Haemodynamic and neurohumoral response in heart failure produced by rapid ventricular pacing

Travill, C M; Williams, T. D. M.; Pate, P.; Song, Gouqing; Chalmers, J. A. C.; Lightman, Stafford L.; Rb, Sutton; Noble, Mark I. M.

doi:10.1093/cvr/26.8.783

Cited by 52 publications

(23 citation statements)

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“…4,5 Furthermore, Weinberg et al 41 demonstrated that chronic administration of amlodipine normalized LV end-diastolic pressure in a model of LV hypertrophy. Consistent with past reports, [25][26][27][28][29][30][31][32] chronic rapid pacing caused LV dilation and pump dysfunction. In the present study, concomitant amlodipine monotherapy, ACE inhibition, or combination therapy instituted during chronic rapid pacing reduced the degree of LV dilation.…”

Section: Function and Systemic Hemodynamicssupporting

confidence: 91%

“…[25][26][27][28][29][30][31][32] Specifically, the development of pacing-induced CHF is associated with severe LV pump failure, heightened catecholamine levels, and increased vascular resistance in several circulatory beds. [25][26][27][28][29][30][31][32] In addition, the pacing model of CHF has been successfully used to examine specific systemic and neurohormonal changes that occur during exercise with the development of CHF. 27,29 Accordingly, in the present study, we used a pacing-induced model of CHF to examine the potentially differential effects of amlodipine treatment, ACE inhibition, and combined treatment on LV pump function, systemic hemodynamics, and regional blood flow patterns both at rest and with treadmill-induced exercise.…”

Section: Rationalementioning

confidence: 99%

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Amlodipine Monotherapy, Angiotensin-Converting Enzyme Inhibition, and Combination Therapy With Pacing-Induced Heart Failure

Kribbs

Merritt²,

Clair

et al. 1998

Hypertension

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Abstract-In patients with congestive heart failure (CHF) receiving therapy with angiotensin-converting enzyme (ACE) inhibition, institution of calcium channel antagonism with amlodipine provided favorable effects. The goal of the present study was to define potential mechanisms for these effects by measuring left ventricular function, hemodynamics, and neurohormonal system activity in a model of CHF in which amlodipine treatment had been instituted either as a monotherapy or in combination with ACE inhibition. Thirty-two pigs were instrumented to allow measurement of cardiac index, total systemic resistance index, and neurohormonal activity in the conscious state and assigned to one of four groups: (1) rapid atrial pacing (240 bpm) for 3 weeks (nϭ8), (2) amlodipine (1.5 mg ⅐ kg Ϫ1 ⅐ d Ϫ1 ) and pacing (nϭ8), (3) ACE inhibition (fosinopril 1.0 mg/kg BID) and pacing (nϭ8), and (4) , respectively, PϽ.05), and was normalized with combination therapy. Plasma catecholamines, renin activity, and endothelin levels were increased threefold with rapid pacing. Amlodipine, either as a monotherapy or in combination with ACE inhibition, did not result in increased plasma catecholamines and renin activity compared with the rapid pacing-only group. Furthermore, combination therapy reduced steady state norepinephrine and normalized epinephrine levels. The results of the present study demonstrated that monotherapy with either amlodipine or ACE inhibition provides beneficial effects in this pacing model of CHF. Combined amlodipine and ACE inhibition provided greater benefit with respect to vascular resistance properties and neurohormonal system activity compared with either monotherapy. (Hypertension. 1998;31:755-765.)

