Impaired Heart Rate Recovery and Chronotropic Incompetence in Patients With Heart Failure With Preserved Ejection Fraction

Phan, Thanh Trung; Shivu, Ganesh Nallur; Abozguia, Khalid; Davies, C. T. M.; Nassimizadeh, Mohammad; Jimenez, Donie; Weaver, Rebekah; Ahmed, Ibrar; Frenneaux, Michael

doi:10.1161/circheartfailure.109.877720

Cited by 180 publications

(144 citation statements)

References 39 publications

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“…Phan et al [8] found that 34% of patients with HFpEF have CI during maximal exercise when defined by %Max PHR and 63% when defined by %HRR. In order to avoid age, functional capacity and resting HR biases of each individual [1,4,5,[20][21][22][23][24], for comparison analysis of patient data we have used %HRR.…”

Section: Discussionmentioning

confidence: 99%

“…A number of recent studies have revealed the existence of depresssed chronotropic reserve in patients with HFpEF even compared with older, age-matched controls and independent of rate-slowing medication use. [7][8][9][10][11]30] Similar to CHF, this is likely to be related to downstream deficits in beta-adrenergic stimulation and/or autonomic dysfunction. [7,8] Data on the relation between the extent of diastolic dysfunction and CI in patients with HFpEF are limited.…”

Section: Discussionmentioning

confidence: 99%

“…[1][2][3] CI is common in patients with cardiovascular disease, produces exercise intolerance, and is an independent predictor of major adverse cardiovascular events and overall mortality even in patients taking drugs that interfere with CI such as beta blockers; [4][5][6] CI is often present in patients with HF, especially in those with preserved ejection fraction (HFpEF), even compared with older, age-matched controls and independent of rate-slowing medication use, and contributes to their prominent exertional symptoms, lower exercise capacity and reduced quality-of-life. [7][8][9][10] Because exercise requires coordinated changes in ventricular function, arterial tone, endothelial function, venous return, and autonomic signalling, CI is one of the mechanisms that are impaired in patients with HFpEF contributing in coordinate fashion to depressed reserve capacity that produce exercise limitation. [9,11] However, recent clinical studies also observed a significant correlation between exercise capacity and diastolic function parameters, i.e.…”

Section: Introductionmentioning

confidence: 99%

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Echocardiographic Predictors of Chronotropic Incompetence to Exercise in Patients with Heart Failure with Preserved Ejection Fraction

Projevska-Donegati

Georgievska-Ismail

2014

Prilozi

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Objective: Exercise intolerance in patients with heart failure with preserved ejection fraction (HFpEF) is most often attributed to diastolic dysfunction (DD); however, chronotropic incompetence (CI) could also play an important role. We intended to examine whether there are predictive echocardiographic parameters of DD for impaired chronotropic response to exercise. Methods and Results: Patients (n = 143) with unexplained dyspnea and/or exercise intolerance who fulfilled clinical and echocardiographic criteria of HFpEF presence underwent a symptom-limited exercise test using a treadmill (ETT) according to the Bruce protocol. CI was defined as an achieved heart rate reserve (HRR) of ≤ 80%. Comparison of the groups with (n = 98) and without CI (n = 45) did not show any statistically significant difference regarding demographic and clinical characterristics except for use of beta blockers (BB) that were more frequently present (p = 0.012) in patients with CI in comparison with those without. Patients with CI had a higher mean E-wave velocity, E/A ratio, increased E/E' septal, lateral as well as average ratio and abnormal IVRT/T E-e' index all consistent with elevated LV filling pressures. E/E' average ratio > 15 was statistically insignificantly more frequently present in patients with CI. In addition, by multivariate stepwise regression analysis value of E' septal (β = 3.697, 95%CI 0.921-6.473, p = 0.009) along with use of BB, current smoking and basal heart rate appeared as statistically significant independent predictors of lower HRR %. Conclusion: Patients with HFpEF frequently have chronotropic incompetence to graded exercise which may partly be predicted with echocardiographic parameters that are consistent with elevated LV filling pressures.

