Dilated cardiomyopathy in children with ventricular preexcitation: the location of the accessory pathway is predictive of this association

Cate, Floris E.A. Udink ten; Kruessell, M; Wagner, Kerstin; Trieschmann, Uwe; Emmel, Mathias; Brockmeier, Konrad; Sreeram, Narayanswami

doi:10.1016/j.jelectrocard.2009.09.007

Cited by 64 publications

(53 citation statements)

References 32 publications

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“…This hypothesis is supported by the fact that various forms of abnormal ventricular activation have been shown to adversely affect left ventricular systolic function including chronic right ventricular pacing, [25][26][27] left bundle branch block 28,29 and ventricular pre-excitation. 30,31 Given this, chronic atrial pacing is likely a more pure model of TIC, as it should result in fewer electromechanical changes in the ventricles beyond increased rate.…”

Section: Introductionmentioning

confidence: 99%

What About Tachycardia-induced Cardiomyopathy?

Ellis¹,

Josephson²

2013

Arrhythmia &Amp; Electrophysiology Review

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Cardiomyopathies are heterogeneous heart muscle disorders with a wide range of aetiologies and clinical manifestations. They are often defined by their causes (i.e. hypertension, prior myocardial infarction, valvular heart disease), although current major society definitions describe cardiomyopathy as the presence of abnormal myocardial structure and/or function in the absence of underlying structural heart disease. Long-standing tachycardia is a well-recognised cause of heart failure and left ventricular dysfunction, and has led to the nomenclature, tachycardia-induced cardiomyopathy (TIC). TIC is generally a reversible cardiomyopathy if the tachycardia can be treated effectively, either with medications, surgery or catheter ablation. TIC can also manifest in patients with baseline left ventricular dysfunction from underlying structural heart disease that develop a worsening of their myocardial dysfunction in the setting of prolonged tachycardia, which can be reversed with control of the tachycardia. The diagnosis is usually made after demonstrating recovery of left ventricular function with normalisation of heart rate in the absence of other identifiable aetiologies.TIC was first described in 1913 in a young patient who presented with congestive heart failure (CHF) and atrial fibrillation (AF) with rapid ventricular response.1 In the subsequent decades, further reports were written documenting cases of complete resolution of CHF after cardioversion of AF to sinus rhythm.2-4 A century after the first reported case, we are still working to expand our understanding of the mechanisms underlying this disorder. A variety of chronic or incessant tachyarrhythmias have been implicated in the pathogenesis of TIC, the most classic being AF, 5-7 atrial flutter, 8 incessant supraventricular tachycardia, 9-12 ventricular tachycardia [13][14][15][16] and premature ventricular depolarizations 17 (see Table 1). The most common presentation is a dilated cardiomyopathy with or without the causative tachycardia.Given that this diagnosis represents a potentially reversible cause of heart failure, its recognition is critically important. In this review, we will discuss the proposed mechanisms of TIC, the causative tachycardias and their treatment, outcomes for patients diagnosed with TIC, and future directions for research and clinical care. Experimental Models BackgroundThe first experimental model of TIC was described by Whipple et al. in 1962 where he demonstrated that rapid, prolonged atrial pacing resulted in low output heart failure.18 This model has since become widely used as a model to study CHF. Animal studies, primarily in dogs and pigs, have shown that sustained rapid atrial or ventricular pacing results in systolic heart failure that is neurohormonally and haemodynamically similar to left ventricular systolic dysfunction in humans. [19][20][21][22][23] The majority of what is known about the pathophysiologic mechanisms underlying TIC is supported by pacing-induced heart failure in animal models (see Table 2). It is ...

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Section: Introductionmentioning

confidence: 99%

What About Tachycardia-induced Cardiomyopathy?

Ellis¹,

Josephson²

2013

Arrhythmia &Amp; Electrophysiology Review

View full text Add to dashboard Cite

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“…However, there have been some reports of decreased cardiac function in patients with WPW in the absence of SVT, and these patients (most of whom were infants or children) tend to exhibit segmental dyskinesia of the myocardium and/or global LV dysfunction. [7][8][9][10][11] Pre-existing areas may lead to dyssynchrony in LV motion and result in global LV dysfunction.…”

Section: Discussionmentioning

confidence: 99%

“…In those reports, most patients exhibited right septal or posteroseptal accessory pathways. [7][8][9][10][11] with WPW syndrome with a right-sided free-wall accessory pathway and dilated cardiomyopathy (DCM), in which LV function improved following RF ablation. 12) In patients with decreased LV cardiac function, such as those with DCM, LV dyssynchrony can further compromise cardiac function.…”

Section: Discussionmentioning

confidence: 99%

An Asymptomatic Case of Wolff‐Parkinson‐White Syndrome with Right‐sided Free‐wall Accessory Pathway and Left Ventricular Dysfunction

Mine

Kodani

Hamaoka

et al. 2011

Journal of Arrhythmia

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A 16-year-old girl with a known history of asymptomatic Wolff-Parkinson-White syndrome exhibited signs of left ventricular (LV) septal akinesia and LV dysfunction during routine follow-up. A 12-lead surface ECG showed pre-excitation, a predominantly negative delta wave in V 1 and left axis deviation, which was consistent with the presence of a right free-wall accessory pathway. Radiofrequency ablation of the anterolateral right atrium around the local shortest atrium-to-ventricle interval created the accessory pathway block. An echocardiogram taken one month after the procedure revealed that LV septal wall motion had normalized and that LV ejection fraction had improved from 50% before the ablation to 64% after the ablation. Most previous reports of asymptomatic patients of WPW with LV septal dyskinesia and dysfunction have described right septal or posteroseptal accessory pathways. This patient reported here represents a rare case with right free-wall accessory pathway and LV dysfunction without tachycardia. (J Arrhythmia 2011; 27: 145-149)

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“…Recent studies have demonstrated that pacing from the RV apex may induce left ventricular dyssynchrony (Thambo et al, 2004;Tops et al, 2007;Cheng et al, 2009). It has long been recognized that ventricular dyssynchrony caused by a variety of cardiovascular diseases, including heart failure, ventricular preexcitation, and left bundle branch block mediate ventricular remodelling and subsequently myocardial dysfunction (Prinzen et al, 1995;Kass, 2008;Udink ten Cate et al, 2010a;Udink ten Cate et al, 2010b). Evidence is now emerging that pacing-induced ventricular dyssynchrony disturbs myocardial regional workload and wall stress, which may result in wall motion abnormalities, myocardial perfusion defects, changes in coronary blood flow, increased left ventricular cavity volume, and asymmetrical changes in left ventricular wall thickness (Karpawich, 2004;Kass, 2008;Cheng et al, 2009).…”

Section: Pacing Induced Ventricular Remodelling and Dysfunctionmentioning

confidence: 99%