Dissociation between reflex sympathetic and forearm vascular responses to lower body negative pressure in heart failure patients with coronary artery disease

2009 ◽  
Vol 297 (5) ◽  
pp. H1760-H1766 ◽  
Author(s):  
Catherine F. Notarius ◽  
Beverley L. Morris ◽  
John S. Floras
Keyword(s):  
Heart Failure ◽  
Negative Pressure ◽  
Lower Body Negative Pressure ◽  
Muscle Sympathetic Nerve Activity ◽  
Left Ventricular ◽  
Left Ventricular Ejection ◽  
Plasma Norepinephrine ◽  
Lower Body ◽  
Ventricular Ejection Fraction ◽  
Vascular Responses

Many heart failure (HF) patients exhibit paradoxical forearm vasodilation when central blood volume is reduced by lower body negative pressure (LBNP). We tested the hypothesis that this response results from reflex sympathetic withdrawal. We recorded simultaneously forearm blood flow, muscle sympathetic nerve activity (MSNA), and plasma norepinephrine (PNE) during four random applications of LBNP, −5, −10, −20, and −40 mmHg, in 12 men with HF (mean left ventricular ejection fraction = 24 ± 2%) and 10 healthy, normal, age-matched men (N). Compared with N, MSNA burst frequency ( P = 0.001) and PNE ( P = 0.005) were significantly higher in the HF group, both at rest and during LBNP. As anticipated in N, LBNP −40 mmHg significantly increased MSNA (+14.2 ± 2.5 bursts/min; P < 0.05) and PNE (+0.83 ± 0.22 nmol/l; P < 0.05) and decreased forearm vascular conductance (FVC) (−11.7 ± 3.2 ml·min−1·mmHg−1; P < 0.05). In the HF group, LBNP elicited similar increases in MSNA (+11.5 ± 2.0; P < 0.05) and PNE (+0.85 ± 0.12; P < 0.05), without affecting FVC significantly (−4.1 ± 2.4; P = 0.01 vs. N, interaction P = 0.03). However, within the HF group, responses were bimodal: LBNP −40 mmHg increased MSNA in all subjects ( P < 0.001), yet the six patients with nonischemic or dilated cardiomyopathy (DCM) exhibited significant vasoconstriction (decrease in FVC; P = 0.001), whereas the six patients with ischemic cardiomyopathy (ICM) exhibited significant vasodilation (increase in FVC; P < 0.02 vs. DCM and N; interaction P = 0.02). Cold pressor testing increased MSNA and decreased FVC in ICM ( n = 4). Thus paradoxical forearm vasodilator responses to LBNP in HF are not mediated by reflex sympathetic withdrawal. ICM and DCM patients differ qualitatively in their vascular responses to hypotensive LBNP.

scholarly journals Training heart failure patients with reduced ejection fraction attenuates muscle sympathetic nerve activation during mild dynamic exercise

2019 ◽  
Vol 317 (4) ◽  
pp. R503-R512 ◽  
Author(s):  
Catherine F. Notarius ◽  
Philip J. Millar ◽  
Daniel A. Keir ◽  
Hisayoshi Murai ◽  
Nobuhiko Haruki ◽  
...  
Keyword(s):  
Heart Failure ◽  
Ejection Fraction ◽  
Sympathetic Nerve ◽  
Muscle Sympathetic Nerve Activity ◽  
Reactive Hyperemia ◽  
Left Ventricular ◽  
Left Ventricular Ejection ◽  
Ventricular Ejection Fraction ◽  
Muscle Metaboreflex ◽  
Reduced Ejection Fraction

