Congestive heart failure following chronic tachycardia

Coleman, Henry Neal; Taylor, Roger R.; Pool, Peter E.; Whipple, Gerald H.; Covell, James W.; Ross, John; Braunwald, Eugene

doi:10.1016/0002-8703(71)90083-4

Cited by 215 publications

(68 citation statements)

References 18 publications

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“…The low-output heart-failure model used in these elation beexperiments was originally described by Whipple et al12 and was expanded by Coleman et al 13 In the present study, eight dogs were continuously paced for a mean duration of 27.6±3.5 days. At the time the acute experiment was performed, there was a significant elevation in LVEDP and a significant reduction in cardiac output in the anesthetized dogs.…”

Section: Discussion Liameter Inmentioning

confidence: 89%

See 1 more Smart Citation

Carotid sinus baroreceptor sensitivity in experimental heart failure.

Wang¹,

Chen²,

Zucker³

1990

Circulation

136

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Single-unit carotid sinus baroreceptor activity was recorded in normal and heart-failure (pacing-induced) dogs. The sensitivity of these units was compared between the two groups of dogs. After development of clinical heart failure, the animals were anesthetized, and the left carotid sinus was vascularly isolated and perfused with oxygenated Krebs-Henseleit solution. Single-unit baroreceptor discharge was recorded from the carotid sinus nerve in response to stepwise increases in carotid sinus pressure (CSP). In addition, the carotid sinus diameter was measured with sonomicrometer crystals. In this way, both CSP-discharge and CSP-diameter curves were constructed for both normal and heart-failure dogs. Analysis of these curves demonstrated that the heart-failure group exhibited a significant decrease in peak discharge (48.1±3.0 vs. 22.2±+ 2.2 spikes/sec; p<0.001) and a significant elevation in threshold pressure compared with the normal animals (91.0 +5.0 vs. 119.1±+4.4 mm Hg; p<0.001). The peak slope of the CSP-discharge curve was also significantly lower in the heart-failure group (0.63 ±0.06 vs. 0.40 ±0.09 spikes/sec/mm Hg; p <0.05). In the heart-failure group, perfusion of the carotid sinus with ouabain (0.01 ,ug/ml) caused a significant decrease in threshold pressure and a significant increase in peak discharge frequency, as well as an increase in slope of the CSP-discharge curve. There were no changes in CSP-diameter relations in response to ouabain. This dose of ouabain had no effect on pressure-discharge relations or carotid sinus diameters in normal dogs. Perfusion of the isolated carotid sinus with a Krebs-Henseleit solution with 50% of the normal potassium ion concentration had no effect on peak discharge or slope, but this perfusion protocol significantly reduced threshold pressure in heart-failure dogs. Low potassium ion concentration had no effect in the normal dogs. From these data, we conclude that there is attenuation of the carotid sinus baroreceptor discharge sensitivity in this model of low-output heart failure. The data are consistent with the view that there is an augmentation of Na+,K+-ATPase activity in the carotid sinus baroreceptor. (Circulation 1990;81:1959-1966 T he reflex control of the circulation is clearly abnormal in heart failure.1-8 The arterial baroreflex is abnormal in both low-and high-output heart failure in humans3'4 and in animals.5-8 The mechanisms for this reflex abnormality are not completely understood. Derangements in any part of the reflex arc could be responsible for the depression in baroreflex sensitivity that has been observed in heart failure.Clearly, data indicate that the efferent components of the baroreflex control of heart rate are abnormal,2'4 and it has also been shown that both catecholamine synthesis and responsiveness are depressed in heart failure. both systemic norepinephrine clearance and spillover are abnormal in heart failure.1" Evidence from this laboratory also suggests that both carotid and aortic baroreceptor discharge sensitivities are depres...

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Section: Discussion Liameter Inmentioning

confidence: 89%

“…The inflow and outflow perfusion catheters were placed in the common carotid and lingual arteries, respectively. An oxygenated Krebs [10][11][12][13][14][15] minutes. There was no effect of time on any parameter of these curves.…”

Section: Preparation Of Isolated Carotid Sinusmentioning

confidence: 99%

Carotid sinus baroreceptor sensitivity in experimental heart failure.

Wang¹,

Chen²,

Zucker³

1990

Circulation

136

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“…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.…”

Section: Introductionmentioning

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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“…34 In contrast, intracellular biochemical changes associated with concentric hypertrophy may depend more on perfusion to the endocardium (especially rate related). 33,37,38 Altered biochemistry is reported by other investigators who studied patients with mitral valve prolapse. The arterial and coronary sinus blood lactate levels were increased 30 in a group with mitral valve prolapse, and right ventricular endomyocardial biopsies 31 demonstrated evidence of mitochondrial degeneration.…”

Section: Figurementioning

confidence: 78%

Mitral Regurgitation

et al. 1998

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Background-A number of phosphorus ( 31 P) magnetic resonance spectroscopy (MRS) studies link alterations of high-energy phosphate metabolism in valvular disease and cardiomyopathy to the clinical severity of heart failure. However, correlations between MRS and indexes of ventricular dysfunction are inconclusive to date. We examined whether changes in 31 P MRS are associated with the impaired contractility, which predisposes to chronic congestive heart failure in patients with mitral regurgitation. Methods and Results-Thirteen normal control subjects and 22 patients with echocardiographically characterized chronic mitral regurgitation were studied by 31 P MRS. The apical phosphocreatine-to-ATP ratio (PCr/ATP) was lower in severe disease (PϽ.02) and those on therapy (nϭ13, 1.29Ϯ0.29, PϽ.01) in contrast to control subjects (nϭ13, 1.61Ϯ0.3). Compared to those with mild mitral regurgitation, patients with more severe incompetence had lower mean myocardial PCr/ATP ratios (mild, nϭ6,

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Congestive heart failure following chronic tachycardia

Cited by 215 publications

References 18 publications

Carotid sinus baroreceptor sensitivity in experimental heart failure.

Carotid sinus baroreceptor sensitivity in experimental heart failure.

What About Tachycardia-induced Cardiomyopathy?

Mitral Regurgitation

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