Effects of resynchronization therapy on sympathetic activity in patients with depressed ejection fraction and intraventricular conduction delay due to ischemic or idiopathic dilated cardiomyopathy

Hamdan, Mohamed H.; Barbera, S; Kowal, Robert C.; Page, Richard L.; Ramaswamy, Karthik; Joglar, José A.; Karimkhani, Valeh; Smith, Michael L.

doi:10.1016/s0002-9149(02)02273-7

Cited by 53 publications

(42 citation statements)

References 10 publications

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“…Although reductions in sympathetic nerve activity occur during abrupt, short-term biventricular pacing in an electrophysiology laboratory setting, 12 the long-term effects of CRT in the present study had no effect on circulating catecholamines. These findings suggest that the beneficial autonomic effects of CRT were mostly associated with increased parasympathetic HR control, although resting ACL was unchanged.…”

Section: Discussioncontrasting

confidence: 58%

Cardiac Resynchronization Therapy Improves Heart Rate Variability in Patients with Symptomatic Heart Failure

et al. 2003

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Background-Cardiac resynchronization therapy (CRT) using biventricular pacing improves symptoms and functional capacity in patients with moderate to severe heart failure. The present study examined whether an improvement in ventricular performance from resynchronization therapy changes the autonomic control of heart rate. Methods and Results-Heart rate variability (HRV) was examined in 50 patients implanted with the InSync biventricular pacing system who were randomized to therapy-on (nϭ25) or therapy-off (nϭ25). HRV was computed as the standard deviation of the atrial cycle length sensed from the system over 2 months of continuous monitoring. HRV was compared between CRT-on and CRT-off groups. HRV was higher in patients randomized to CRT-on compared with CRT-off (148Ϯ47 ms for CRT-on versus 118Ϯ45 ms for CRT-off; Pϭ0.02), despite the lack of difference in mean atrial cycle length (844Ϯ129 ms for CRT-on versus 851Ϯ110 ms for CRT-off; Pϭ0.82). Changes in plasma catecholamines were not different between the CRT-on and CRT-off groups from baseline to the 3-month follow-up. Conclusions-Improvement in ventricular performance from CRT shifts cardiac autonomic balance toward a more favorable profile that is less dependent on sympathetic activation. (Circulation. 2003;108:266-269.)

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Section: Discussioncontrasting

confidence: 58%

Cardiac Resynchronization Therapy Improves Heart Rate Variability in Patients with Symptomatic Heart Failure

et al. 2003

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“…Biventricular pacing was shown to reduce muscle sympathetic nerve activity when compared with right ventricular pacing 137 or right atrial pacing. 138 These beneficial effects persisted ≤6 months after resynchronization therapy. 139,140 Cha et al 141 examined the effect of CRT on neurohormonal integrity by studying cardiac presynaptic sympathetic function, as determined by nuclear cardiac imaging modalities ( 123 I-MIBG scintigraphy), in patients with HF who received CRT and found that CRT reverses cardiac autonomic remodeling by upregulating presynaptic receptor function, as evidenced by increased 123 I-MIBG heart/mediastinum ratio and attenuated heart/mediastinum washout rate, with concomitantly improved HRV.…”

Section: Effect Of Cardiac Resynchronization Therapy On Cardiac Autonmentioning

confidence: 98%

The Autonomic Nervous System and Heart Failure

Florea

Cohn

2014

Circulation Research

439

366

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Abstract:The pathophysiology of heart failure (HF) is characterized by hemodynamic abnormalities that result in neurohormonal activation and autonomic imbalance with increase in sympathetic activity and withdrawal of vagal activity. Alterations in receptor activation from this autonomic imbalance may have profound effects on cardiac function and structure. Inhibition of the sympathetic drive to the heart through β-receptor blockade has become a standard component of therapy for HF with a dilated left ventricle because of its effectiveness in inhibiting the ventricular structural remodeling process and in prolonging life. Several devices for selective modulation of sympathetic and vagal activity have recently been developed in an attempt to alter the natural history of HF. The optimal counteraction of the excessive sympathetic activity is still unclear. A profound decrease in adrenergic support with excessive blockade of the sympathetic nervous system may result in adverse outcomes in clinical HF. In this review, we analyze the data supporting a contributory role of the autonomic functional alterations on the course of HF, the techniques used to assess autonomic nervous system activity, the evidence for clinical effectiveness of pharmacological and device interventions, and the potential future role of autonomic nervous system modifiers in the management of this syndrome. (Circ Res. 2014;114:1815-1826.) Key Words: autonomic nervous system ■ heart failure ■ norepinephrine ■ receptors, adrenergicThe Autonomic Nervous System and Heart Failure Viorel G. Florea, Jay N. Cohn This Review is in a thematic series on The Autonomic Nervous System and the Cardiovascular System, which includes the following articles: Role of the Autonomic Nervous System in Modulating Cardiac Arrhythmias [Circ Res. 2014;114:1004-1021 The Autonomic Nervous System and Hypertension [Circ Res. 2014;114:1804-1814 The Autonomic Nervous System and Heart Failure Renal Denervation for the Treatment of Cardiovascular High Risk-Hypertension or Beyond? Original received February 10, 2014; revision received April 29, 2014; accepted April 29, 2014. In March 2014, the average time from submission to first decision for all original research papers submitted to Circulation Research was 12.63 days.From the Minneapolis VA Health Care System, Section of Cardiology (V.G.F.) and Rasmussen Center for Cardiovascular Disease Prevention, Department of Medicine (J.N.C.), University of Minnesota Medical School.Correspondence to Jay N. endocardium. Parasympathetic effects are carried by the right and left vagus nerves, originating in the medulla. The vagus nerve further divides into the superior and inferior cardiac nerves, finally merging with the postganglionic sympathetic neurons to form a plexus of nerves at the base of the heart, known as the cardiac plexus. 1The 2 mediators of the SNS, norepinephrine and epinephrine, derive from 2 major sources in the body: the sympathetic nerve endings, which release norepinephrine directly into the synaptic cleft, and the adren...

