Atrial flutter and thromboembolic risk: a systematic review

Vadmann, Henrik; Nielsen, Peter Brønnum; Hjortshøj, Søren Pihlkjær; Riahi, Sam; Rasmussen, Lars Hvilsted; Lip, Gregory Y.H.; Larsen, Torben Bjerregaard

doi:10.1136/heartjnl-2015-307550

Cited by 61 publications

(43 citation statements)

References 60 publications

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“…Dostępne dowody wskazują, że ryzyko udaru mózgu u pacjentów z trzepotaniem przedsionków nie różni się bardzo od ryzyka w przypadku AF [827]. Co więcej, u wielu pacjentów, u których rozpoznaje się trzepotanie przedsionków, później pojawia się AF [993][994][995].…”

Section: Postępowanie W Trzepotaniuunclassified

2016 ESC Guidelines for the management of atrial fibrillation developed in collaboration with EACTS

Kirchhof

Benussi

Kotecha³

et al. 2016

Kardiol Pol

2,379

4,206

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Section: Postępowanie W Trzepotaniuunclassified

2016 ESC Guidelines for the management of atrial fibrillation developed in collaboration with EACTS

Kirchhof

Benussi

Kotecha³

et al. 2016

Kardiol Pol

2,379

4,206

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“…A recent systematic review of the literature on atrial flutter and thromboembolic risk concluded that while a risk certainly exists, the exact estimate is challenging. 44 There have not been any randomized controlled trials examining this association, and atrial flutter often coexists with AF and likely derives from a common pathophysiological mechanism. Although atrial flutter is not mentioned in guidelines for the primary prevention of stroke, guidelines on the secondary prevention of stroke recommend that similar treatment parameters should be followed for atrial flutter as for AF.…”

Section: Epidemiology and Pathogenesismentioning

confidence: 99%

Cardioembolic Stroke: Mechanisms and Therapeutics

2017

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Cardioembolic stroke accounts for nearly 30% of all known stroke mechanisms. This percentage may be underestimated, however, when considering the large proportion of cryptogenic strokes that likely have a covert cardiac source. Although it is well known that cardioembolic stroke can occur in the setting of atrial fibrillation, other mechanisms such as a systolic heart failure, patent foramen ovale, valvular dysfunction, and aortic arch atheroma are commonly encountered in daily practice. The authors provide an overview on the epidemiology, pathogenesis, diagnostic evaluation, and secondary prevention treatment strategies for cardioembolic stroke.

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“…The same recommendation applies to patients with atrial fibrillation, who can be assumed to have a comparably high risk of thrombembolism [52]. In addition to the vitamin K antagonists, 4 preparations are currently available from the group of non-vitamin K antagonist anticoagulants (NOAC) (▶ table 4), including the direct thrombin inhibitor dabigatran as well as 3 factor Xa antagonists (rivaroxaban, apixaban, edoxaban).…”

Section: Antithrombotic Therapymentioning

confidence: 99%

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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Atrial flutter and thromboembolic risk: a systematic review

Cited by 61 publications

References 60 publications

2016 ESC Guidelines for the management of atrial fibrillation developed in collaboration with EACTS

2016 ESC Guidelines for the management of atrial fibrillation developed in collaboration with EACTS

Cardioembolic Stroke: Mechanisms and Therapeutics

Cardiac Arrhythmia following Stroke

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