Muscle sympathetic nerve activity (MSNA) decreases during low-intensity dynamic one-leg exercise in healthy subjects but increases in patients with heart failure with reduced ejection fraction (HFrEF). We hypothesized that increased peak oxygen uptake (V̇o2peak) after aerobic training would be accompanied by less sympathoexcitation during both mild and moderate one-leg dynamic cycling, an attenuated muscle metaboreflex, and greater skin vasodilation. We studied 27 stable, treated HFrEF patients (6 women; mean age: 65 ± 2 SE yr; mean left ventricular ejection fraction: 30 ± 1%) and 18 healthy age-matched volunteers (6 women; mean age: 57 ± 2 yr). We assessed V̇o2peak (open-circuit spirometry) and the skin microcirculatory response to reactive hyperemia (laser flowmetry). Fibular MSNA (microneurography) was recorded before and during one-leg cycling (2 min unloaded and 2 min at 50% of V̇o2peak) and, to assess the muscle metaboreflex, during posthandgrip ischemia (PHGI). HFrEF patients were evaluated before and after 6 mo of exercise-based cardiac rehabilitation. Pretraining V̇o2peak and skin vasodilatation were lower ( P < 0.001) and resting MSNA higher ( P = 0.01) in HFrEF than control subjects. Training improved V̇o2peak (+3.0 ± 1.0 mL·kg−1·min−1; P < 0.001) and cutaneous vasodilation and diminished resting MSNA (−6.0 ± 2.0, P = 0.01) plus exercise MSNA during unloaded (−4.0 ± 2.5, P = 0.04) but not loaded cycling (−1.0 ± 4.0 bursts/min, P = 0.34) and MSNA during PHGI ( P < 0.05). In HFrEF patients, exercise training lowers MSNA at rest, desensitizes the sympathoexcitatory metaboreflex, and diminishes MSNA elicited by mild but not moderate cycling. Training-induced downregulation of resting MSNA and attenuated reflex sympathetic excitation may improve exercise capacity and survival.

Abstract 15563: Neurovascular Control and Spontaneous Baroreflex Sensitivity in Heart Failure Patients with Preserved Ejection Fraction

Circulation ◽  
2014 ◽  
Vol 130 (suppl_2) ◽  
Author(s):  
Ana Luiza C Sayegh ◽  
Marcelo R dos Santos ◽  
Francis R de Souza ◽  
Vera Maria C Salemi ◽  
Carlos Augusto P Oliveira ◽  
...  
Keyword(s):  
Heart Failure ◽  
Ejection Fraction ◽  
Baroreflex Sensitivity ◽  
Muscle Sympathetic Nerve Activity ◽  
Left Ventricular ◽  
Left Ventricular Ejection ◽  
Normal Ejection Fraction ◽  
Preserved Ejection Fraction ◽  
Ventricular Ejection Fraction ◽  
Spontaneous Baroreflex

Introduction: Muscle sympathetic nerve activity (MSNA) and forearm blood flow (FBF) are markers of mortality in Systolic Heart Failure (S-HF). Endomyocardial Fibrosis (EMF) is a Heart Failure (HF) with Preserved Ejection Fraction (PEF-HF). Although mortality in PEF-HF can be similar to S-HF, it is still unknown if neurovascular control is impaired in PEF-HF. Hypothesis: Our hypothesis is that even though PEF-HF show normal ejection fraction, they have the same autonomic dysfunction as S-HF. The aim was to evaluate MSNA, FBF and spontaneous baroreflex sensitivity (SBS) in PEF-HF compared to S-HF and healthy subjects (HS). Methods: Nineteen females HF, NYHA class II and III, were divided in two groups: PEF-HF (n=10) and S-HF (n=9), and were compared to HS (n=7). Left Ventricular Ejection Fraction (LVEF), by echocardiography (Simpson); MSNA, by microneurography; FBF, by venous occlusion plethysmography; mean blood pressure (MBP) and heart rate (HR) by Finometer; SBS, by sequence method, were measured. Significance was considered p<0.05. Results: Age was not different between PEF-HF, S-HF and HS (57±2 vs. 55±2 vs. 52±1 years; p<0.15, respectively). LVEF was higher in PEF-HF and HS compared to S-HF (55±3 vs. 65±1 vs. 33±2%; p<0.02, respectively). MSNA in bursts per minute (35±3 vs. 40±2 vs. 20±1 bursts/min; p<0.001) and MSNA per 100 heart beats (50±4 vs. 57±3 vs. 26±2 bursts/100 HB; p<0.001) were higher in PEF-HF and S-HF compared to HS, respectively. FBF was lower in PEF-HF and S-HF compared to HS (1.45±0.2 vs. 1.78±0.3 vs. 2.70±0.3 ml/min/100ml; p<0.047). Forearm vascular conductance was lower in PEF-HF compared to HS (1.63±0.2 vs. 2.98±0.3 units; p<0.008) but PEF-HF was not different compared to S-HF (1.63±0.2 vs. 2.04±0.3 units; p<0.28). MBP (92±3 vs. 89±4 vs. 92±4 mmHg; p=0.87) and HR (71±3 to 70±3 vs. 75±3 beats/min; p<0.46) were not different between groups. However, SBS was not different between PEF-HF and S-HF (2.3±0.5 vs. 6.9±4.4 ms/mmHg; p=0.089, respectively) but PEF-HF was lower when compared to HS (2.3±0.5 vs. 8.1±0.7 ms/mmHg; p=0.047, respectively). Conclusion: These results point out that even though PEF-HF have a normal ejection fraction, they showed neurovascular control as impaired as S-HF with lower SBS compared to HS.

