Heart-brain interactions in patients with heart failure, including takotsubo syndrome: a need to monitor autonomic sympathetic activity: reply

The upper limit of incidence of muscle sympathetic neural bursts can lead to underestimation of sympathetic activity in patients with severe heart failure. This study aimed to evaluate the pulse-synchronous burst power of muscle sympathetic nerve activity (MSNA) as a more specific indicator that could discriminate sympathetic activity in patients with heart failure. In 54 patients with heart failure, the pulse-synchronous burst power at the mean heart rate was quantified by spectral analysis of MSNA. Thirteen patients received a central sympatholytic agent (guanfacine) for 5 days to validate the feasibility of this new index. Both burst incidence and plasma norepinephrine level showed no significant difference between patients in New York Heart Association functional class III (94 ± 6 per 100 heartbeats and 477 ± 219 pg/ml, respectively) and class II (79 ± 14 per 100 heartbeats and 424 ± 268 pg/ml, respectively). In contrast, the burst power was useful for discriminating patients in class III from those in class II (61 ± 8% vs. 39 ± 10%; P < 0.05). Inhibition of sympathetic nerve activity by guanfacine was more sensitively reflected by the change of burst power (−36 ± 25%) than by that of burst incidence (−12 ± 14%; P < 0.001). The sympathetic burst power reflects both burst frequency and amplitude independently of the absolute values and provides a sensitive new index for interindividual comparisons of sympathetic activity in patients with heart failure.

Download Full-text

Effectiveness of inspiratory muscle training associated with a cardiac rehabilitation program on sympathetic activity and functional capacity in patients with heart failure: a study protocol for a randomized controlled trial

Trials ◽

10.1186/s13063-020-04363-6 ◽

2020 ◽

Vol 21 (1) ◽

Author(s):

Jéssica Costa Leite ◽

Daniella Cunha Brandão ◽

Simone Cristina Soares Brandão ◽

Helen Kerlen Bastos Fuzari ◽

Tainá Maria Vidal ◽

...

Keyword(s):

Heart Failure ◽

Randomized Controlled Trial ◽

Functional Capacity ◽

Sympathetic Activity ◽

Controlled Trial ◽

Rehabilitation Program ◽

Cardiac Rehabilitation Program ◽

Muscle Training ◽

Randomized Controlled ◽

Patients With Heart Failure

Download Full-text

Statin therapy and cardiac sympathetic activity in patients with heart failure: A 123Iodine-metaiodobenzylguanidine myocardial scintigraphy study

International Journal of Cardiology ◽

10.1016/j.ijcard.2014.07.243 ◽

2014 ◽

Vol 176 (3) ◽

pp. 1181-1183 ◽

Cited By ~ 1

Author(s):

Igor A. Fernandes ◽

Lauro C. Vianna ◽

Raphael A. Freitas ◽

Sandra Marina Miranda ◽

Evandro Tinoco Mesquita ◽

...

Keyword(s):

Heart Failure ◽

Statin Therapy ◽

Sympathetic Activity ◽

Myocardial Scintigraphy ◽

Cardiac Sympathetic Activity ◽

Patients With Heart Failure

Download Full-text

Acute effects of angiotensin-converting enzyme inhibition versus angiotensin II receptor blockade on cardiac sympathetic activity in patients with heart failure

AJP Regulatory Integrative and Comparative Physiology ◽

10.1152/ajpregu.00095.2017 ◽

2017 ◽

Vol 313 (4) ◽

pp. R410-R417 ◽

Cited By ~ 3

Author(s):

Eduardo R. Azevedo ◽

Susanna Mak ◽

John S. Floras ◽

John D. Parker

Keyword(s):

