Ventricular remodeling during development and recovery from modified tachycardia-induced cardiomyopathy model

Yamamoto, Kazuhide; Burnett, John C.; Meyer, L; Sinclair, Lisa M.; Stevens, Tracy L.; Redfield, Margaret M.

doi:10.1152/ajpregu.1996.271.6.r1529

Cited by 25 publications

(33 citation statements)

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“…An early study reported that patients with a PVC burden of 20 % were more likely to have impaired LV function compared with those patients with a PVC burden of <20 %. 76 A later study found that a PVC burden of 16 % by a receiver operating characteristic (ROC) curve analysis best separated patients with and without TIC. 109 Most recently, a PVC burden of 24 % was reported to be strongly associated with the presence of cardiomyopathy, although this cut-off value failed to identify every individual at risk of cardiomyopathy and the critical burden for some patients was noted to be lower.…”

Section: Ventricular Tachycardiamentioning

confidence: 99%

“…33,38,40,50 Changes in intracardiac filling pressures, cardiac output and systemic vascular resistance are generally reversible with cessation of rapid pacing, although in some cases ejection fraction may not return to baseline and abnormalities in contractile function may persist. 33,76 Within 48 hours of cessation of pacing, intracardiac filling pressures, systemic arterial pressures, systemic vascular resistance and cardiac index have been shown to return to levels similar to control animals. 34 Significant improvements in LVEF have been shown by 24-48 hours with normalisation after 1-2 weeks.…”

Section: Time Course and Recoverymentioning

confidence: 99%

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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: Ventricular Tachycardiamentioning

confidence: 99%

Section: Time Course and Recoverymentioning

confidence: 99%

What About Tachycardia-induced Cardiomyopathy?

Ellis¹,

Josephson²

2013

Arrhythmia &Amp; Electrophysiology Review

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“…6 After a 2-week recovery period, the pacemaker was programmed to 180 bpm for 10 days, after which the pacing rate was increased at 7-day intervals sequentially to 200, 210, 220, and 240 bpm as previously described. 6,7 …”

Section: Hf Modelmentioning

confidence: 99%

“…TRCM is associated with marked left ventricular (LV) dilatation, systolic dysfunction, and disruption of the fibrillar collagen network. [1][2][3][4][5][6][7] Further, reduced myocyte adhesion to constituents of the basement membrane 4,8 has been reported in TRCM and may contribute to myocyte elongation, chamber remodeling, dysfunction, and altered mechanotransduction because of the decreased coupling of the myocyte sarcolemma to the extracellular matrix (ECM).…”

mentioning

confidence: 99%

Titin Isoforms, Extracellular Matrix, and Global Chamber Remodeling in Experimental Dilated Cardiomyopathy

Maniu

Krysiak

Shapiro

et al. 2008

Circ: Heart Failure

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Background-Altered titin isoforms may modify cardiac function in heart failure (HF), but the nature of isoform switches and associated functional implications are not well defined. Limited studies have reported an increased compliant isoform (N2BA) expression in human systolic HF. Titin may also modulate stretch-regulated responses such as myocardial natriuretic peptide production. Methods and Results-We characterized titin isoform expression and extracellular matrix in all 4 cardiac chambers and the left ventricular (LV) epicardium and endocardium in normal dogs (nϭ6) and those with HF (nϭ6) due to tachypacing and characterized functional implications at the LV myofiber and chamber level. Recognizing the potential for uncoupling of the extracellular matrix and cardiomyocyte in tachypacing, myocardial natriuretic peptide production, a molecular marker of stretch-regulated responses, was also assessed. All chambers were dilated in HF, but the extracellular matrix was not increased. HF dogs had markedly lower N2BA in the atria and right ventricle. In failing LVs, N2BA was decreased only in the epicardium, where myofiber passive stiffness was increased. However, LV chamber mechanics were driven by the marked LV dilatation, with no increase in LV diastolic stiffness. Natriuretic peptide concentrations increased markedly in the endocardium in relation to increases in LV wall stress. Conclusions-Tachypacing HF is characterized by decreases in compliant titin isoform expression in the atria, right ventricle, and LV epicardium. However, LV chamber mechanics are principally determined by geometric and extracellular matrix changes rather than titin-based myofiber stiffness in this model. Stretch-regulated myocardial responses (natriuretic peptide production) appeared intact, suggesting that the mechanotransduction role of titin was not impaired in HF. (Circ Heart Fail. 2008;1:192-199.)

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“…In some publications, left ventricular ejection fraction (LVEF) reduced up to 24-28% and moderate to severe MR was developed after rapid pacing 77,78,80 . One drawback of this model is that after recovery from rapid pacing, LV function return to levels seen in the healthy animals 81 . In light of this observation, researchers should pay attention to this fact with regard to evaluation of device efficacy.…”

Section: Mitral Valve Repairmentioning

confidence: 99%