Cardiorenal and neurohumoral function in a canine model of early left ventricular dysfunction.

Redfield, MM; Aarhus, Lawrence L.; Wright, R. Scott; Burnett, Jr Jc

doi:10.1161/01.cir.87.6.2016

Cited by 70 publications

(45 citation statements)

References 26 publications

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“…Three additional ELVD-INTACT dogs were studied where the surgical preparation was identical to the ELVD-APPX dogs in that bilateral pericardial incisions were made over the atrial appendages, however no atrial appendectomy was performed. Hemodynamic, neurohumoral, and renal data in the three ELVD-INTACT dogs was not significantly different from the group of five ELVD-INTACT dogs from the original study (7). The remaining seven ELVD-INTACT dogs comprised the acute antagonism group which received HS-142-1.…”

Section: Methodsmentioning

confidence: 74%

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A functional role for endogenous atrial natriuretic peptide in a canine model of early left ventricular dysfunction.

Stevens¹,

Burnett²,

Kinoshita³

et al. 1995

J. Clin. Invest.

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115

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Asymptomatic or early left ventricular dysfunction in humans is characterized by increases in circulating atrial natriuretic peptide (ANP) without activation of the renin-angiotensin-aldosterone system (RAAS). We previously reported a canine model of early left ventricular dysfunction (ELVD) produced by rapid ventricular pacing and characterized by an identical neurohumoral profile and maintenance of the natriuretic response to volume expansion (VE). To test the hypothesis that elevated endogenous ANP suppresses the RAAS and maintains sodium excretion in ELVD, we assessed the effects of antagonism of ANP on cardiorenal and neurohumoral function in ELVD. Chronic ANP suppression was produced by bilateral atrial appendectomies before the production of ELVD by rapid ventricular pacing (ELVD-APPX, n = 5). This group was compared with a separate group with ELVD and intact atrial appendages (ELVD-INTACT, n = 8). ELVD-APPX was characterized by lower circulating ANP (50±11 vs. 158±37 pg/ml, P < 0.05), activation of plasma renin activity (PRA) (9.4±2.4 vs. 0.6±0.4 ng/ml per h, P < 0.05) and aldosterone (36.4±12.5 vs. 2.5±0.0 ng/dl, P < 0.05) when compared to ELVD-INTACT. In comparison to the ELVD-INTACT group, sodium excretion was decreased before and during VE in the ELVD-APPX group. Acute ANP antagonism was produced by administration of the particulate guanylate cyclase coupled natriuretic peptide receptor antagonist, HS-142-1, to seven conscious dogs with ELVD and intact atrial appendages (ELVD-INTACT). HS-142-1 decreased plasma concentrations and renal generation of the ANP second messenger, cGMP, and was associated with activation of PRA and sodium retention with enhanced tubular sodium reabsorption. These data support a significant role for elevated endogenous ANP in the maintenance of sodium excretion

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Section: Methodsmentioning

confidence: 74%

“…We have reported a canine model of ELVD produced by rapid ventricular pacing at 180 beats per minute for 10 d (7). This model of ELVD results in a neurohumoral profile identical to that observed in humans with ELVD as reported in SOLVD (6).…”

Section: Introductionmentioning

confidence: 76%

A functional role for endogenous atrial natriuretic peptide in a canine model of early left ventricular dysfunction.

Stevens¹,

Burnett²,

Kinoshita³

et al. 1995

J. Clin. Invest.

Self Cite

115

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show abstract

“…By pacing at a slower rate or for a shorter duration, a lesser degree of left ventricular dysfunction can be produced. [32][33][34][35] Although both chronic atrial and ventricular pacing result in left ventricular dysfunction, deterioration of left ventricular ejection fraction (LVEF) and left ventricular cavity dilation are more marked with chronic ventricular pacing than chronic atrial pacing. 36 Intermittent ventricular pacing appears to produce a less advanced syndrome of heart failure compared with continuous ventricular pacing.…”

