Mediastinal Nerve Research Articles

Spinal cord stimulation suppresses bradycardias and atrial tachyarrhythmias induced by mediastinal nerve stimulation in dogs

Spinal cord stimulation (SCS) applied to the dorsal aspect of the cranial thoracic cord imparts cardioprotection under conditions of neuronally dependent cardiac stress. This study investigated whether neuronally induced atrial arrhythmias can be modulated by SCS. In 16 anesthetized dogs with intact stellate ganglia and in five with bilateral stellectomy, trains of five electrical stimuli were delivered during the atrial refractory period to right- or left-sided mediastinal nerves for up to 20 s before and after SCS (20 min). Recordings were obtained from 191 biatrial epicardial sites. Before SCS (11 animals), mediastinal nerve stimulation initiated bradycardia alone (12 nerve sites), bradycardia followed by tachyarrhythmia/fibrillation (50 sites), as well as tachyarrhythmia/fibrillation without a preceding bradycardia (21 sites). After SCS, the number of responsive sites inducing bradycardia was reduced by 25% (62 to 47 sites), and the cycle length prolongation in residual bradycardias was reduced. The number of responsive sites inducing tachyarrhythmia was reduced by 60% (71 to 29 sites). Once elicited, residual tachyarrhythmias arose from similar epicardial foci, displaying similar dynamics (cycle length) as in control states. In the absence of SCS, bradycardias and tachyarrhythmias induced by repeat nerve stimulation were reproducible (five additional animals). After bilateral stellectomy, SCS no longer influenced neuronal induction of bradycardia and atrial tachyarrhythmias. These data indicate that SCS obtunds the induction of atrial arrhythmias resulting from excessive activation of intrinsic cardiac neurons and that such protective effects depend on the integrity of nerves coursing via the subclavian ansae and stellate ganglia.

Differential effects of cervical vagosympathetic and mediastinal nerve activation on atrial arrhythmia formation in dogs

To investigate the influence of the thoracic autonomic neuronal hierarchy on atrial arrhythmia formation, we compared the characteristics of atrial tachyarrhythmias induced by electrical stimulation of 1) the right vagosympathetic nerve complex at the cervical level and 2) the more caudal juxta-cardiac mediastinal nerves located on the anterior surface of the superior vena cava. Unipolar electrograms were recorded from 191 sites on the entire epicardial atrial surface and, in some experiments, from 63 right atrial endocardial sites. The sites of origin of initial beats at the onset of atrial tachyarrhythmias so induced were investigated analysing atrial activation maps. Neural effects on repolarization were determined by computing the integral surface subtended by unipolar recordings under basal conditions and at maximum neurally induced bradycardia, and calculating differences at each recording site. The mean area affected by nerve stimulation in all animals was significantly greater in response to vagosympathetic than mediastinal nerve stimulation. Atrial cycle length prolongation prior to tachyarrhythmia onset was more pronounced in response to vagosympathetic than mediastinal nerve stimulation. The earliest epicardial activations in early tachyarrhythmia beats were localized in the right atrial free wall and Bachmann bundle region in both cases, but with a higher incidence of double breakthroughs from septal sites of origin in response to vagosympathetic versus mediastinal nerve stimulation. Sites of early activation were associated with the areas of neurally induced repolarization changes. Thus, differential contributions are made to the electrophysiologic substrate of neurally induced atrial tachyarrhythmias depending on the pattern of engagement of neural elements within the autonomic neuronal hierarchy.

Origin and pharmacological response of atrial tachyarrhythmias induced by activation of mediastinal nerves in canines

We sought to determine the sites of origin of atrial tachyarrhythmias induced by activating mediastinal nerves, as well as the response of such arrhythmias to autonomic modulation. Under general anaesthesia, atrioventricular block was induced after thoracotomy in 19 canines. Brief trains of 5 electrical stimuli were delivered to right-sided mediastinal nerves during the atrial refractory period. Unipolar electrograms were recorded from 191 right and left atrial epicardial sites under several conditions, i.e. (i) with intact nervous systems and following (ii) acute decentralization of the intrathoracic nervous system or administration of (iii) atropine, (iv) timolol, (v) hexamethonium. Concomitant right atrial endocardial mapping was performed in 7 of these dogs. Mediastinal nerve stimulation consistently initiated bradycardia followed by atrial tachyarrhythmias. In the initial tachyarrhythmia beats, early epicardial breakthroughs were identified in the right atrial free wall (28/50 episodes) or Bachmann bundle region (22/50), which corresponded to endocardial sites of origin associated with the right atrial subsidiary pacemaker complex, i.e. the crista terminalis and dorsal locations including the right atrial aspect of the interatrial septum. Neuronally induced responses were eliminated by atropine, modified by timolol and unaffected by acute neuronal decentralization. After hexamethonium, responses to extra-pericardial but not intra-pericardial nerve stimulation were eliminated. It is concluded that concomitant activation of cholinergic and adrenergic efferent intrinsic cardiac neurons induced by right-sided efferent neuronal stimulation initiates atrial tachyarrhythmias that originate from foci anatomically related to the right atrial pacemaker complex and tissues underlying major atrial ganglionated plexuses.