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Section: Function and Systemic Hemodynamicssupporting

confidence: 91%

Section: Rationalementioning

confidence: 99%

Amlodipine Monotherapy, Angiotensin-Converting Enzyme Inhibition, and Combination Therapy With Pacing-Induced Heart Failure

Kribbs

Merritt²,

Clair

et al. 1998

Hypertension

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“…First, we studied an animal model of RV pacing-induced HF that reproduces many of the functional and neurohormonal features (5,7,8,29,33,54) of clinical HF. Although this experimental model demonstrated biventricular chamber dilatation with increased LV and RV filling pressures and striking abnormalities in systolic and diastolic function similar to those found in patients with dilated cardiomyopathy, we cannot be certain that our results apply to HF of other causes such as hypertrophic cardiomyopathy.…”

Section: Study Limitationsmentioning

confidence: 99%

Levosimendan restores the positive force-frequency relation in heart failure

Masutani

Cheng

Tachibana

et al. 2011

American Journal of Physiology-Heart and Circulatory Physiology

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Masutani S, Cheng HJ, Tachibana H, Little WC, Cheng CP. Levosimendan restores the positive force-frequency relation in heart failure. Am J Physiol Heart Circ Physiol 301: H488 -H496, 2011. First published May 13, 2011; doi:10.1152/ajpheart.01116.2010.-Frequency potentiation of contractile function is a major mechanism of the increase in myocardial performance during exercise. In heart failure (HF), this positive force-frequency relation is impaired, and the abnormal left ventricular (LV)-arterial coupling is exacerbated by tachycardia. A myofilament Ca 2ϩ sensitizer, levosimendan, has been shown to improve exercise tolerance in HF. This may be due to its beneficial actions on the force-frequency relation and LV-arterial coupling (end-systolic elastance/arterial elastance, EES/EA). We assessed the effects of therapeutic doses of levosimendan on the forcefrequency relation and EES/EA in nine conscious dogs after pacinginduced HF using pressure-volume analysis. Before HF, pacing tachycardia increased E ES, shortened , and did not impair EES/EA and mechanical efficiency (stroke work/pressure-volume area, SW/PVA). In contrast, after HF, pacing at 140, 160, 180, and 200 beat/min (bpm) produced smaller a increase of EES or less shortening of , whereas EES/EA (from 0.56 at baseline to 0.42 at 200 bpm) and SW/PVA (from 0.52 at baseline to 0.43 at 200 bpm) progressively decreased. With levosimendan, basal E ES increased 27% (6.2 mmHg/ml), decreased 11% (40.8 ms), EES/EA increased 34% (0.75), and SW/PVA improved by 15% (0.60). During tachycardia, E ES further increased by 23%, 37%, 68%, and 89%; decreased by 9%, 12%, 15%, and 17%; and EES/EA was augmented by 11%, 16%, 31%, and 33%, incrementally, with pacing rate. SW/PVA was improved (0.61 to 0.64). In conclusion, in HF, treatment with levosimendan restores the normal positive LV systolic and diastolic force-frequency relation and prevents tachycardia-induced adverse effect on LV-arterial coupling and mechanical efficiency.drugs; contractility; diastole; heart rate UNDER NORMAL CONDITIONS, an increase in heart rate (HR) augments myocardial contractility and the rate of relaxation (15,39,44). This force-frequency behavior is determined by both calcium handling and myofilament properties (26). It has been shown that the integrated dynamic balance of the intracellular Ca 2ϩ concentration ([Ca 2ϩ ] i ) is the primary cellular mechanism responsible for the force-frequency relation (FFR) and is determined by sarcoplasmic reticulum (SR) Ca 2ϩ load and Ca 2ϩ flux through the sarcolemma via L-type Ca 2ϩ channels and the Na ϩ -Ca 2ϩ exchanger (13). The positive FFR and relaxation-frequency relation (RFR) enhance cardiac performance during stress or exercise (7,36,39,44,52). In heart failure (HF), the positive FFR and RFR are impaired (16,24,28,29,44), and the abnormal left ventricular (LV)-arterial coupling is exacerbated by tachycardia. This contributes to exercise intolerance in HF (44, 52). The altered responses of LV contraction and relaxation to HR in HF may at least partially ...

