Exhaustion of Frank-Starling mechanism in conscious dogs with heart failure

Komamura, Kazuo; Shannon, Richard P.; Ihara, Tadashi; Shen, You‐Tang; Mirsky, Israel; Bishop, Sanford P.; Vatner, Stephen F.

doi:10.1152/ajpheart.1993.265.4.h1119

Cited by 76 publications

(70 citation statements)

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“…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%

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

Spinale¹

2007

Physiological Reviews

1,004

1,023

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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.

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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

1,004

1,023

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“…34,42,44,45 Loss of myocardial contractility has also been demonstrated as shown by a diminished or absent response to inotropic agents, volume loading and postextrasystolic potentiation. 46 Disturbed elastic properties of the left ventricle (LV) have also been reported, which result in a stiffer ventricle and worsening LV diastolic function. In a normal heart, LV torsion reduces transmural fiber strain during systole, and recoil in early diastole is thought to enhance left ventricular filling.…”

Section: Haemodynamic Changesmentioning

confidence: 99%

“…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. 55 Chamber dilation and wall thinning has been shown to correlate with loss of myocytes and an increase in volume of the remaining myocytes, 56 although other studies have shown remodeling without myocyte hypertrophy.…”

Section: Structural Changesmentioning

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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“…In healthy people, the heart respond to increased venous return with an augmented stroke volume (Frank-Starling relationship) (5). However, in patients with heart failure, stroke volume can not be further augmented due to exhaustion of Frank Starling reserve (6). Both of the patients had been tested if they could stay in supine position for 2 or 3 hours in the day before the procedure, so this mechanism can not solely explain the situation.…”

Section: Discussionmentioning

confidence: 99%