Heart Rate and Heart Failure  - Not a Simple Relationship -

Heusch, Gerd

doi:10.1253/circj.cj-10-0925

Cited by 54 publications

(19 citation statements)

References 134 publications

(65 reference statements)

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“…Although chronic elevations in HR can contribute to stress-related illness such as cardiovascular disease [72, 73], the elevation in heart rate in rats exposed to controllable stress was temporary since within 48 hours after stress the heart rate in rats with control had almost returned to pre-stress levels (Figure 4B, Day 2). It is possible that the temporary elevation in HR following ES reflects an adaptive, preparatory response to facilitate fighting or fleeing from subsequent challenges.…”

Section: Discussionmentioning

confidence: 99%

Effects of stressor controllability on diurnal physiological rhythms

Thompson

Christianson

Maslanik

et al. 2013

Physiology & Behavior

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Disruptions in circadian and diurnal rhythms are associated with stress-related psychiatric disorders and stressor exposure can disrupt these rhythms. The controllability of the stressor can modulate various behavioral and neurochemical responses to stress. Uncontrollable, but not controllable, stress produces behaviors in rats that resemble symptoms of anxiety and depression. Whether acute stress-induced disruptions in physiological rhythms are sensitive to controllability of the stressor, however, remains unknown. To examine the role of controllability in diurnal rhythm disruption, adult male Sprague Dawley rats were implanted with Data Sciences International (DSI) biotelemetry devices. Real-time measurements were obtained before, during and after exposure to a controllable or yoked uncontrollable stressor. Controllable and uncontrollable stress equally disrupted diurnal rhythms of locomotor activity and body temperature but not heart rate. The diurnal heart rate the day following stressor exposure was flattened to a greater extent and was significantly higher in rats with control over stress suggesting a relationship between stressor controllability and the heart rate response. Our results are consistent with the conclusion that acute stress-induced disruptions in diurnal physiological rhythms likely contribute little to the behavioral and affective consequences of stress that are sensitive to stressor controllability.

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Section: Discussionmentioning

confidence: 99%

Effects of stressor controllability on diurnal physiological rhythms

Thompson

Christianson

Maslanik

et al. 2013

Physiology & Behavior

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“…A well-established large animal model of HF, induced by continuous cardiac pacing at a frequency three- to fourfold higher than the spontaneous heart rate, is mostly applied to dogs, pigs, sheep, and monkeys [15, 34]. One characteristic of this model is the presence of regional differences in functional and molecular remodeling.…”

Section: Introductionmentioning

confidence: 99%

Cell-to-cell variability in troponin I phosphorylation in a porcine model of pacing-induced heart failure

et al. 2012

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We tested the hypothesis that myocardial contractile protein phosphorylation and the Ca2+ sensitivity of force production are dysregulated in a porcine model of pacing-induced heart failure (HF). The level of protein kinase A (PKA)-dependent cardiac troponin I (TnI) phosphorylation was lower in the myocardium surrounding the pacing electrode (pacing site) of the failing left ventricle (LV) than in the controls. Immunohistochemical assays of the LV pacing site pointed to isolated clusters of cardiomyocytes exhibiting a reduced level of phosphorylated TnI. Flow cytometry on isolated and permeabilized cardiomyocytes revealed a significantly larger cell-to-cell variation in the level of TnI phosphorylation of the LV pacing site than in the opposite region in HF or in either region in the controls: the interquartile range (IQR) on the distribution histogram of relative TnI phosphorylation was wider at the pacing site (IQR = 0.53) than that at the remote site of HF (IQR = 0.42; P = 0.0047) or that of the free wall of the control animals (IQR = 0.36; P = 0.0093). Additionally, the Ca2+ sensitivities of isometric force production were higher and appeared to be more variable in single permeabilized cardiomyocytes from the HF pacing site than in the healthy myocardium. In conclusion, the level of PKA-dependent TnI phosphorylation and the Ca2+ sensitivity of force production exhibited a high cell-to-cell variability at the LV pacing site, possibly explaining the abnormalities of the regional myocardial contractile function in a porcine model of pacing-induced HF.Electronic supplementary materialThe online version of this article (doi:10.1007/s00395-012-0244-x) contains supplementary material, which is available to authorized users.

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“…A retrospective subgroup analysis demonstrated that the benefit of ivabradine treatment in terms of reduced mortality and hospitalization for acute MI in patients with anginal symptoms, LV dysfunction, and heart rate greater than 70 bpm was much larger than to be expected from a modest (at most 7 bpm) placebo‐corrected heart rate reduction alone 44, 45. In SHIFT, however, the benefit from ivabradine correlated with the magnitude of HR reduction 4, 46. In order to elucidate the effects of ivabradine on LV remodeling beyond pure heart rate reduction, a remodeling study could be performed in paced ivabradine‐treated animals 47…”

Section: Discussionmentioning

confidence: 99%

Heart Rate Reduction With Ivabradine Protects Against Left Ventricular Remodeling by Attenuating Infarct Expansion and Preserving Remote‐Zone Contractile Function and Synchrony in a Mouse Model of Reperfused Myocardial Infarction

O’Connor

Smith

Piras

et al. 2016

JAHA

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BackgroundIvabradine selectively inhibits the pacemaker current of the sinoatrial node, slowing heart rate. Few studies have examined the effects of ivabradine on the mechanical properties of the heart after reperfused myocardial infarction (MI). Advances in ultrasound speckle‐tracking allow strain analyses to be performed in small‐animal models, enabling the assessment of regional mechanical function.Methods and ResultsAfter 1 hour of coronary occlusion followed by reperfusion, mice received 10 mg/kg per day of ivabradine dissolved in drinking water (n=10), or were treated as infarcted controls (n=9). Three‐dimensional high‐frequency echocardiography was performed at baseline and at days 2, 7, 14, and 28 post‐MI. Speckle‐tracking software was used to calculate intramural longitudinal myocardial strain (Ell) and strain rate. Standard deviation time to peak radial strain (SD Tpeak Err) and temporal uniformity of strain were calculated from short‐axis cines acquired in the left ventricular remote zone. Ivabradine reduced heart rate by 8% to 16% over the course of 28 days compared to controls (P<0.001). On day 28 post–MI, the ivabradine group was found to have significantly smaller end‐systolic volumes, greater ejection fraction, reduced wall thinning, and greater peak Ell and Ell rate in the remote zone, as well as globally. Temporal uniformity of strain and SD Tpeak Err were significantly smaller in the ivabradine‐treated group by day 28 (P<0.05).ConclusionsHigh‐frequency ultrasound speckle‐tracking demonstrated decreased left ventricular remodeling and dyssynchrony, as well as improved mechanical performance in remote myocardium after heart rate reduction with ivabradine.

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Heart Rate and Heart Failure - Not a Simple Relationship -

Cited by 54 publications

References 134 publications

Effects of stressor controllability on diurnal physiological rhythms

Effects of stressor controllability on diurnal physiological rhythms

Cell-to-cell variability in troponin I phosphorylation in a porcine model of pacing-induced heart failure

Heart Rate Reduction With Ivabradine Protects Against Left Ventricular Remodeling by Attenuating Infarct Expansion and Preserving Remote‐Zone Contractile Function and Synchrony in a Mouse Model of Reperfused Myocardial Infarction

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