynchronization devices

Martin, David T.; Bersohn, Malcolm; Waldo, Albert L.; Wathen, Mark S.; Choucair, Wassim; Lip, Gregory Y. H.; Ip, John; Holcomb, Richard; Akar, Joseph G.; Halperin, Jonathan L.

doi:10.1093/eurheartj/ehv115

Cited by 334 publications

(238 citation statements)

References 27 publications

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“…Much more frequently, the episodes occurred more than 30 days earlier, or occurred for the first time after a stroke [32]. Two further studies with similar methodologies also concluded that the majority of cardiac embolisms occur without immediately preceding episodes of atrial fibrillation [33,34]. Modern concepts are therefore based on the assumption that episodes of atrial fibrillation are only "the tip of the iceberg" and the epiphenomena of a complex disease of the atria, with risk of stroke persisting even after conversion to sinus rhythm [35,36].…”

Section: Embolies In Atrial Fibrillation: Complex Pathophysiologymentioning

confidence: 97%

“…This approach appears to be intuitively correct but fails to convince as far an understanding of the large number of atrial fibrillation-associated stroke events is concerned. Most recently, newer data have raised serious questions about this approach [32][33][34]: In the AS-SERT study, involving 2 580 patients with implanted cardiac pacemaker or AICD aggregate groups, a total of 51 patients during follow-up of 2.5 years suffered an ischemic stroke or a systemic embolism. A reading of the pacemaker memory allowed to study the temporal relationship between atrial fibrillation episodes and the occurrence of stroke: In a period of 30 days before the occurrence of stroke, atrial fibrillation episodes > 6 min were detectable in only n 8 % of the cases.…”

Section: Embolies In Atrial Fibrillation: Complex Pathophysiologymentioning

confidence: 99%

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Cardiac Arrhythmia following Stroke

Kallmünzer

Schwab

2017

Neurology International Open

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The autonomous innervation of the heart is based on a complex interaction of central and peripheral mechanisms in sympathetic and parasympathetic parts of the autonomic nervous system (▶Fig. 1). An extrinsic cardiac innervation is distinguished from an intrinsic one. Extrinsic systemTo put it simply, a center of the efferent parasympathetic innervation of the heart is found in the nucleus of the medulla oblongata, especially in the nucleus dorsalis [1]. The preganglionic fibers leave the central nervous system along with the vagus nerve and are connected to the second neuron in cardiac ganglion cells. Sympath etic fibers, on the other hand, originate from the nucleus intermediolateralis of the upper thoracic cord [2]. They reach the plexus cardiacus by means of the so-called "cardiac nerves" (usually 4 right-sided and 3 left-sided nervi cardiaci), after interposition in the border ganglia, especially in the ganglion stellatum. For the control of cardiac functions, the profound part of the plexus cardiacus is decisive; it extends between the tracheal bifurcation and the aortic arch, divides into a right and left half and in its further course follows the right or left coronary artery. The function of the efferent limb is modified by afferents from various organ systems, including the gastrointestinal tract or the carotissinus, by means of multisynaptic reflex arcs (e. g., baroreflex) [1]. In addition, in the blood circulating catecholamine, the release of which in the adrenal system is also subject to the autonomic system, mediates beta-adrenergic effects on the myocardium. It is postulated that dysbalances in the extrinsic system, in particular the pathological disinhibition of sympathetic activity, are relevant to the development of cardiac arrhythmias [1,[3][4][5]. For example, extensive brain stem damage can lead to suppression of central parasympathetic functions and overcoming of sympathetic tone [6], thus promoting the occurrence of cardiac arrhythmias. Conversely, blockade of the ganglion stellatum or renal sympathetic denervation should reduce the risk of ventricular arrhythmias in patients with prolonged-QT syndromes [7]. It is noteworthy in this context that extensive cardiac denervation, which may be present after orthotopic heart transplantation, is associated with a lower risk of supra ventricular rhythm disturbances, especially atrial fibrillation [8]. In these cases, the denervation should have protective effects and protect the myocardium from the autonomic imbalances of the extrinsic system before transmission. It should be noted, however, that organ donors are usually much younger and the vascular damage to the donor organs is often less pronounced, which significantly reduces the risk of atrial fibrillation independent of cardiac denervation [9].

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Section: Embolies In Atrial Fibrillation: Complex Pathophysiologymentioning

confidence: 97%

Section: Embolies In Atrial Fibrillation: Complex Pathophysiologymentioning

confidence: 99%

Cardiac Arrhythmia following Stroke

Kallmünzer

Schwab

2017

Neurology International Open

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“…48 In retrospect, this study likely failed due to low rates of AF (only 264 out of 2,718 patients had AF during the study); low rates of thromboembolism (only 69 patients experienced a thromboembolic event); and the fact that warfarin was the primary method of anticoagulation, with a suboptimal time in therapeutic range of approximately 59%. 49 More recent pilot studies using DOACs in lowto-intermediate risk patients with a low burden of AF, however, have shown more promising results. The Rhythm Evaluation for Anticoagulation with Continuous Monitoring (REACT.COM) pilot study was a multicenter single-arm study that enrolled 59 patients (mean age: 67 years ± eight years, 75% male, mean CHADS 2 score: 1.3 ± 0.5) with implanted Reveal XT™ (Medtronic, Minneapolis, MN, USA) ILRs; nonpermanent AF on a DOAC (apixaban, dabigatran, or rivaroxaban); and a CHADS 2 score of 1 to 2.…”

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confidence: 99%

Tailored Anticoagulation for Thromboembolic Risk Reduction in Paroxysmal Atrial Fibrillation

Matos

Waks

Zimetbaum

2018

J Innov Cardiac Rhythm Manage

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“…7 Another puzzle is that asymptomatic episodes of SCAF detected by continuous monitoring in many, if not most, studies seem not to correlate closely with the timing of stroke. 4,[6][7][8]15 It may be that AF and thrombus formation might occur some days, weeks, or even months before the clot dislodges from the atrium and causes an embolic stroke, but it is difficult to incriminate AF as the stroke mechanism when the AF occurs only after the stroke. In addition, there are many causes of ischemic stroke other than AF, none of which is unlikely in patients with AF.…”

mentioning

confidence: 99%