Sympathetic Nerve Activity In Patients Research Articles

Augmented muscle sympathetic nerve activity in liver cirrhosis with ascites

Muscle sympathetic-nerve activity (MSNA) was measured in six patients with liver cirrhosis and eight healthy age-matched subjects, by means of microneurography, to determine what changes may occur in sympathetic nerve activity in patients with cirrhosis with ascites. Muscle sympathetic-nerve activity was recorded at rest for 30 min or longer, venous blood samples were obtained simultaneously from an antecubital veins, and plasma norepinephrine, plasma renin activity, and plasma aldosterone levels were measured. Muscle sympathetic-nerve activity and norepinephrine, renin and aldosterone plasma levels were significantly higher in the subjects with cirrhosis than in healthy subjects; muscle sympathetic-nerve activity and norepinephrine levels, and muscle sympathetic-nerve activity and plasma renin activity presented a positive correlation in all subjects.

Effect of Atorvastatin versus Rosuvastatin on Cardiac Sympathetic Nerve Activity in Patients with Dilated Cardiomyopathy

Effect of Atorvastatin versus Rosuvastatin on Cardiac Sympathetic Nerve Activity in Patients with Dilated Cardiomyopathy

Increased Postprandial Colonic Motility is Associated With Sympathetic Nerve Activity in Patients With Irritable Bowel Syndrome

Increased Postprandial Colonic Motility is Associated With Sympathetic Nerve Activity in Patients With Irritable Bowel Syndrome

Effect of Atorvastatin vs. Rosuvastatin on Cardiac Sympathetic Nerve Activity in Non-Diabetic Patients With Dilated Cardiomyopathy

Effects of statin therapy on cardiac sympathetic nerve activity in patients with chronic heart failure (CHF) have not previously been evaluated. To compare the effects of lipophilic atorvastatin and hydrophilic rosuvastatin on cardiac sympathetic nerve activity in CHF patients with dilated cardiomyopathy (DCM), 63 stable outpatients with DCM, who were already receiving standard therapy for CHF, were randomized to atorvastatin (n = 32) or rosuvastatin (n = 31). We evaluated cardiac sympathetic nerve activity by cardiac ¹²³I-metaiodobenzylguanidine (MIBG) scintigraphy, hemodynamic parameters and neurohumoral factors before and after 6 months of treatment. There were no differences in the baseline characteristics of the 2 groups. In the rosuvastatin group, there were no changes in MIBG parameters, left ventricular ejection fraction or plasma levels of N-terminal pro-B-type natriuretic peptide (NT-proBNP) after 6 months of treatment. In contrast, the atorvastatin group showed a significant increase in the delayed heart/mediastinum count ratio (2.18 ± 0.4 vs. 2.36 ± 0.4, P < 0.0001), and the washout rate was significantly decreased (34.8 ± 5.7 vs. 32.6 ± 6.3%, P = 0.0001) after 6 months of treatment compared with the baseline values. The plasma NT-proBNP level was also significantly decreased (729 ± 858 vs. 558 ± 747 pg/ml, P = 0.0139). Lipophilic atorvastatin but not hydrophilic rosuvastatin improves cardiac sympathetic nerve activity in CHF patients with DCM.

Short term effect of adaptive servo-ventilation on muscle sympathetic nerve activity in patients with heart failure

Chronic heart failure (HF) is characterized by sympathetic overactivation and periodic breathing. We examined whether adaptive servo-ventilation (ASV) exerts a sympathoinhibitory effect in patients with HF via normalizing respiratory pattern. Muscle sympathetic nerve activity (MSNA), heart rate, blood pressure, respiratory pattern and oxygen saturation were examined in 29 HF patients without obstructive sleep apnea (age, 61 ± 15 years; ejection fraction, 0.32 ± 0.09; obstructive apnea index, < 5/h) before (10 min), during (30 min) and after (10 min) the application of ASV. Periodic breathing was defined as a repeated oscillation of tidal volume with regularly recurring hyperpnea and hypopnea with a variation in tidal volume of greater than 25%. The severity of respiratory instability was determined using the coefficient of variation of tidal volume (CV-TV). Of 29 patients with HF, 11 had periodic breathing and 18 did not. There was a modest positive correlation between MSNA and CV-TV ( n = 29, p < 0.05). ASV reduced respiratory rate, CV-TV and MSNA only in the group with periodic breathing ( p < 0.01). Change in MSNA significantly correlated with changes in respiratory rate, CV-TV and presence of periodic breathing. However, multivariate analyses revealed that respiratory rate and CV-TV were independent predictors of change in MSNA. ASV reduces MSNA by slowing respiratory rates and stabilizing respiratory patterns in patients with HF.