Effects of beta-blockade on neurohumoral responses and neurochemical markers in pacing-induced heart failure

1994 ◽  
Vol 266 (2) ◽  
pp. H468-H475 ◽  
Author(s):  
J. M. Levett ◽  
C. C. Marinelli ◽  
D. D. Lund ◽  
B. J. Pardini ◽  
S. Nader ◽  
...  
Keyword(s):  
Heart Failure ◽  
High Plasma ◽  
Left Ventricular ◽  
Left Ventricular Ejection ◽  
Control Group ◽  
Beta Blockade ◽  
Plasma Norepinephrine ◽  
Adrenergic Blockade ◽  
Ventricular Ejection Fraction ◽  
Cardiac Denervation

We investigated neurohumoral profiles and transmitter and neuroenzyme markers of cardiac autonomic innervation in control (unpaced) dogs and three groups of dogs with pacing-induced heart failure (paced, paced + beta-adrenergic blockade, and paced + cardiac denervation). Left ventricular ejection fraction decreased significantly and to a comparable extent in all paced groups. Pacing increased plasma norepinephrine (NE); increases in NE were not attenuated but instead tended to be exaggerated by treatment with propranolol or cardiac denervation. Atrial hypertrophy occurred in all paced groups compared with the control group. However, atrial and right ventricular hypertrophy were not as pronounced in the paced plus cardiac denervation group as in the paced and paced plus propranolol groups. Pacing also depleted neuropeptide Y and NE from all heart chambers; propranolol treatment did not modify these local tissue changes. Pacing caused selective depletion of neuroenzymes predominantly in the left ventricle; again, propranolol did little to modify these changes. In this study of paced animals with experimentally maintained cardiac dysfunction, failure to modify noradrenergic responses with intrapericardial cardiac denervation suggests that noncardiac sources contribute predominantly to high plasma NE. Failure to modify neurohumoral, neuropeptide, and neuroenzyme responses with beta-antagonist suggests this treatment has little practical direct influence on sympathetic vasomotor activity or neuronal function in heart failure.

scholarly journals Prostaglandin modulation of venoconstriction to physiological stress in normals and heart failure patients

2003 ◽  
Vol 284 (3) ◽  
pp. H790-H797 ◽  
Author(s):  
T. Nancy Dzeka ◽  
J. Malcolm O. Arnold
Keyword(s):  
Heart Failure ◽  
Mental Arithmetic ◽  
Physiological Stress ◽  
Lower Body Negative Pressure ◽  
Cold Pressor Test ◽  
Cold Pressor ◽  
Left Ventricular ◽  
Left Ventricular Ejection ◽  
Ventricular Ejection Fraction ◽  
Hand Vein

Prostaglandins released from blood vessels modulate vascular tone, and inhibition of their production during exogenous infusions of catecholamines causes increased venoconstriction. To determine the influence of prostaglandin production on venoconstriction during physiological stimuli known to cause sympathetic activation, and to assess its importance in chronic heart failure (CHF), we studied 11 normal subjects (62 ± 4 yr) and 14 patients with CHF (64 ± 2 yr, left ventricular ejection fraction 23 ± 1%, New York Heart Association classes II and III) (means ± SE). Dorsal hand vein distension was measured during mental arithmetic (MA), cold pressor test (CPT), and lower body negative pressure (LBNP; −10 and −40 mmHg), with saline infusion in one hand and local indomethacin (cyclooxygenase inhibitor) infusion (3 μg/min) in the other. Acetylcholine (0.01–1 nmol/min) dilated veins preconstricted with PGF2α in normals but, consistent with endothelial dysfunction, barely did so in CHF patients ( P = 0.001). Nonendothelial venodilation to sodium nitroprusside (0.3–10 nmol/min) was not different between normals and CHF patients. Resting venous norepinephrine levels were higher in CHF patients (2,812 ± 420 pmol/l) than normals (1,418 ± 145 pmol/l, P = 0.007). In normals, indomethacin caused increased venoconstriction to MA (from 4.9 ± 1.5 to 19.2 ± 4.5%, P = 0.022) and CPT (from 2.9 ± 3.8 to 17.6 ± 4.2%, P = 0.007). In CHF, indomethacin caused increased venoconstriction to MA (from 6.6 ± 3.9% to 19.0 ± 4.5%, P = 0.014), CPT (from 9.6 ± 2.1% to 20.1 ± 3.7%, P = 0.001), and −40 mmHg LBNP (from 10.7 ± 3.0% to 23.2 ± 3.8%, P= 0.041). Control responses for all tests were not different between normals and CHF patients. The effects of indomethacin on venoconstriction to MA and CPT were not different between normals and CHF patients, but venoconstriction to −40 mmHg LBNP was accentuated in CHF patients ( P = 0.036). Inhibition of prostaglandins by indomethacin significantly enhances hand vein constriction to physiological stimuli in both normals and CHF patients, although a differential effect exists for LBNP.