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“…In patients with cardiomyopathy, biventricular pacing resulted in decreased sympathetic nerve activity along with improvement in blood pressure compared with intrinsic conduction in patients with left ventricular dysfunction and intraventricular conduction delay. 115 Furthermore, in 50 patients implanted with biventricular pacemakers and randomized to therapy-on (n = 25) vs therapyoff (n = 25), HRV was significantly improved in patients receiving resynchronization therapy despite a lack of difference between mean atrial cycle length. Therefore, improvement in ventricular performance via resynchronization therapy shifts the cardiac autonomic balance toward a more favorable profile of less sympathetic and more parasympathetic activation.…”

Section: Effect Of Resynchronization Therapy On Sympathetic Activitymentioning

confidence: 98%

The Role of the Autonomic Nervous System in Sudden Cardiac Death

Vaseghi

Shivkumar²

2008

Progress in Cardiovascular Diseases

328

233

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The cardiac autonomic nervous system consists of 2 branches-the sympathetic and the parasympathetic systems-that work in a delicately tuned, yet opposing fashion in the heart. This extrinsic control mechanism can dominate intrinsic regulatory mechanisms that modulate heart rate and cardiac output. These branches differ in their neurotransmitters (norepinephrine and acetylcholine) and exert stimulatory or inhibitory effects on target tissue via adrenergic and muscarinic receptors. Stimulation of the sympathetic branch exerts facilitatory effects on function, increasing heart rate and myocardial contractility, whereas the stimulation of the parasympathetic branch exerts inhibitory effects that decrease heart rate and contractility. The interplay between these two branches is complex and susceptible to control at several levels, from centrally mediated baroreceptors and chemoreceptors to local interneuronal interactions.Alterations in autonomic function occur in several interrelated cardiac conditions including sudden cardiac death, congestive heart failure, diabetic neuropathy, and myocardial ischemia. Although the full extent of these changes has not been elucidated, multiple autonomic remodeling mechanisms have been observed at both the neuronal fiber and myocardial cellular level that contribute to an arrhythmogenic substrate. We describe the anatomy of both systems in this review. However, the review will premdominantly focus on the sympathetic system, whose role in the modulation of cardiac arrhythmias is slightly better delineated. Cardiac Autonomic Innervation: NeuroanatomyBoth branches of the autonomic nervous system are composed of both afferent and efferent as well interneuronal fibers (Fig 1). Sympathetic innervation originates mainly in the right and left stellate ganglia. These fibers travel along the epicardial vascular structures of the heart and penetrate into the underlying myocardium similar to coronary vessels and end as sympathetic nerve terminals reaching the endocardium. Based on norepinephrine content studies, a gradient exists in sympathetic innervation from atria to the ventricles and from base to apex of the heart. Therefore, the atria are most densely innervated, but the ventricles are also supplied with a sympathetic network, most densely at the base. 1 Parasympathetic effects are carried by the right and left vagus nerves, originating in the medulla. The vagus nerve further divides into the superior and inferior cardiac nerves, finally merging with the postganglionic sympathetic neurons to form a plexus of nerves at the base of the heart, known as the cardiac plexus. In contrast to sympathetic neurons, after parasympathetic fibers cross the atrioventricular (AV) groove along the surface of the heart,

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Effects of resynchronization therapy on sympathetic activity in patients with depressed ejection fraction and intraventricular conduction delay due to ischemic or idiopathic dilated cardiomyopathy

Cited by 53 publications

References 10 publications

Cardiac Resynchronization Therapy Improves Heart Rate Variability in Patients with Symptomatic Heart Failure

Cardiac Resynchronization Therapy Improves Heart Rate Variability in Patients with Symptomatic Heart Failure

The Autonomic Nervous System and Heart Failure

The Role of the Autonomic Nervous System in Sudden Cardiac Death

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