Late Gadolinium Enhancement CMR in Patients with Tachycardia‐Induced Cardiomyopathy Caused by Idiopathic Ventricular Arrhythmias

Hasdemir, Can; Yüksel, Alper; Camlı, Dilsat; Kartal, Yildirim; Şimşek, Evrim; Musayev, Oktay; İsayev, Elnur; Aydın, Mehmet; Can, Levent

doi:10.1111/j.1540-8159.2011.03324.x

Cited by 80 publications

(62 citation statements)

References 23 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…In 2 studies of adult patients with focal atrial tachycardia (AT), the incidence of AIC was 8.3% to 10% (5,6), whereas in a pediatric multicenter study of atrial ectopic tachycardia (AET), 28% had AIC (7). The incidence of AIC was 9% to 34% in patients with frequent premature ventricular complexes (PVCs) and/or nonsustained ventricular tachycardia referred for electrophysiological evaluation (8–10). …”

Section: Epidemiologymentioning

confidence: 99%

Arrhythmia-Induced Cardiomyopathies

Gopinathannair

Etheridge

Marchlinski

et al. 2015

Journal of the American College of Cardiology

307

116

View full text Add to dashboard Cite

Arrhythmia-induced cardiomyopathy (AIC) is a potentially reversible condition in which left ventricular dysfunction is induced or mediated by atrial or ventricular arrhythmias. Cellular and extracellular changes in response to the culprit arrhythmia have been identified, but specific pathophysiological mechanisms remain unclear. Early recognition of AIC and prompt treatment of the culprit arrhythmia using pharmacological or ablative techniques results in symptom resolution and recovery of ventricular function. Although cardiomyopathy in response to an arrhythmia may take months to years to develop, recurrent arrhythmia can result in rapid decline in ventricular function with development of heart failure, suggesting residual ultrastructural abnormalities. Reports of sudden death in patients whose left ventricular ejection fraction have normalized cast doubt on the complete reversibility of this condition. Several aspects of AIC, including specific pathophysiological mechanisms, predisposing factors, optimal therapeutic strategies to prevent ultrastructural changes, and long-term risk of sudden death remain unresolved and need further research.

show abstract

Section: Epidemiologymentioning

confidence: 99%

Arrhythmia-Induced Cardiomyopathies

Gopinathannair

Etheridge

Marchlinski

et al. 2015

Journal of the American College of Cardiology

307

116

View full text Add to dashboard Cite

show abstract

“…Of note, five patients with primary cardiomyopathy were also scanned with CMR and four of the five patients had evidence of LGE. 127 The investigators concluded that PVC-induced cardiomyopathy is less likely to have LGE on CMR as compared with other forms of cardiomyopathy. Consistent with this finding, a recent canine model of PVC-induced cardiomyopathy failed to demonstrate increased inflammation, fibrosis or changes in apoptosis or mitochondrial function.…”

Section: Imaging Studies In Tachycardia-induced Cardiomyopathymentioning

confidence: 99%

What About Tachycardia-induced Cardiomyopathy?

Ellis¹,

Josephson²

2013

Arrhythmia &Amp; Electrophysiology Review

View full text Add to dashboard Cite

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 ...

show abstract

“…This suggested that tachycardia-induced cardiomyopathy may have been involved in the decreased cardiac function. However, because LGE of CMRI is usually unobserved in tachycardia-induced cardiomyopathy,29 30 we cannot explain the LGE positivity in our patient. In addition, as IVCD was noted 3 years earlier, we presume that the patient may have experienced cardiomyopathy that caused latent myocardial damage.…”

Section: Discussionmentioning

confidence: 66%

Antimitochondrial antibodies-positive myositis accompanied by cardiac involvement

et al. 2017

View full text Add to dashboard Cite

We report a 55-year-old man who experienced proximal muscle weakness accompanied by the atrial flutter (AFL) with 1:1 conduction. Detailed examination revealed elevated antimitochondrial antibodies (AMA) and creatine kinase (CK). AFL was converted to sinus rhythm by cardioversion. He was diagnosed as AMA-positive myositis-associated AFL and was treated by prednisolone. Although his muscle weakness and CK level improved, AFL with 1:1 conduction reappeared. Therefore, radiofrequency catheter ablation (RFCA) was needed to treat the AFL, resulting in maintenance of sinus rhythm. This case report describes cardiac involvement in a patient with AMA-positive myositis.

show abstract

Late Gadolinium Enhancement CMR in Patients with Tachycardia‐Induced Cardiomyopathy Caused by Idiopathic Ventricular Arrhythmias

Cited by 80 publications

References 23 publications

Arrhythmia-Induced Cardiomyopathies

Arrhythmia-Induced Cardiomyopathies

What About Tachycardia-induced Cardiomyopathy?

Antimitochondrial antibodies-positive myositis accompanied by cardiac involvement

Contact Info

Product

Resources

About