Section: Haemodynamic 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 an experimental model of CHF, sodium extrusion and natriuresis in response to volume expansion was intact and renal function was preserved, 21 suggesting that retention of both sodium and fluid is increased by renal dysfunction. Renal dysfunction induces anemia mainly because of impaired erythropoietin production.…”

Section: Relation Between Renal Dysfunction and Chf Re-hospitalizationmentioning

confidence: 99%

Decreased Renal Function as an Independent Predictor of Re-Hospitalization for Congestive Heart Failure

Komukai

Ogawa

Yagi

et al. 2008

Circ J

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atients with congestive heart failure (CHF) are frequently re-hospitalized, worsening their quality of life, and re-hospitalization for CHF is also associated with increased mortality rates. 1,2 Therefore, re-hospitalization for CHF should be avoided. Renal insufficiency increases the risk of CHF, [3][4][5] but most studies that have investigated the role of renal function in CHF have included only subjects with no known CHF or mild-to-moderate CHF and excluded patients with severe renal dysfunction. Patients hospitalized for CHF have more severe disease and impaired renal function, but little is known about the relation between renal dysfunction and re-hospitalization because of CHF. Thus, the aim of the present study was to investigate whether renal dysfunction is associated with rehospitalization for CHF after successful discharge. MethodsThe study protocol was approved by the Ethics Committee of The Jikei University School of ).Patients with CHF who had been admitted from January 2003 through December 2004 and followed up after discharge at the outpatient clinic were reviewed. CHF was diagnosed by 2 or more cardiologists on the basis of the Framingham criteria. Patients were excluded if they had CHF complicated by acute myocardial infarction, were undergoing or starting dialysis during the follow-up period, or had undergone cardiac surgery during the follow-up period. With these selection criteria, 109 patients were enrolled. The duration of follow-up was 6-1,466 days (mean, 496 days; median, 348 days). The estimated glomerular filtration rate (GFR) was calculated using the Modification of Diet in Renal Disease equation 6 coefficient modified for Japanese patients: estimated GFR = 0.741×175× Cr -1.154 × age -0.203 (ml · min -1 · 1.73 m -2 ). For women, the estimated GFR was multiplied by a correction factor of 0.742.The 109 patients were divided into 2 groups: decreased renal function (estimated GFR on admission <45 ml·min -1 · 1.73 m -2 ; 42 patients) and preserved renal function (estimated GFR on admission ≥45 ml·min -1 ·1.73 m -2 ; 67 patients). The 2 groups were compared on the basis of age, sex, New York Heart Association (NYHA) class on admission, prescribed anti-CHF drugs at discharge, and the rates of coronary artery disease, valvular heart disease, cardiomyopathy, atrial fibrillation, hypertension, diabetes mellitus (DM), dyslipidemia, anemia, systolic dysfunction, previous hospitalization for CHF, and worsening renal function during hospitalization. Cardiomyopathy was defined according to heart catheterization or previous diagnosis. Hypertension was defined as systolic blood pressure ≥140 mmHg, diastolic blood pressure ≥90 mmHg, or previous history. DM was defined as fasting plasma glucose concentration ≥126 mg/dl, Background Patients with congestive heart failure (CHF) are often re-hospitalized, worsening both their quality of life and prognosis. Although renal dysfunction reportedly increases the risk of CHF, the association between renal dysfunction and re-hospitalization for CHF remains unclear...

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Cardiorenal and neurohumoral function in a canine model of early left ventricular dysfunction.

Abstract: The current study demonstrates that significant ventricular dysfunction with peripheral vasoconstriction can be associated with normal renal function and thus suggests an important functional role for the neurohumoral profile of ALVD in preserving sodium balance.

Cited by 70 publications

References 26 publications

A functional role for endogenous atrial natriuretic peptide in a canine model of early left ventricular dysfunction.

A functional role for endogenous atrial natriuretic peptide in a canine model of early left ventricular dysfunction.

What About Tachycardia-induced Cardiomyopathy?

Decreased Renal Function as an Independent Predictor of Re-Hospitalization for Congestive Heart Failure

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