Rapid fall in sympathetic nerve hyperactivity in patients with heart failure after cardiac transplantation

Rundqvist, Bengt; Casale, Roberto; Bergmann-Sverrisdottir, Yrsa; Friberg, Peter; Mortara, Andrea; Elam, I Mikael

doi:10.1016/s1071-9164(97)90005-1

Cited by 18 publications

(18 citation statements)

References 16 publications

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“…However, sympathoexcitation as a compensatory response, elicited by still-functioning baroreceptors sensing an increasingly lowered blood pressure, may contribute. The improved hemodynamic situation and the normalization of baroreflex function within weeks after HTx 31 could both be responsible for the rapid postoperative reduction in MSNA 15 and the normalization of MSNA burst amplitude distribution shown in this study.…”

Section: Burst Amplitude Distribution Illustrates Sympathoexcitation mentioning

confidence: 56%

“…However, reciprocal changes in MSNA median burst amplitude and blood pressure during pharmacological baroreflex provocations have been demonstrated in normal subjects with intact baroreflex function. 6 The present data include reanalysis of several previous studies from our laboratory, 15,16,18 precluding the addition of a baroreflex test, and we base our suggestion of baroreflex involvement on the previously published evidence for decreased baroreflex control of sympathetic outflow in CHF that is normalized after HTx and on the evidence for normal sympathetic baroreflex control in aging. Baroreflex control of MSNA is usually investigated with short-term pharmacological interventions, raising blood pressure with phenylephrine and/or lowering blood pressure with nitroprusside.…”

Section: Study Limitationsmentioning

confidence: 77%

“…15 The patients in the severe CHF group were classified as being in NYHA functional class IIIB to IV, 5 with coronary artery disease and 7 with idiopathic dilated cardiomyopathy.…”

Section: Cardiac Transplant Recipientsmentioning

confidence: 99%

“…The first condition was CHF, in which increased MSNA burst frequency is a well-established finding 7,8 considered to be at least partly elicited peripherally by malfunctioning baroreflex mechanisms. 9,10 Because several studies have shown that the sympathoexcitation in CHF is normal-ized after orthotopic heart transplantation, [11][12][13][14][15] we also analyzed the burst amplitude distribution before and after transplantation. The second group consisted of patients with pituitary deficiency and untreated growth hormone deficiency (GHD), a neuroendocrine disease recently shown to be associated with increased MSNA burst frequency, in all probability of central origin.…”

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confidence: 99%

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Sympathetic Neural Burst Amplitude Distribution

et al. 2000

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Background —Human muscle sympathetic nerve activity (MSNA) is usually measured as the number of pulse-synchronous bursts in multiunit mean voltage recordings. We recently suggested burst amplitude distribution as a more sensitive indicator of altered MSNA in congestive heart failure (CHF). Here, we test whether this distribution can discriminate between different conditions with increased MSNA burst frequency and whether it reflects single vasoconstrictor fiber firing intensity. Methods and Results —We analyzed resting multiunit MSNA in 36 CHF patients (24 with mild to moderate CHF, 12 with severe CHF investigated before and after heart transplantation), 14 patients with pituitary deficiency, 25 matched healthy control subjects, and an additional 56 healthy men with a wider age range (21 to 71 years). Pituitary deficiency was associated with increased MSNA burst frequency (60 versus 37 bursts/min in control subjects), equivalent to that in mild to moderate CHF (61 bursts/min). However, burst amplitude distribution in hypopituitary patients (median burst amplitude, 37%) did not deviate from matched control subjects (36%), whereas amplitudes increased with disease severity in CHF (43% in mild to moderate, 52% in severe) and normalized after transplantation (36%). In the larger healthy group, MSNA burst frequency increased with age, and burst amplitude distribution remained unaffected. In 8 CHF patients, single-unit firing frequency showed a close positive relationship to multiunit burst amplitude distribution ( r =0.82, P <0.01) but none to burst frequency ( r =0.39, P =0.3). Conclusions —Muscle vasoconstrictor fiber activity is better reflected by multiunit MSNA burst amplitude distribution than by burst frequency, at least in CHF. This distribution can discriminate between conditions with increased burst frequency.