Modulation of neurohormonal activity after treatment of children in heart failure with carvedilol

2003 ◽  
Vol 13 (4) ◽  
pp. 333-336 ◽  
Author(s):  
Alessandro Giardini ◽  
Roberto Formigari ◽  
Gabriele Bronzetti ◽  
Daniela Prandstraller ◽  
Andrea Donti ◽  
...  
Keyword(s):  
Heart Failure ◽  
Left Ventricular Function ◽  
Ventricular Function ◽  
Standard Treatment ◽  
Left Ventricular ◽  
Muscle Disease ◽  
Left Ventricular Ejection ◽  
Plasma Norepinephrine ◽  
Neurohormonal Activation ◽  
Ventricular Ejection Fraction

Background:In adults with heart failure, neurohormonal overstimulation is related to the progression of the disease, and influences prognosis. β-blockers, which modulate neurohormonal activation, now play an essential role in the pharmacological management of heart failure in adults, but their use in children is very limited.Patients and Methods:To investigate the effects of carvedilol administration on neurohormonal activation and left ventricular function, carvedilol was added to standard treatment for heart failure in 9 patients with dilated cardiomyopathy due to heart muscle disease. Standard treatment has been in place for at least 1 month. The protocol consisted in a baseline evaluation to assess neurohormonal activation, and echocardiographic evaluation of left ventricular function. This was followed by a final evaluation at 12 months from carvedilol loading. Carvedilol was started at 0.05 mg/kg/day, and increased every two weeks until the target dose of 0.8 mg/kg/day was reached.Results:Carvedilol administration was associated with a significant reduction in plasma norepinephrine (p = 0.00001), dopamine (p = 0.0001), aldosterone (p = 0.00001) and activation of the renin-angiotensin system (p = 0.0006). Similar reductions in vanilmandelic and homovanillic acid were noted. After 12 months, a positive remodeling took place, with significant reductions in end-diastolic (p = 0.004) and end-systolic diameters (p = 0.009), and an increase in left ventricular ejection fraction (p = 0.001). No adverse effects needing reduction or interruption in the dosage were noted in the run-in phase, nor in the period of maintenance.Conclusion:Carvedilol is a safe complement to standard therapy for heart failure in children, allowing a significant reduction of neurohormonal activation with evident benefits on both ventricular function and the clinical condition.

Efficacy of Vitamin D on Chronic Heart Failure Among Adults

2020 ◽  
Vol 90 (1-2) ◽  
pp. 49-58 ◽  
Author(s):  
Wang Chunbin ◽  
Wang Han ◽  
Cai Lin
Keyword(s):  
Heart Failure ◽  
Vitamin D ◽  
Chronic Heart Failure ◽  
Left Ventricular Ejection Fraction ◽  
Confidence Interval ◽  
Left Ventricular ◽  
Left Ventricular Ejection ◽  
Controlled Trials ◽  
Ventricular Ejection Fraction ◽  
Randomized Controlled