The effects of clonidine on arterial baroreflex sensitivity and cardiopulmonary barorefex control of sympathetic nerve activity in patients with left ventricular dysfunction

Clonidine is a potent sympatholytic drug with central neural effects. The aim of this study was to evaluate the effects of clonidine on arterial baroreflex sensitivity (BRS) and cardiopulmonary (CP) baroreflex control of muscle sympathetic nerve activity (MSNA) in patients with left ventricular (LV) dysfunction. Twenty patients were randomly assigned to either clonidine or placebo groups (10 in each group). BRS (by phenylephrine method) and CP baroreflex (by lower body negative pressure) effects on sympathetic nerve activity (circulating norepinephrine and MSNA recordings) were measured before and after a 4-week treatment period. Clonidine lowered blood pressure and heart rate. Clonidine was accompanied not only by a decrease in plasma noradrenaline (from 444±196 to 260±144 pg ml(-1) ) but also by a reduction in directly measured MSNA (from 47±16 to 36±16 bursts min(-1) ). BRS increased significantly from 3·01±1·19 to 6·86±2·84 ms mmHg(-1) after clonidine. When expressed as per cent change in MSNA during CP baroreceptor stimulation, CP baroreflex control of MSNA was significantly increased from 9·26±8·93% to 28·83±11·96% after clonidine. However, there were no significant changes in the measured variables in the control group. Clonidine enhanced BRS and CP baroreflex control of MSNA while reducing baseline sympathetic activity in patients with LV dysfunction.

Improvement of autonomic nervous activity by Waon therapy in patients with chronic heart failure

We have reported previously that Waon therapy improves cardiac and vascular function, and prognosis of patients with chronic heart failure (CHF). CHF is characterized by generalized sympathetic activation and parasympathetic withdrawal. The purpose of this study was to evaluate the effect of Waon therapy on autonomic nervous activity in patients with CHF. Fifty-four patients with CHF, who were receiving conventional therapy for CHF, were divided into Waon therapy and control groups. In the Waon therapy group, 27 patients were treated with medication and Waon therapy. In the control group, 27 patients were treated with only conventional CHF therapy. Cardiac function including cardiac output (CO) and left ventricular ejection fraction (LVEF) was evaluated by echocardiography. The heart rate variability, such as the coefficient of variation of RR intervals (CVRR), the low-frequency (LF) component, high-frequency (HF) component, the LF norm [LF/(LF+HF)], and HF norm [HF/(LF+HF)], were measured at admission and 4 weeks after treatment. Echocardiography demonstrated that CO and LVEF significantly increased after 4 weeks in the Waon therapy group, but did not change in the control group. In the Waon therapy group, CVRR, HF, and HF norm significantly increased 4 weeks after Waon therapy. In addition, the LF/HF ratio and LF norm significantly decreased 4 weeks after Waon therapy. In contrast, these parameters remained unchanged in the control group. Moreover, the HF and HF norm were significantly higher, and the LF/HF ratio and LF norm were significantly lower after 4 weeks of Waon therapy group than after 4 weeks of only conventional therapy. Waon therapy improved cardiac function and autonomic nervous activity by increasing parasympathetic and decreasing sympathetic nervous activity in patients with CHF.