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“…Because the development of tachycardia-induced HF is reversible and the termination of rapid ventricular pacing results in improved cardiac and hormonal functions, 30 we performed these experiments with ongoing rapid ventricular pacing even though it is very important to assess the effects of the antagonist on changes in heart rate.…”

Section: Limitations Of the Studymentioning

confidence: 99%

“…30 However, even shorter-term pacing induces hemodynamic deterioration and some neurohormonal activation. Although it is important to assess exercise capacity, which is reduced in HF, to ascertain whether HF has been induced in this model, we could not assess it in the present study.…”

Section: Limitations Of the Studymentioning

confidence: 99%

Short-Term and Long-Term Inhibition of Endogenous Atrial Natriuretic Peptide in Dogs With Early-Stage Heart Failure

et al. 1998

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n congestive heart failure, neurohormonal factors such as the renin-angiotensin-aldosterone system (RAAS) and the sympathetic nervous system are activated, and the RAAS activation may lead to deterioration of heart failure (HF) due to the vasoconstrictive and volume-retaining effects. 1 Atrial natriuretic peptide (ANP) demonstrates increased secretion in proportion to the severity of HF, and may act to counterbalance the adverse effects of the RAAS through its direct vasodilatory action, inhibition of the excessive release of renin and aldosterone, and by its direct diuretic and natriuretic effects. [2][3][4] As reported in the Study of Left Ventricular Dysfunction (SOLVD), early-stage HF is characterized by an increase in circulating ANP without activation of the RAAS or body fluid retention. 5 Considering these hormonal profiles and the body fluid balance, ANP may be one of the principal factors inhibiting the activation of the RAAS and body fluid retention in early-stage HF. However, in advanced HF the intracardiac pressure increases, volume overload develops, and the RAAS activates in spite of the fact that the plasma ANP level remains elevated above basal values. Elevated plasma ANP in advanced HF may not be as effective as expected. In addition, the responsiveness to exogenous ANP decreases in renin suppression or renal excretion in advanced HF. 6 Thus the decreased responsiveness to endogenous ANP may play a part in the pathogenesis of vasoconstriction, activation of the RAAS and body fluid retention in HF. However, it has not been demonstrated experimentally whether hyporesponsiveness to ANP is directly related to the progression of HF.We and others have attempted to clarify the role of endogenous ANP in HF through short-term inhibition of ANP activity using an ANP receptor antagonist, HS-142-1. 4,[7][8][9][10][11] However, the influence of long-term inhibition of endogenous ANP activity by an ANP receptor antagonist in established HF, in which ANP has previously exerted an effect, has not been determined. We assumed that longterm inhibition of endogenous ANP activity in early-stage HF provokes the progression to advanced HF. It is important to examine how long-term inhibition of endogenous ANP affects cardiorenal and neurohormonal factors in early-stage HF in order to clarify the exact role of ANP in the progression from early-stage to advanced HF.The objective of the present study is to clarify whether endogenous ANP inhibits the deterioration of early-stage HF by investigating the effects of long-term suppression of endogenous ANP activity by HS-142-1 in dogs with earlystage HF. Furthermore, since it is expected that the longterm inhibition of endogenous ANP will cause the activation of various substances that affect vascular tone, hormonal secretion and renal functions, we compared the differences in the effects of short-term and long-term inhibition, and determined the direct and indirect influences of the suppression of endogenous ANP in early-stage HF. Short-Term and Long-Term Inhibition of Endoge...

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Haemodynamic and neurohumoral response in heart failure produced by rapid ventricular pacing

Abstract: These findings are compatible with a major role of one or more of renin, vasopressin, and noradrenaline in the pathophysiology of the fluid retention of heart failure; the manifestations are not counteracted by the rise in atrial natriuretic factor.

Cited by 52 publications

References 0 publications

Amlodipine Monotherapy, Angiotensin-Converting Enzyme Inhibition, and Combination Therapy With Pacing-Induced Heart Failure

Amlodipine Monotherapy, Angiotensin-Converting Enzyme Inhibition, and Combination Therapy With Pacing-Induced Heart Failure

Levosimendan restores the positive force-frequency relation in heart failure

Short-Term and Long-Term Inhibition of Endogenous Atrial Natriuretic Peptide in Dogs With Early-Stage Heart Failure

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