Improvement of cardiac function and neurological remodeling in a patient with tachycardia-induced cardiomyopathy after catheter ablation

Omichi, Chikaya; Tanaka, Takeshi; Kakizawa, Yoshiko; Yamada, Ayako; Ishii, Yasuhiro; Nagashima, Hirotaka; Kanmatsuse, Katsuo; Endo, Masahiro

doi:10.1016/j.jjcc.2008.10.002

Cited by 11 publications

(13 citation statements)

References 8 publications

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“…68 It has also been shown to normalise in the setting of rate control. 69 However, it is not clear whether these changes contribute to myocardial dysfunction or whether they are a consequence of prolonged rapid pacing and chronically enhanced sympathetic activity. 70 Abnormal calcium handling also seems to play a role in the pathogenesis of TIC.…”

Section: Cellular Changesmentioning

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: Cellular Changesmentioning

confidence: 99%

What About Tachycardia-induced Cardiomyopathy?

Ellis¹,

Josephson²

2013

Arrhythmia &Amp; Electrophysiology Review

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“…Increases in circulating epinephrine and norepinephrine trigger remodeling, which is associated with a decrease in β-adrenergic responsiveness, a decrease in β-1 receptor density and downregulation of β-receptors. This remodeling can normalize with rate control [26]. Elevated levels of angiotensin-II, atrial natriuretic peptide, and endothelin-1 levels are seen, potentially contributing to abnormal sodium handling and ultimately myocardial fi brotic changes [2].…”

Section: Pathophysiologymentioning

confidence: 99%

Tachycardia-mediated cardiomyopathy: Recognition and management

Gopinathannair¹,

Sullivan²,

Olshansky

2009

Curr Heart Fail Rep

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Tachycardia-mediated cardiomyopathy is a cause of ventricular dysfunction due to, at least partially, persistent tachycardia leading to cellular and extracellular perturbations. Cardiomyopathy may take years to develop, but pharmacologic management to achieve rate control and reverse remodeling, as well as cardioversion or ablative strategies to stop the tachycardia, can result in rapid recovery from symptoms and gradual improvement in left ventricular ejection fraction. However, ultrastructural changes can remain and may lead to a rapid decline in ventricular function if tachycardia recurs. Ultrastructural changes may also explain a propensity toward sudden death even if the ejection fraction normalizes. Although the etiology, pathophysiology, and late clinical manifestations of tachycardia-mediated cardiomyopathy are beginning to be understood, investigation continues, focusing on prevention, early recognition, and acute and long-term management in an attempt to lessen heart failure and prevent risk of sudden death.

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“…A right ventricular outflow tract-PVC was defined as follows: (1) PVC had a left bundle branch block (LBBB) morphology in V 1, (2) the R/S transition zones (first precordial lead with R/S ratio ≥1) in the PVCs were present in V 2 –V 4 , and (3) the R/S transition zones of the PVCs in the precordial lead did not occur earlier than the R/S transition zones of the sinusal QRS on the same 12-lead surface ECG. Ventricular tachycardia was defined by standard electrocardiographic criteria of at least five consecutive PVCs at a rate of more than 120 beats/min.…”

Section: Definition Of Rvot-pvc and Evaluation Of Cardiac Structure Amentioning

confidence: 99%

“…Persistent tachycardia can induce dilated cardiomyopathy, and the suppression of it can reverse the changes in cardiac structure and function in these patients (2,3). One of tachycardia, frequent premature ventricular contraction (FPVC), has been generally considered as benign (4), although some recent studies suggest that long-term FPVC may cause progressive ventricular dysfunction and dilatation and may induce dilated cardiomyopathy (tachycardiomyopathy) or even heart failure (4-8).…”

Section: Introductionmentioning

confidence: 99%

Radiofrequency ablation can reverse the structural remodeling caused by frequent premature ventricular contractions originating from the right ventricular outflow tract even in a “normal heart”

Fang¹,

Wen²,

Yang³

et al. 2013

Clinics

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OBJECTIVE:The aim of this study was to evaluate whether frequent premature ventricular contractions originating from the right ventricular outflow tract remodel the cardiac structure and function in patients with a “seemingly normal heart” and whether radiofrequency ablation can reverse this remodeling.METHODS:Sixty-eight patients with idiopathic frequent premature ventricular contractions originating from the right ventricular outflow tract and normal heart structure and function were enrolled in this study. The patients were divided into three groups according to the therapeutic method: radiofrequency ablation group (24 cases), anti-arrhythmia drug group (26 cases), and control group (18 cases without any treatment). Clinical Registration number: ChiCTR-ONRC-12002834RESULTS:The basic patient characteristics were comparable between the three groups, except for the premature ventricular contraction rate, which was significantly lower in the control group. After six months of follow up, the premature ventricular contraction rate was significantly reduced in the radiofrequency ablation group, which was accompanied by a significant decrease in the following cardiac cavity inner diameters, as determined by echocardiography: right atrium (33.33±3.78 vs. 30.05±2.60 mm, p = 0.001), right ventricle (23.24±2.40 vs. 21.05±2.16 mm, p = 0.020), and left ventricle (44.76±4.33 vs. 41.71±3.44 mm, p = 0.025). These results were similar in the anti-arrhythmia drug group, although this group exhibited a smaller extent of change (right atrium: 33.94±3.25 vs. 31.27±3.11 mm, p = 0.024; right ventricle: 22.97±3.09 vs. 21.64±2.33 mm, p = 0.049; left ventricle: 45.92±6.38 vs. 43.84±5.67 mm, p = 0.039), but not in the control group (p>0.05). There was a tendency toward improvement in the cardiac functions in both the radiofrequency ablation and anti-arrhythmia drug groups. However, these differences were not statistically significant (p>0.05).CONCLUSIONS:These results indicate that radiofrequency ablation can potentially reverse the cardiac remodeling caused by frequent premature ventricular contractions even in structurally normal hearts and that frequent premature ventricular contractions should be abated even in structurally normal hearts.

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Improvement of cardiac function and neurological remodeling in a patient with tachycardia-induced cardiomyopathy after catheter ablation

Cited by 11 publications

References 8 publications

What About Tachycardia-induced Cardiomyopathy?

What About Tachycardia-induced Cardiomyopathy?

Tachycardia-mediated cardiomyopathy: Recognition and management

Radiofrequency ablation can reverse the structural remodeling caused by frequent premature ventricular contractions originating from the right ventricular outflow tract even in a “normal heart”

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