Effects of moxonidine on sympathetic nerve activity in patients with end-stage renal disease

End-stage renal disease (ESRD) is characterized by markedly increased sympathetic outflow that contributes to increased cardiovascular mortality in these patients. The central sympatholytic drug moxonidine (MOX) has been shown to reduce muscle sympathetic nerve activity (MSNA) in initial stages of chronic kidney disease; however, the effects in ESRD are not known. The aim of this study was to test the hypothesis that low-dose MOX causes sustained decreases in sympathetic outflow in ESRD patients. Twenty-three ESRD patients (mean age 46.4 +/- 16 years, 14 men, seven women, no diabetic patients) were randomized to a daily treatment of 0.3 mg MOX or placebo (PLA) in addition to pre-existing antihypertensive therapy. At baseline and after 1 and 6 months of treatment, heart rate (HR, ECG), blood pressure (mean arterial pressure, automatic sphygmanometer), calf blood flow (CBF, venous occlusion plethysmography), muscle sympathetic nerve activity (MSNA) (microneurography at the peroneal nerve) were measured. Data are mean +/- SEM. MOX acutely decreased MSNA within 2 h after oral intake (from 45 +/- 3.7 to 35 +/- 3.9 bursts/min, P < 0.05). This decrease was sustained over 6 months (MSNA 45 +/- 3.7, 35 +/- 4.6, 33 +/- 4.5 bursts/min at 0, 1 and 6 months, P < 0.05). PLA had no effect. Neither MOX nor PLA resulted in any significant acute or long-term changes in HR, MAP or CBF. In ESRD patients, low-dose MOX produced sustained and substantial reductions in sympathetic outflow without hemodynamically compromising them. We suggest that the inhibition of central sympathetic outflow may improve cardiovascular prognosis in ESRD.

Effect of Adaptive Servo-Ventilation on Muscle Sympathetic Nerve Activity in Patients With Heart Failure and Renal Insufficiency

Effect of Adaptive Servo-Ventilation on Muscle Sympathetic Nerve Activity in Patients With Heart Failure and Renal Insufficiency

Reply to Young et al.

LETTERS TO THE EDITORReply to Young et al.Holly R. Middlekauff and Jeanie ParkHolly R. Middlekauff and Jeanie ParkPublished Online:01 May 2009https://doi.org/10.1152/japplphysiol.00017.2009MoreSectionsPDF (30 KB)Download PDF ToolsExport citationAdd to favoritesGet permissionsTrack citations ShareShare onFacebookTwitterLinkedInEmailWeChat to the editor: We thank Drs. Young, Keller, Crandall, and Fadel (2) for their interest in our work (1), and their opinions regarding the impracticality of comparing skin sympathetic nerve activity (SSNA) between subjects in different groups. Since single SSNA bursts can include multiple small peaks, they ask, “Does a multiple peak burst represent one or more bursts?” In our study, such bursts were counted as one by the blinded investigator who analyzed all neurograms, thereby providing uniformity to burst quantification.Second, they correctly point out that the SSNA recordings may represent multiple fiber types and that any given neurogram may have varying contributions from each fiber type. They are concerned that in our multiunit recordings, we could miss the fiber type that potentially has elevated activity. Although this is true in theory, it is extremely unlikely. The SSNA neurogram is a random sample of total SSNA activity, and it is against the odds that during the 8 (or 16 total SSNA recordings if one includes healthy controls), we always missed the overactive skin fiber type. A more likely explanation for the absence of elevated SSNA in our recordings in end-stage renal disease patients is that it is not present.We invite Drs. Young, Keller, Crandall, and Fadel to review, once again, Fig. 1 in our paper. These representative neurograms lay to rest any real question whether SSNA is elevated in ESRD patients compared with healthy controls. In this case, a picture is truly worth a thousand words.REFERENCES1 Park J, Campese VM, Nobakht N, Middlekauff HR. Differential distribution of muscle and skin sympathetic nerve activity in patients with end-stage renal disease. J Appl Physiol 105: 1873–1876, 2008.Link | ISI | Google Scholar2 Young CN, Keller DM, Crandall CG, Fadel PJ. Comparing resting skin sympathetic nerve activity between groups: caution needed. J Appl Physiol; doi:10.1152/japplphysiol.91538.2008.Link | ISI | Google ScholarAUTHOR NOTESAddress for reprint requests and other correspondence: J. Park, Emory Univ., Renal Division, WMRB, 1639 Pierce Drive, Suite 338, Atlanta, GA 30322 (e-mail: [email protected]) Download PDF Previous Back to Top Next FiguresReferencesRelatedInformation More from this issue > Volume 106Issue 5May 2009Pages 1753-1753 Copyright & PermissionsCopyright © 2009 the American Physiological Societyhttps://doi.org/10.1152/japplphysiol.00017.2009History Published online 1 May 2009 Published in print 1 May 2009 Metrics

