Cardiac geometry and mass changes associated with pacing-induced cardiomyopathy in the dog

Scott, Brook D.; Sharma, Mukesh Kumar; Levett, James M.; Marinelli, Carlos C; Kieso, Robert A.; Schmid, Phillip G.; Kerber, Richard E.

doi:10.1016/0002-8703(93)90113-n

Cited by 17 publications

(8 citation statements)

References 17 publications

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“…Several experimental studies have demonstrated that ventricular dysfunction was significantly related to the pacing duration and frequency in animal models. 25,26 In the clinical scenario, the incessant pattern of tachycardia, in contrast to episodic of sporadic patterns, may be the most important determinant of the duration and density of tachycardia, and consequently would be strongly associated with the development of myocardial dysfunction. 16 Considering that focal ATs originating from atrial appendage account for 41.9% (18/43) of persistent ATs it could be speculated that the preference for appendage originating ATs patients to develop TCM could be attributed to the fact that the appendage tachycardias are characterized by being incessant and had poor response to antiarrhythmic treatment.…”

Section: The Association Between the Persistent Nature Of At And Tcmmentioning

confidence: 99%

Tachycardiomyopathy Complicated by Focal Atrial Tachycardia: Incidence, Risk Factors, and Long‐Term Outcome

Yang

et al. 2014

Cardiovasc electrophysiol

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Section: The Association Between the Persistent Nature Of At And Tcmmentioning

confidence: 99%

Tachycardiomyopathy Complicated by Focal Atrial Tachycardia: Incidence, Risk Factors, and Long‐Term Outcome

Yang

et al. 2014

Cardiovasc electrophysiol

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“…38,39,54 Commonly, left ventricular cavity dilation is accompanied by little or no change in LV wall mass with a normal or reduced LV wall thickness. 22,39 Cellular changes accompanying the change in chamber size include cellular elongation, decreased myocyte cross-sectional area and disruption of normal myofibril alignment. 23,46 Other studies have reported increased numbers of cells in both the longitudinal and transverse sections of intact myocardium from animals with pacing-induced heart failure.…”

Section: Structural Changesmentioning

confidence: 99%

“…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 important to recognise that although rapid pacing likely provides a close approximation to the effects of native tachyarrhythmias, this supposition cannot be definitively confirmed.…”

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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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“…Specifically, we have shown in the canine tachypacing model of dilated cardiomyopathy that conduction slowing was dependent on the presence of LV mechanical dysfunction indexed by increased LV end diastolic pressure (8). However, this model does not include the element of ventricular hypertrophy (28), which has been shown in in vitro studies of neonatal rat ventricular myocyte monolayers (29) and very recently in ex vivo murine studies (27) to alter conduction properties. Hence, we investigated conduction delays at the early, intermediate, and late stages of PoH in which mechanical alterations (both increased and decreased function) caused by the hypertrophic response are accounted for.…”

Section: Conduction Abnormalities During Disease Progressionmentioning

confidence: 99%

Mechanoelectrical remodeling and arrhythmias during progression of hypertrophy

et al. 2009

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Despite a clear association between left ventricular (LV) mechanical dysfunction in end-stage heart failure and the incidence of arrhythmias, the majority of sudden cardiac deaths occur at earlier stages of disease development. The mechanisms by which structural, mechanical, and molecular alterations predispose to arrhythmias at the tissue level before the onset of LV dysfunction remain unclear. In a rat model of pressure overload hypertrophy (PoH) produced by ascending aortic banding, we correlated mechanical and structural changes measured in vivo with key electrophysiological changes measured ex vivo in the same animals. We found that action potential prolongation, a hallmark of electrical remodeling at the tissue level, is highly correlated with changes in LV wall thickness but not mechanical function. In contrast, conduction delays are not predicted by either mechanical or structural changes during disease development. Moreover, disrupted Cx43 phosphorylation at intermediate (increased) and late (decreased) stages of PoH are associated with moderate and severe conduction delays, respectively. Interestingly, the level of interaction between Cx43 and the cytoskeletal protein ZO-1 is exclusively decreased at the late stage of PoH. Closely coupled action potentials consistent with afterdepolarization-mediated triggered beats were readily observed in 6 of 15 PoH hearts but never in controls. Similarly, PoH (8/15) but not control hearts exhibited sustained episodes of ventricular tachycardia after rapid stimulation. The initiation and early maintenance of arrhythmias in PoH were formed by rapid and highly uniform activation wavefronts emanating from sites distal to the former site of stimulation. In conclusion, repolarization but not conduction delays are predicted by structural remodeling in PoH. Cx43 phosphorylation is disrupted at intermediate (increased) and late (decreased) stages, which are associated with conduction delays. Dephosphorylation of Cx43 is associated with loss of interaction with ZO-1 and severe conduction delays. Remodeling at all stages of PoH predisposes to triggers and focal arrhythmias.

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Cardiac geometry and mass changes associated with pacing-induced cardiomyopathy in the dog

Cited by 17 publications

References 17 publications

Tachycardiomyopathy Complicated by Focal Atrial Tachycardia: Incidence, Risk Factors, and Long‐Term Outcome

Tachycardiomyopathy Complicated by Focal Atrial Tachycardia: Incidence, Risk Factors, and Long‐Term Outcome

What About Tachycardia-induced Cardiomyopathy?

Mechanoelectrical remodeling and arrhythmias during progression of hypertrophy

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