Abstract. Vitamin D deficiency commonly occurs in chronic heart failure. Whether additional vitamin D supplementation can be beneficial to adults with chronic heart failure remains unclear. We conducted a meta-analysis to derive a more precise estimation. PubMed, Embase, and Cochrane databases were searched on September 8, 2016. Seven randomized controlled trials that investigated the effects of vitamin D on cardiovascular outcomes in adults with chronic heart failure, and comprised 592 patients, were included in the analysis. Compared to placebo, vitamin D, at doses ranging from 2,000 IU/day to 50,000 IU/week, could not improve left ventricular ejection fraction (Weighted mean difference, WMD = 3.31, 95% confidence interval, CL = −0.93 to 7.55, P < 0.001, I2 = 92.1%); it also exerts no beneficial effects on the 6 minute walk distance (WMD = 18.84, 95% CL = −24.85 to 62.52, P = 0.276, I2 = 22.4%) and natriuretic peptide (Standardized mean difference, SMD = −0.39, 95% confidence interval CL = −0.48 to 0.69, P < 0.001, I2 = 92.4%). However, a dose-response analysis from two studies demonstrated an improved left ventricular ejection fraction with vitamin D at a dose of 4,000 IU/day (WMD = 6.58, 95% confidence interval CL = −4.04 to 9.13, P = 0.134, I2 = 55.4%). The results showed that high dose vitamin D treatment could potentially benefit adults with chronic heart failure, but more randomized controlled trials are required to confirm this result.

Emerging Cardiac Resynchronisation Therapy Indications

2011 ◽  
Vol 7 (1) ◽  
pp. 29
Author(s):  
Charlotte Eitel ◽  
Gerhard Hindricks ◽  
Christopher Piorkowski ◽  
◽  
◽  
...  
Keyword(s):  
Heart Failure ◽  
Systolic Heart Failure ◽  
Cardiac Resynchronisation Therapy ◽  
Left Ventricular ◽  
Left Ventricular Ejection ◽  
Current Evidence ◽  
Class Iii ◽  
Ventricular Ejection Fraction ◽  
Cardiac Resynchronisation ◽  
Resynchronisation Therapy

Cardiac resynchronisation therapy (CRT) is an efficacious and cost-effective therapy in patients with highly symptomatic systolic heart failure and delayed ventricular conduction. Current guidelines recommend CRT as a class I indication for patients with sinus rhythm, New York Heart Association (NYHA) functional class III or ambulatory class IV, a QRS duration ≥120ms, and left ventricular ejection fraction (LVEF) ≤35%, despite optimal pharmacological therapy. Recent trials resulted in an extension of current recommendations to patients with mild heart failure, patients with atrial fibrillation, and patients with an indication for permanent right ventricular pacing with the aim of morbidity reduction. The effectiveness of CRT in patients with narrow QRS, patients with end-stage heart failure and cardiogenic shock, and patients with an LVEF >35% still needs to be proved. This article reviews current evidence and clinical applications of CRT in heart failure and provides an outlook on future developments.

Heart Failure with Preserved Ejection Fraction – A Review

2012 ◽  
Vol 9 (1) ◽  
pp. 90-95 ◽  
Author(s):  
Otto A Smiseth ◽  
Anders Opdahl ◽  
Espen Boe ◽  
Helge Skulstad
Keyword(s):  
Heart Failure ◽  
Ejection Fraction ◽  
Diastolic Heart Failure ◽  
The Elderly ◽  
Left Ventricular ◽  
Filling Pressure ◽  
Left Ventricular Ejection ◽  
Ventricular Ejection Fraction ◽  
Reduced Ejection Fraction ◽  
Objective Evidence

Heart failure with preserved left ventricular ejection fraction (HF-PEF), sometimes named diastolic heart failure, is a common condition most frequently seen in the elderly and is associated with arterial hypertension and left ventricular (LV) hypertrophy. Symptoms are attributed to a stiff left ventricle with compensatory elevation of filling pressure and reduced ability to increase stroke volume by the Frank-Starling mechanism. LV interaction with stiff arteries aggravates these problems. Prognosis is almost as severe as for heart failure with reduced ejection fraction (HF-REF), in part reflecting co-morbidities. Before the diagnosis of HF-PEF is made, non-cardiac etiologies must be excluded. Due to the non-specific nature of heart failure symptoms, it is essential to search for objective evidence of diastolic dysfunction which, in the absence of invasive data, is done by echocardiography and demonstration of signs of elevated LV filling pressure, impaired LV relaxation, or increased LV diastolic stiffness. Antihypertensive treatment can effectively prevent HF-PEF. Treatment of HF-PEF is symptomatic, with similar drugs as in HF-REF.

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