Alterations in myocyte shape and basement membrane attachment with tachycardia-induced heart failure.

Zellner, James L.; Spinale, Francis G.; Eble, Diane M.; Hewett, Kenneth W.; Crawford, Fred A.

doi:10.1161/01.res.69.3.590

Cited by 100 publications

(65 citation statements)

References 38 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Left ventricular torsional abnormalities 27 and mitral regurgitation 31 occur in sheep. Independent of LVEF measurements, myocyte elongation and misalignment and disruption of basement membrane/sarcolemmal interfaces 32 with developing sarcolemmal festoons 33 and changes in myocyte attachment to laminin, fibronectin, and the extracellular collagen matrix 32,33 may be seen.…”

Section: Animal Modelsmentioning

confidence: 97%

Heart Failure and Sudden Death in Patients With Tachycardia-Induced Cardiomyopathy and Recurrent Tachycardia

et al. 2004

View full text Add to dashboard Cite

Background-Tachycardia-induced cardiomyopathy is a reversible cause of heart failure. We hypothesized that although left ventricular ejection fraction measurements normalize after heart rate or rhythm control in patients with tachycardia-induced cardiomyopathy, recurrent tachycardia may have abrupt and deleterious consequences. Methods and Results-Patients with tachycardia-induced cardiomyopathy that developed over years were evaluated and treated. Tachycardia episodes and outcomes were assessed. Twenty-four patients were identified. All had NYHA functional class III heart failure or greater on presentation. One third were heart transplant candidates. There were 17 men and 7 women with a mean age of 46Ϯ16 years and mean left ventricular ejection fraction of 0.26Ϯ0.09 at the index visit. The cause was atrial fibrillation (nϭ13), atrial flutter (nϭ4), atrial tachycardia (nϭ3), idiopathic ventricular tachycardia (nϭ1), permanent junctional reciprocating tachycardia (nϭ2), and bigeminal ventricular premature contractions (nϭ1). Within 6 months of rate control or correction of the rhythm, left ventricular ejection fraction improved or normalized and symptoms abated in all. Five patients had tachycardia recur. In these patients, left ventricular ejection fraction dropped precipitously and heart failure ensued within 6 months, even though the initial impairment took years. Rate control eliminated heart failure and improved or normalized ejection fraction in 6 months. Three of 24 patients died suddenly and unexpectedly. Conclusions-Tachycardia-induced cardiomyopathy develops slowly and appears reversible by left ventricular ejection fraction improvement, but recurrent tachycardia causes rapid decline in left ventricular function and development of heart failure. Sudden death is possible.

show abstract

Section: Animal Modelsmentioning

confidence: 97%

Heart Failure and Sudden Death in Patients With Tachycardia-Induced Cardiomyopathy and Recurrent Tachycardia

et al. 2004

View full text Add to dashboard Cite

show abstract

“…For example, in idiopathic DCM, the alterations in normal ECM architecture are associated with reduced collagen cross-linking, which will make the ECM more susceptible to degradation (146,206). Animal models of pacing-induced DCM have demonstrated a time-dependent alteration in normal ECM structure and composition that is accompanied by the progressive changes in LV geometry and function (208,410,490,537). Specifically, in this model of DCM, the progressive loss of normal myocardial ECM is accompanied by LV myocyte lengthening and a loss of myocyte adhesion to critical ECM components (208,537).…”

Section: Myocardial Remodeling In Cardiomyopathic Diseasementioning

confidence: 99%

“…Animal models of pacing-induced DCM have demonstrated a time-dependent alteration in normal ECM structure and composition that is accompanied by the progressive changes in LV geometry and function (208,410,490,537). Specifically, in this model of DCM, the progressive loss of normal myocardial ECM is accompanied by LV myocyte lengthening and a loss of myocyte adhesion to critical ECM components (208,537). These early changes in myocardial ECM structure and composition likely contribute to the progression of LV dilation and dysfunction in this nonischemic model of DCM.…”

Section: Myocardial Remodeling In Cardiomyopathic Diseasementioning

confidence: 99%

Myocardial Matrix Remodeling and the Matrix Metalloproteinases: Influence on Cardiac Form and Function

Spinale¹

2007

Physiological Reviews

1,005

1,023

View full text Add to dashboard Cite

It is now becoming apparent that dynamic changes occur within the interstitium that directly contribute to adverse myocardial remodeling following myocardial infarction (MI), with hypertensive heart disease and with intrinsic myocardial disease such as cardiomyopathy. Furthermore, a family of matrix proteases, the matrix metalloproteinases (MMPs) and the tissue inhibitors of MMPs (TIMPs), has been recognized to play an important role in matrix remodeling in these cardiac disease states. The purpose of this review is fivefold: 1) to examine and redefine the myocardial matrix as a critical and dynamic entity with respect to the remodeling process encountered with MI, hypertension, or cardiomyopathic disease; 2) present the remarkable progress that has been made with respect to MMP/TIMP biology and how it relates to myocardial matrix remodeling; 3) to evaluate critical translational/clinical studies that have provided a cause-effect relationship between alterations in MMP/TIMP regulation and myocardial matrix remodeling; 4) to provide a critical review and analysis of current diagnostic, prognostic, and pharmacological approaches that utilized our basic understanding of MMP/TIMPs in the context of cardiac disease; and 5) most importantly, to dispel the historical belief that the myocardial matrix is a passive structure and supplant this belief that the regulation of matrix protease pathways such as the MMPs and TIMPs will likely yield a new avenue of diagnostic and therapeutic strategies for myocardial remodeling and the progression to heart failure.

show abstract

“…47 These changes have been attributed to changes in the geometric orientation of the ventricle with changes in cardiac structural proteins as well as alterations in basement membrane and extracellular matrix function. 48,49 As a response to these changes, similar to other forms of CHF, pacing-induced CHF in animal models results in upregulation of the neurohormonal axis leading to elevated levels of serum atrial natriuretic peptide (ANP), renin, aldosterone, angiotensin-II, epinephrine and norepinephrine. 50,51 Interestingly, the vasodilator, natriuretic and renin-lowering effects of ANP are blunted in the canine model of TIC due to reduced cyclic guanosine monophosphate (GMP) expression in response to ANP.…”

Section: Haemodynamic Changesmentioning

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

Alterations in myocyte shape and basement membrane attachment with tachycardia-induced heart failure.

Cited by 100 publications

References 38 publications

Heart Failure and Sudden Death in Patients With Tachycardia-Induced Cardiomyopathy and Recurrent Tachycardia

Heart Failure and Sudden Death in Patients With Tachycardia-Induced Cardiomyopathy and Recurrent Tachycardia

Myocardial Matrix Remodeling and the Matrix Metalloproteinases: Influence on Cardiac Form and Function

What About Tachycardia-induced Cardiomyopathy?

Contact Info

Product

Resources

About