Heart Failure ◽

Angiotensin Ii ◽

Angiotensin Converting Enzyme ◽

Sympathetic Activity ◽

Ang Ii ◽

Converting Enzyme ◽

Acute Effects ◽

Beneficial Effects ◽

Patients With Heart Failure ◽

Total Body

The beneficial effects of angiotensin-converting enzyme (ACE) inhibitors and angiotensin II (ANG II) receptor antagonists in patients with heart failure secondary to reduced ejection fraction (HFrEF) are felt to result from prevention of the adverse effects of ANG II on systemic afterload and renal homeostasis. However, ANG II can activate the sympathetic nervous system, and part of the beneficial effects of ACE inhibitors and ANG II antagonists may result from their ability to inhibit such activation. We examined the acute effects of the ACE inhibitor captopril (25 mg, n = 9) and the ANG II receptor antagonist losartan (50 mg, n = 10) on hemodynamics as well as total body and cardiac norepinephrine spillover in patients with chronic HFrEF. Hemodynamic and neurochemical measurements were made at baseline and at 1, 2, and 4 h after oral dosing. Administration of both drugs caused significant reductions in systemic arterial, cardiac filling, and pulmonary artery pressures ( P < 0.05 vs. baseline). There was no significant difference in the magnitude of those hemodynamic effects. Plasma concentrations of ANG II were significantly decreased by captopril and increased by losartan ( P < 0.05 vs. baseline for both). Total body sympathetic activity increased in response to both captopril and losartan ( P < 0.05 vs. baseline for both); however, there was no change in cardiac sympathetic activity in response to either drug. The results of the present study do not support the hypothesis that the acute inhibition of the renin-angiotensin system has sympathoinhibitory effects in patients with chronic HFrEF.

Download Full-text

Decreased renal sympathetic activity in response to cardiac unloading with nitroglycerin in patients with heart failure*

European Journal of Heart Failure ◽

10.1016/j.ejheart.2004.11.001 ◽

2005 ◽

Vol 7 (6) ◽

pp. 1003-1010 ◽

Cited By ~ 10

Author(s):

Magnus Petersson ◽

Peter Friberg ◽

Gavin Lambert ◽

Bengt Rundqvist

Keyword(s):

Heart Failure ◽

Sympathetic Activity ◽

Patients With Heart Failure ◽

Cardiac Unloading ◽

Renal Sympathetic

Download Full-text

Abstract 2404: Sympathetic Cardiorenal Interaction Becomes Exaggerated When Cardiac and Renal Functions Are Both Deteriorated

Circulation ◽

10.1161/circ.118.suppl_18.s_719-b ◽

2008 ◽

Vol 118 (suppl_18) ◽

Author(s):

Yoshitaka Oda ◽

Shuji Joho ◽

Tadakazu Hirai ◽

Hidetsugu Asanoi ◽

Hiroshi Inoue

Keyword(s):

Heart Failure ◽

Cardiac Dysfunction ◽

Sympathetic Activity ◽

Plasma Norepinephrine ◽

Renal Functions ◽

Patients With Heart Failure ◽

Muscle Nerve ◽

The Difference ◽

Estimated Glomerular Filtration Rates ◽

Resting Muscle

The pathophysiology of the cardiorenal interaction remains poorly understood. We tested the hypothesis that renal insufficiency (RI) and cardiac dysfunction would contribute to the elevated sympathetic activity in patients with heart failure. In 79 patients with heart failure (ejection fraction (EF) < 0.45), the resting muscle nerve sympathetic activity (MSNA), plasma norepinephrine (NE), brain natriuretic peptide (BNP) were determined. Estimated glomerular filtration rates (eGFR) less than 60ml/min/1.73m 2 measured by simplified Modification of Diet in Renal Disease equation for Japanese was used to identify RI. Although NE and BNP were comparable between RI group (n = 30, eGFR 45 ± 10) and no RI group (n = 49, eGFR 76 ± 10), MSNA was higher in RI group (burst rate, 54 ± 14 versus 46 ± 14 bursts/minute, p < 0.05; burst incidence, 77 ± 19 versus 68 ± 18 bursts/100beats, p < 0.05). For patients with preserved EF (≥ 0.30), MSNA was similar between those with and without RI, while for patients with low EF (< 0.30), MSNA was significantly higher in those with RI than in those without RI (burst rate, 62 ± 10 versus 49 ± 15 bursts/minute, p < 0.01; burst incidence, 88 ± 12 versus 68 ± 18 bursts/ 100beats, p < 0.01). The difference of MSNA between patients with low EF and with preserved EF was significantly greater in RI group than in no RI group (interaction, p < 0.05). These findings suggest that sympathetic cardiorenal interaction might become exaggerated when cardiac and renal functions are both deteriorated.

Download Full-text