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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Echocardiographic Predictors of Chronotropic Incompetence to Exercise in Patients with Heart Failure with Preserved Ejection Fraction

Projevska-Donegati

Georgievska-Ismail

2014

Prilozi

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“…32) In HFpEF, baroreflex sensitivity is reduced and impaired heart rate recovery. 33,34) Patients with HFpEF have multiple arteriosclerotic risk factors, and stiffened arterial walls in the baroreceptor regions impair baroreflex function.…”

Section: 14-17)mentioning

confidence: 99%

Heart Failure as a Disruption of Dynamic Circulatory Homeostasis Mediated by the Brain

Kishi

2016

Int. Heart J.

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SummaryCirculatory homeostasis is associated with interactions between multiple organs, and the disruption of dynamic circulatory homeostasis could be considered as heart failure. The brain is the central unit integrating neural and neurohormonal information from peripheral organs and controlling peripheral organs using the autonomic nervous system. Heart failure is worsened by abnormal sympathoexcitation associated with baroreflex failure and/or chemoreflex activation, and by vagal withdrawal, and autonomic modulation therapies have benefits for heart failure. Recently, we showed that baroreflex failure induces striking volume intolerance independent of left ventricular dysfunction. Many studies have indicated that an overactive renin-angiotensin system, excess oxidative stress and excess inflammation, and/or decreased nitric oxide in the brain cause sympathoexcitation in heart failure. We have demonstrated that angiotensin II type 1 receptor (AT 1 R)-induced oxidative stress in the rostral ventrolateral medulla (RVLM), which is known as a vasomotor center, causes prominent sympathoexcitation in heart failure model rats. Interestingly, systemic infusion of angiotensin II directly affects brain AT 1 R with sympathoexcitation and left ventricular diastolic dysfunction. Moreover, we have demonstrated that targeted deletion of AT 1 R in astrocytes strikingly improved survival with prevention of left ventricular remodeling and sympathoinhibition in myocardial infarction-induced heart failure. From these results, we believe it is possible that AT 1 R in astrocytes, not in neurons, have a key role in the pathophysiology of heart failure. We would like to propose a novel concept that the brain works as a central processing unit integrating neural and hormonal input, and that the disruption of dynamic circulatory homeostasis mediated by the brain causes heart failure. (Int Heart J 2016; 57: 145-149)

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“…Beta-blockers inconsistentlyinverse these modifications, contracting sympathetic drive and proliferating β-receptor susceptibility. Up-to-the minute HF with conserved LVEF (HFpEF), [19,20] plasma catecholamine concentrations are not elevated; however, even in the lack of epicardial coronary artery disease HFpEF patients do not generally have an increase in EF in reaction to exercise or β-adrenergic stimulation, [20] symptomatic of β-adrenergic receptor desensitization [21].…”

Section: Introductionmentioning

confidence: 99%

A Review study on “The effect of Metoprolol and Losartan on Isoprenaline Induced Heart Failure Mice”.

Nepal¹,

Chen²,

Yasmeen³

et al. 2017

Int. J. Adv. Res. Biol. Sci.

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Heart failure, the one, and only cardiovascular disease is the primary cause of mortality and morbidity with increasing incidence and possess a considerable economic burden. The abrasions seen after Isoprenaline treatment are even more severe than those induced by epinephrine or norepinephrine. This severeness implies that the administration of Isoprenaline diminishes the efficacy of cardiac muscle cells and causes complex biochemical and structural alterations leading to cell damage and necrosis. Moreover, the abrasions demonstrated that ACE inhibitors reduce blood pressure, enhance left ventricular hypertrophy, decrease morbidity and mortality in cardiac failure, and inhibit progression to explicit cardiac failure in patients with depressed ventricular function or myocardial infarction. On the other hand, Beta-blockers decrease heart rate, lower blood pressure and cardiac contractility prominent to diminished oxygen consumption which may, in turn, stimulate the metoprolol-induced enhancement in function and structure.

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Impaired Heart Rate Recovery and Chronotropic Incompetence in Patients With Heart Failure With Preserved Ejection Fraction

Cited by 180 publications

References 39 publications

Echocardiographic Predictors of Chronotropic Incompetence to Exercise in Patients with Heart Failure with Preserved Ejection Fraction

Echocardiographic Predictors of Chronotropic Incompetence to Exercise in Patients with Heart Failure with Preserved Ejection Fraction

Heart Failure as a Disruption of Dynamic Circulatory Homeostasis Mediated by the Brain

A Review study on “The effect of Metoprolol and Losartan on Isoprenaline Induced Heart Failure Mice”.

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