Arterial baroreflex control of heart rate and sympathetic nerve activity in patients with type II diabetes

Previous studies have indicated that diabetes is associated with postural hypotension and greater arterial blood pressure (BP) reactivity to acute cardiovascular stressors. However, whether impairments in arterial baroreflex (ABR) function contribute to alterations in BP control in diabetes remains unclear. To begin to address this question, muscle sympathetic nerve activity (MSNA), heart rate, and BP were continuously recorded in 8 type II diabetic patients and 4 healthy age‐matched control subjects during intravenous bolus injections of sodium nitroprusside followed 60s later by phenylephrine hydrochloride. The sensitivity (i.e., gain) of ABR‐cardiac and ABR‐MSNA control were identified from the linear relationships between RR‐interval and systolic BP and total MSNA and diastolic BP, respectively. ABR‐cardiac gain tended to be lower in diabetic patients compared to healthy controls [4.95±0.67 diabetics (n=8) vs. 9.25±3.90 controls, ms/mmHg; P=0.18]. In contrast, the ABR‐MSNA gain was similar between the two groups [‐8.32±3.03 diabetics (n=5) vs. ‐9.67±1.40 controls, units/beat/mmHg; P=0.72]. These preliminary data suggest that type II diabetic patients exhibit differential alterations in ABR function demonstrating ∼46% reductions in ABR‐cardiac control, whereas ABR‐MSNA control appears to be better preserved (∼14% reduction vs. controls).

MIBG-Szintigrafie des Herzens

l23Iod-MIBG-Untersuchungen des Myokards können wichtige Informationen über pathophysiologische Prozesse im Hinblick auf die sympathische Innervation des Herzens liefern. Viele Autoren bestätigen die gleichzeitige Existenz eines durch hohe Affinität charakterisierten neuronalen Aufnahmemechanismus für MIBG in die sympathischen, postganglionären präsynaptischen Nervenstrukturen neben einem unspezifischen, jedoch mit hoher Transportleistung ausgestatteten, extraneuronalen Mechanismus. Das szintigrafische Verteilungsmuster bei erhaltenem MIBG-Transportmechanismus stellt zuverlässig die linksventrikuläre sympathische Nervenversorgung und deren pathologische Veränderungen wie beispielsweise bei Myokardischämien, Herzinsuffizienz oder Arrhythmien dar; dazu erlaubt diese Bildgebung die Früherkennung der autonomen Neuropathie im Rahmen des Diabetes mellitus. Für Patienten mit Herzinsuffizienz oder hypertrophischer Kardiomyopathie konnte gezeigt werden, dass durch die MIBG-Szintigrafie solche mit erhöhtem Ri-siko für das Auftreten eines plötzlichen Herztodes identifiziert werden können. Darüber hinaus können therapeutische Effekte verschiedener Behandlungsstrategien evaluiert werden.

Effectiveness of Nocturnal Home Oxygen Therapy to Improve Exercise Capacity, Cardiac Function and Cardiac Sympathetic Nerve Activity in Patients With Chronic Heart Failure and Central Sleep Apnea

Central sleep apnea, often found in patients with chronic heart failure (CHF), has a high risk of poor prognosis. This study involved 20 patients with CHF (left ventricular ejection fraction (LVEF) <45%, M/F =19/1, age 65+/-10 years) and an apnea-hypopnea index (AHI) >5 times/h who were divided into 2 groups: 10 patients treated with nocturnal home oxygen therapy (HOT) and 10 patients without HOT (non-HOT). All patients had dilated cardiomyopathy and underwent overnight polysomnography, cardiopulmonary exercise testing, and nuclear cardiac examinations to evaluate AHI, exercise capacity according to the specific activity scale and oxygen uptake at anaerobic threshold and peak exercise (peak VO(2)). Cardiac function according to (99m)Tc-MIBI QGS, and the total defect score (TDS), H/M ratio and the washout rate (WR) on (123)I-metaiodobenzylguanidine (MIBG) imaging were calculated for all patients. As compared with the non-HOT group, the HOT group demonstrated a greater reduction in AHI (26.1+/-9.1 to 5.1+/-3.4), (123)I-MIBG TDS (31+/-8 to 25+/-9), and (123)I-MIBG WR (48+/-8% to 41+/-5%) and a greater increase in the specific activity scale (4.0+/-0.9 to 5.8+/-1.2 Mets), peak VO(2) (16.0+/-3.8 to 18.3+/-4.7 ml . min(-1) . kg(-1)), and LVEF (27+/-9% to 37+/-10%). HOT improves exercise capacity, cardiac function, and cardiac sympathetic nerve activity in patients with CHF and central sleep apnea.