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Section: Burst Amplitude Distribution Illustrates Sympathoexcitation mentioning

confidence: 56%

Section: Study Limitationsmentioning

confidence: 77%

“…15 The patients in the severe CHF group were classified as being in NYHA functional class IIIB to IV, 5 with coronary artery disease and 7 with idiopathic dilated cardiomyopathy.…”

Section: Cardiac Transplant Recipientsmentioning

confidence: 99%

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confidence: 99%

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Sympathetic Neural Burst Amplitude Distribution

et al. 2000

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“…The reduction was similar in those patients who became hypertensive compared to those who were normotensive following transplantation. 82 Andreassen and colleagues 83 used the Valsalva manoeuvre and cold pressor test to stimulate sympathetic neural outflow and a vasodilator test that is dependent on the presence of a functionally intact endothelium (postocclusive hyperaemia) in 16 cardiac transplant and matched healthy controls. They found endothelial dysfunction in transplant recipients on cyclosporin with intact functional capacity of the sympathetic nervous system.…”

Section: Cyclosporin and Vasodilator Activitymentioning

confidence: 99%

Hypertension in thoracic transplant recipients

Jenkins

Singer

1998

J Hum Hypertens

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There are many mechanisms underlying the hypertension which occurs after thoracic transplantation. Previous disease, effects of cyclosporin, tacrolimus and steroid immunosuppression and cardiac denervation are major contributory factors. Abnormal sodium and water balance is an important common mediating factor. A new approach is clearly needed for classifying the severity of hypertension in these patients taking into account day-night variation and total blood pressure

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Sympathetic vasoconstrictor activity before and after left ventricular assist device implantation in patients with end‐stage heart failure

Heusser

Wittkoepper

Bara

et al. 2021

European J of Heart Fail

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Aims Sympathetic overactivity, which predicts poor outcome in patients with heart failure, normalizes following cardiac transplantation. We tested the hypothesis that haemodynamic improvement following left ventricular assist device (LVAD) implantation is also associated with reductions in centrally generated sympathetic activity. Methods and results In eight patients with heart failure (two women, six men, age 44–66 years), we continuously recorded electrocardiogram, beat‐to‐beat finger blood pressure, respiration, and muscle sympathetic nerve activity (MSNA) before and after implantation of the continuous‐flow LVAD devices HeartWare HVAD (n = 4) and HeartMate II (n = 2), and the non‐continuous‐flow device HeartMate 3 (n = 2). LVAD implantation increased cardiac output by 1.29 ± 0.88 L/min (P = 0.060) and mean arterial pressure by 16.2 ± 7.9 mmHg (P < 0.001), while reducing pulse pressure by 25.3 ± 9.8 mmHg (P < 0.001). LVAD implantation did not change MSNA burst frequency (−1.3 ± 7.5 bursts/min, P = 0.636), total activity (+0.62 ± 1.83 au, P = 0.369), or normalized activity (+0.63 ± 4.23, P = 0.685). MSNA burst incidence was decreased (−7.8 ± 9.3 bursts/100 heart beats, P = 0.049). However, cardiac ectopy altered MSNA bursting patterns that could be mistaken for sympatholysis. Conclusion Implantation of current design LVAD does not consistently normalize sympathetic activity in patients with end‐stage heart failure despite haemodynamic improvement.

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Rapid fall in sympathetic nerve hyperactivity in patients with heart failure after cardiac transplantation

Cited by 18 publications

References 16 publications

Sympathetic Neural Burst Amplitude Distribution

Sympathetic Neural Burst Amplitude Distribution

Hypertension in thoracic transplant recipients

Sympathetic vasoconstrictor activity before and after left ventricular assist device implantation in patients with end‐stage heart failure

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