Persistent left ventricular dilatation in tachycardia-induced cardiomyopathy patients after appropriate treatment and normalization of ejection fraction

Dandamudi, Gopi; Rampurwala, Abbas Y.; Mahenthiran, Jothiharan; Miller, John M.; Das, Mithilesh K.

doi:10.1016/j.hrthm.2008.04.023

Cited by 76 publications

(47 citation statements)

References 7 publications

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“…The mean time interval between pre-treatment and post-treatment echocardiograms was 14 months in this group. 126 These findings are consistent with previously discussed animal models of TIC, which found that after ejection fraction and other haemodynamic parameters normalised, LV volumes remained increased. However, in these animal models such persistent changes were only documented out to 12 weeks.…”

Section: Imaging Studies In Tachycardia-induced Cardiomyopathysupporting

confidence: 92%

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: Imaging Studies In Tachycardia-induced Cardiomyopathysupporting

confidence: 92%

What About Tachycardia-induced Cardiomyopathy?

Ellis¹,

Josephson²

2013

Arrhythmia &Amp; Electrophysiology Review

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“…For example, tachycardia-induced cardiomyopathy in large animals is reversible to some extent on reversal of the tachycardia. 72,73 Moreover, myocyte hypertrophy and fibrosis do not feature prominently in this form of cardiomyopathy despite changes in hemodynamics, neurohormonal activation, and chamber structure and function that replicate clinical DCM. [73][74][75] Animal Models Currently Used for the DCM Phenotype A variety of animal models (large and small) have been used to mimic the human DCM phenotype and HF.…”

Section: Critical Features Of the Animal Modelmentioning

confidence: 92%

Animal Models of Heart Failure

Houser¹,

Margulies²,

Murphy³

et al. 2012

Circulation Research

384

223

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“…4) Chronic tachycardia-mediated DCM is a recognized clinical condition. 6,7) This disease model closely replicates the mechanical, structural, neurohormonal, and myocyte functional alterations of DCM in humans. [8][9][10][11] The predictability and reproducibility of the model, and its parallels to the hemodynamic and mechanical phenotype of DCM in humans, render this an attractive model.…”

Section: Ilated Cardiomyopathy (Dcm) Is An Important Causementioning

confidence: 56%

“Pacing Bigeminal”

Gong¹,

Qin²,

Huang³

et al. 2016

Int. Heart J.

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SummaryA rapid pacing-induced heart failure model is commonly used in developing dilated cardiomyopathy (DCM). Traditionally, the right ventricular lead was connected with a single chamber pacemaker specific for animals that had a high frequency. However, the pacemaker used in this model is commercially unavailable. We developed a "pacing bigeminal" method using a commercially available dual-chamber (DDD) pacemaker to achieve high-frequency pacing. Twenty beagles were assigned to group A (n = 10) (pacing bigeminal method) and group B (n = 10) (traditional method). Echocardiographic measurements and electrocardiograms were obtained at baseline, at two weeks of pacing, and at 4 weeks of end pacing. LV anterior wall cardiac samples were obtained at 2 weeks of pacing and 4 weeks of end pacing for myocardial microscopic evaluation. Clinical manifestation and exposure time were also observed. After pacing for 10.5 ± 2.3 (7-14) days, the beagles in group B experienced heart failure, whereas in group A, only 7.9 ± 2.5 (5-12) days (P < 0.05) were needed to reach heart failure. Both methods could induce wide QRS duration, heart rate elevation, and myocardial microscopic changes (P > 0.05). In conclusion, this pacing bigeminal-induced heart failure method is feasible and can induce heart failure faster than the traditional method, which makes it a promising alternative method. (Int Heart J 2016; 57: 747-752) Key words: Animal model, Cardiac resynchronization therapy, Dilated cardiomyopathy D ilated cardiomyopathy (DCM) is an important cause of heart failure that is characterized by unexplained left ventricular (LV) dilatation and impaired systolic function.1) Cardiac resynchronization therapy (CRT) is a device therapy for end-stage HF, especially that caused by idiopathic DCM. In the wide application of CRT, the establishment of a suitable big-animal heart failure model is essential in basic research on DCM and CRT, because the devices are not easily used in small-animal models.Current DCM heart failure models of large animals include myocardial infarction, coronary microembolization, pacing-induced tachycardia, and toxic injury, 2,3) described in detail in the AHA Scientific Statement. 4) Regional myocardial infarction models mimic human ischemic cardiomyopathy, which mainly uses pigs instead of dogs because dogs have a well-developed collateral circulation, 5) which can result in higher variability in infarct size and subsequent remodeling. Coronary microembolization also resembles human ischemic cardiomyopathy, but it is time consuming and requires repeated injection with polystyrene microspheres. The limitations of the toxic model include variability of the response to doxorubicin and the degree of LV dysfunction and animal mortality caused by arrhythmias. 4)Chronic tachycardia-mediated DCM is a recognized clinical condition. 6,7) This disease model closely replicates the mechanical, structural, neurohormonal, and myocyte functional alterations of DCM in humans. [8][9][10][11] The predictability and reproducibility...

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Persistent left ventricular dilatation in tachycardia-induced cardiomyopathy patients after appropriate treatment and normalization of ejection fraction

Cited by 76 publications

References 7 publications

What About Tachycardia-induced Cardiomyopathy?

What About Tachycardia-induced Cardiomyopathy?

Animal Models of Heart Failure

“Pacing Bigeminal”

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