Augmented sympathoinhibitory effect of valsartan when added to angiotensin-converting enzyme inhibitor in patients with left ventricular dysfunction

Angiotensin-converting enzyme (ACE) inhibitors and angiotensin receptor blockers (ARBs) effectively interfere with the sympathetic nerve activity in patients with left ventricular (LV) dysfunction. The aim of this study was to examine the effect of ARBs on sympathetic nerve activity and baroreflex function in patients with LV dysfunction already receiving ACE inhibitors. Twenty patients with LV dysfunction already treated with ACE inhibitor (enalapril 5 mg/day) were randomly divided into two groups: treatment with 10 mg/day enalapril (control group) or 5 mg/day enalapril plus 80 mg/day valsartan (combination group). In both groups, resting muscle sympathetic nerve activity (MSNA; microneurography), arterial baroreflex sensitivity, and cardiopulmonary baroreflex sensitivity were measured at baseline and 4 weeks after the treatment. Arterial baroreflexes were perturbed by phenylephrine method, and cardiopulmonary baroreflexes were perturbed by lower body negative pressure (-10 mmHg). Baseline characteristics in both groups were similar. Resting MSNA decreased significantly from 35.4+/-10.8 to 26.4+/-5.1 burst/min (p<0.05), while arterial baroreflex sensitivity improved significantly from 6.0+/-2.0 to 10.1+/-2.6 ms/mmHg in the combination group. Moreover, cardiopulmonary baroreflex control of MSNA improved significantly from 15.8+/-12.2 to 42.0+/-26.7% (p<0.05) in the combination group. However, there were no significant changes in arterial baroreflex sensitivity and cardiopulmonary baroreflex of MSNA in the control group. Addition of ARB to ACE inhibitor treatment reduced sympathetic nerve activity and augmented arterial and cardiopulmonary baroreflex sensitivity in patients with LV dysfunction.

Differential distribution of muscle and skin sympathetic nerve activity in patients with end-stage renal disease

End-stage renal disease (ESRD) is characterized by resting sympathetic overactivity. Baseline muscle sympathetic nerve activity (MSNA), which is governed by baroreflexes and chemoreflexes, is elevated in ESRD. Whether resting skin sympathetic nerve activity (SSNA), which is independent from baroreflex and chemoreflex control, is also elevated has never been reported in renal failure. The purpose of this study was to determine whether sympathetic overactivity of ESRD is generalized to include the skin distribution. We measured sympathetic nerve activity to both muscle and skin using microneurography in eight ESRD patients and eight controls. MSNA was significantly (P = 0.025) greater in ESRD (37.3 +/- 3.6 bursts/min) when compared with controls (23.1 +/- 4.4 bursts/min). However, SSNA was not elevated in ESRD (ESRD vs. controls, 17.6 +/- 2.2 vs. 16.1 +/- 1.7 bustst/min, P = 0.61). Similar results were obtained when MSNA was quantified as bursts per 100 heartbeats. We report the novel finding that although sympathetic activity directed to muscle is significantly elevated, activity directed to skin is not elevated in ESRD. The differential distribution of sympathetic outflow to the muscle vs. skin in ESRD is similar to the pattern seen in other disease states characterized by sympathetic overactivity such as heart failure and obesity.

Muscle sympathetic nerve activity in patients with Chagas' disease

Background The progression of heart failure in Chagas' disease has been explained by remodeling, leading to neurohumoral activation, or by the direct parasite damage to parasympathetic neurons during acute phase, leading to early sympathetic activation and progressive heart failure. To help distinguish between these hypotheses we studied muscle sympathetic nerve activity (MSNA) at rest and during handgrip exercise (30% of maximal voluntary contraction) in patients with Chagas' disease and normal ejection fraction vs. patients with heart failure. Methods A consecutive study of 72 eligible out-patients/subjects was conducted between July 1998 and November 2004. The participants were classified in three advanced heart failure groups (New York Heart Association Functional Classes II–III): Chagas' disease ( n = 15), ischemic ( n = 15) and idiopathic cardiomyopathy ( n = 15). Twelve Chagas' disease patients without heart failure and normal ejection fraction, and 15 normal controls were also studied. MSNA was recorded directly from the peroneal nerve by microneurography technique. Results MSNA was greater in heart failure patients when compared with Chagas' disease patients without heart failure (51 ± 3 vs. 20 ± 2 bursts/min P = 0.0001). MSNA in Chagas' patients with normal ejection fraction and normal controls was not different. During exercise, MSNA was similar in all 3 heart failure groups. And, was lower in the Chagas' patients with normal ejection fraction than in patients with Chagas' disease and heart failure (28 ± 1 vs. 63 ± 5 bursts/min, respectively). Conclusion MSNA is not elevated in patients with Chagas' disease with normal ejection fraction. These findings support the concept of remodeling and neurohumoral activation as a common pathway following significant cardiac injury.

The acute effect of atrioventricular pacing on sympathetic nerve activity in patients with normal and depressed left ventricular function

Although modest elevations in pacing rate improve cardiac output and induce reflex sympathoinhibition, the threshold rate above which hemodynamic perturbations induce reflex sympathoexcitation remains unknown. Systolic blood pressure (SBP), diastolic blood pressure (DBP), and mean arterial pressures (MAP) and sympathetic nerve activity (SNA) were measured during normal sinus rhythm (NSR) and atrioventricular (AV) sequential pacing in 25 patients. Pacing was performed at 100, 120, and 140 beats/min with an AV interval of 100 ms. Patients were divided into two groups based on normal or abnormal left ventricular ejection fraction (LVEF): group 1 (n = 11; mean LVEF, 55%) and group 2 (n = 14; mean LVEF, 31%). In group 1, relative to NSR, SBP decreased an average of 2%, 3%, and 8% at 100, 120, and 140 beats/min (P < 0.001), respectively. DBP and MAP increased 9%, 15%, and 15% (P = 0.001) and 3%, 6%, and 5% [P = not significant (NS)], respectively. In group 2, SBP reductions were even greater, with an average decrease of 4%, 8%, and 16% (P < 0.001). Whereas DBP increased 9%, 9%, and 8% at 100, 120, and 140 beats/min (P = NS), MAP increased 3% and 2% at 100 and 120 beats/min but decreased 3% at 140 beats/min (P = 0.001). SNA recordings were obtained in 11 patients (6 in group 1 and 5 in group 2). In group 1, SNA decreased during all rates, with a mean 21% reduction. In group 2, however, SNA decreased at 100 and 120 beats/min (49% and 38%) but increased 24% at 140 beats/min. Patients with depressed LVEF exhibited altered hemodynamic and sympathetic responses to rapid sequential pacing. The implications of these findings in device programming and arrhythmia rate control await future studies.

Does infusion of ANG II increase muscle sympathetic nerve activity in patients with primary aldosteronism?

Patients with primary aldosteronism (PA) were shown to have suppressed muscle sympathetic nerve activity (MSNA) in our previous study. Although baroreflex inhibition probably accounts in part for this reduced MSNA in PA, we hypothesized that the lowered activity of the renin-angiotensin system in PA may also contribute to the suppressed SNA. We recorded MSNA in 9 PA and 16 age-matched normotensive controls (NC). In PA, the resting mean blood pressure (MBP) and serum sodium concentrations were increased, and MSNA was reduced. We examined the effects of infusion of a high physiological dose of ANG II (5.0 ng.kg(-1).min(-1)) on MSNA in 6 of 9 PA and 9 of 16 NC. Infusion of ANG II caused a greater pressor response in PA than NC, but, in spite of the greater increase in pressure, MSNA increased in PA, whereas it decreased in NC. Simultaneous infusion of nitroprusside and ANG II, to maintain central venous pressure at the baseline level and reduce the elevation in MBP induced by ANG II, caused significantly greater increases in MSNA in PA than in NC. Baroreflex sensitivity of heart rate, estimated during phenylephrine infusions, was reduced in PA, but baroreflex sensitivity of MSNA was unchanged in PA compared with NC. All the abnormalities in PA were eliminated following unilateral adrenalectomy. In conclusion, the suppressed SNA in PA depends in part on the low level of ANG II in these patients.

Anti-beta1-adrenoreceptor autoantibodies and myocardial sympathetic nerve activity in chronic heart failure

Background The autoantibodies stimulate the beta1-adrenoreceptors on cardiac myocytes similar to norepinephrine, and are associated with reduced cardiac function. Iodine-123 metaiodobenzylguanidine ( 123I-MIBG) is metabolized similarly to norepinephrine. This study was undertaken to investigate the relationship between cardiac stimulation by anti-beta1-adrenoreceptor autoantibodies and myocardial sympathetic nervous activity in patients with chronic heart failure. Methods We screened for the anti-beta1-adrenoreceptor autoantibodies in 52 patients with chronic heart failure by conducting an enzyme-linked immunosorbent assay, and underwent 123I-MIBG scintigraphy in 27 of the patients. Anterior planar images of 123I-MIBG were obtained 15 min and 3 h after the injection. We determined the heart to mediastinum radioactivity ratio (H/M), and calculated the rate of washout of 123I-MIBG from the heart. Results Patients with New York Heart Association functional class III or IV had higher levels of anti-beta1-adrenoreceptor autoantibodies than those with class I or II ( p < 0.01). The autoantibody level was significantly correlated with delayed H/M ( r = − 0.65, p < 0.001) and washout rate ( r = 0.65, p < 0.001). Sixteen patients with a cardiac event showed higher levels of the autoantibodies ( p < 0.05). Cardiac event-free survival was poorer in patients with the autoantibody levels > 10 U/ml than that < 10 U/ml (log–rank = 12.1, p < 0.001). Conclusion The anti-beta1-adrenoreceptor autoantibodies are closely associated with cardiac sympathetic nervous activity assessed by 123I-MIBG and cardiac event in patients with chronic heart failure.

Combined therapy with carvedilol and amiodarone is more effective in improving cardiac symptoms, function, and sympathetic nerve activity in patients with dilated cardiomyopathy: Comparison with carvedilol therapy alone

Carvedilol therapy has been reported to be more effective than other beta-blockers in patients with chronic heart failure (CHF). Amiodarone is an anti-arrhythmic medicine that has also been reported to be effective in patients with CHF. But the usefulness of combined therapy with carvedilol and amiodarone has not been reported. We compared 15 patients (M/F = 3/12, age = 57 +/- 8 y) with dilated cardiomyopathy (DCM) receiving carvedilol and amiodarone with 15 patients (M/F = 3/12, age = 61 +/- 9 y) receiving carvedilol alone. Patients were studied before and after 1 year of treatment (1Y). NYHA class and exercise capacity based on the specific-activity-scale (SAS), were assessed. Cardiac sympathetic nerve activity was estimated using total defect score (TDS), H/M ratio and washout rate (WR) of 123I-MIBG imaging. Cardiac function was evaluated using 99mTc-MIBI QGS. Combined therapy improved several parameters much more than carvedilol alone (p < 0.05) including delta-TDS (15.0 +/- 8.6 vs. 7.6 +/- 7.2) and delta-WR (15.9 +/- 11.0% vs. 7.3 +/- 10.0%) for 123I-MIBG imaging, delta-LVEF (26.1 +/- 11.4% vs. 15.5 +/- 13.8%), delta-end-systolic volume (100 +/- 63.8 ml vs. 58.9 +/- 47.3 ml), 1Y NYHA class (1.5 +/- 0.5 vs. 1.9 +/- 0.5), 1Y SAS (7.3 +/- 0.7 Mets vs. 6.2 +/- 1.0 Mets), and delta-SAS (3.4 +/- 0.8 Mets vs. 2.6 +/- 1.1 Mets). Combined therapy with carvedilol and amiodarone is more effective in improving cardiac symptoms, exercise capacity, cardiac function and cardiac sympathetic nerve activity in patients with DCM.