Treatment of a Humeral Metastasis with a Composite Allograft-Prosthetic Reconstruction

The treatment of impending pathological fractures and symptomatic metastases involving the upper extremity articulations remains a challenge for the trauma surgeon. While the goals of treatment of bony metastases are clearly defined (early restoration of function, excellent pain control and minimal surgical trauma), these are not always easy to realize in upper extremity periarticular metastases. A patient with a metastasis of a mediastinal nerve sheet tumor, involving the proximal 12 cm of the right humerus, including the whole head and both the tubercles, is described. A complete resection up to the level of the deltoid insertion was performed. In order to restore maximal function, the shoulder joint was reconstructed using a reversed total shoulder prosthesis. A fresh frozen cadaver proximal humerus was used as an allograft to obtain a secure stabilization of the prosthesis. Short-term results were very promising with restoration of ADL (activities of daily living) functionality within 3 months. Abduction and elevation > 100°, exorotation up to 20° and gluteal endorotation could be performed at that time. To the authors’ knowledge, this report is the first to describe reconstruction of the shoulder joint using a reversed shoulder prosthesis-allograft construction in case of a resection for malignancy.

Morphology, distribution, and variability of the epicardiac neural ganglionated subplexuses in the human heart.

Concomitant with the development of surgical treatment of cardiac arrythmias and management of myocardial ischemia, there is renewed interest in morphology of the intrinsic cardiac nervous system. In this study, we analyze the topography and structure of the human epicardiac neural plexus (ENP) as a system of seven ganglionated subplexuses. The morphology of the ENP was revealed by a histochemical method for acetylcholinesterase in whole hearts of 21 humans and examined by stereoscopic, contact, and bright-field microscopy. According to criteria established to distinguish ganglionated subplexuses, they are epicardiac extensions of mediastinal nerves entering the heart through discrete sites of the heart hilum and proceeding separately into regions of innervation by seven pathways, on the courses of which epicardiac ganglia, as wide ganglionated fields, are plentifully located. It was established that topography of epicardiac subplexuses was consistent from heart to heart. In general, the human right atrium was innervated by two subplexuses, the left atrium by three, the right ventricle by one, and the left ventricle by three subplexuses. The highest density of epicardiac ganglia was identified near the heart hilum, especially on the dorsal and dorsolateral surfaces of the left atrium, where up to 50% of all cardiac ganglia were located. The number of epicardiac ganglia identified for the human hearts in this study ranged from 706 up to 1,560 and was not correlated with age in most heart regions. The human heart contained on average 836 +/- 76 epicardiac ganglia. The structural organization of ganglia and nerves within subplexuses was observed to vary considerably from heart to heart and in relation to age. The number of neurons identified for any epicardiac ganglion was significantly fewer in aged human compared with infants. By estimating the number of neurons within epicardiac ganglia and relating this to the number of ganglia in the human epicardium, it was calculated that approximately 43,000 intrinsic neurons might be present in the ENP in adult hearts and 94,000 neurons in young hearts (fetuses, neonates, and children). In conclusion, this study demonstrates the total ENP in humans using staining for acetylcholinesterase, and provides a morphological framework for an understanding of how intrinsic ganglia and nerves are structurally organized within the human heart.

Endoscopic Esophagectomy: A Better Way to Atraumatic Surgery?

This paper describes the technique and clinical results of endoscopic dissection (endodissection) of the thoracic esophagus during transhiatal esophagectomy (THE). The method eliminates the ‘blind angle’ of conventional THE and reduces intraoperative traction on mediastinal tissues. Mediastinal structures such as the trachea, main bronchi and mediastinal nerves can be identified, and bleeding from minor mediastinal vessels can be controlled under vision. The mortality rate of the first 30 patients operated on was 6.6%, and only two major intraoperative complications occurred (one lesion of the right main bronchus, 2 bleedings). The rate of recurrent nerve palsy in these patients was low (6.6%).

Thoracoscopic Resection of a Posterior Mediastinal Neurogenic Tumor

Advances in endoscopic instrumentation and a growing enthusiasm for minimally invasive surgical techniques have sparked renewed interest in therapeutic thoracoscopy. We report the successful thoracoscopic resection of a posterior mediastinal nerve sheath tumor. A 35-year-old asymptomatic woman was found to have a posterior mediastinal mass on chest roentgenogram. Computed tomography and magnetic resonance imaging confirmed the presence of the lesion and showed no evidence of intraspinal extension. Exploratory thoracoscopy revealed a localized lesion without intraspinal extension. Thoracoscopic resection of the lesion was then performed. The patient's postoperative course was uncomplicated and she was discharged on the fifth postoperative day. The therapeutic potential of thoracoscopy continues to be realized as experience with the technique grows.

Plexiform neurofibromatosis of the mediastinum: CT appearance.

We studied the CT findings in four patients with pathologically proved thoracic plexiform neurofibromatosis. In all four patients, CT showed an infiltrative process and masses that involved the mediastinum along the distribution of the sympathetic chains, phrenic, and vagus nerves. The lesions had lower attenuation values than did chest-wall muscle. In one patient, CT revealed calcifications and peripheral enhancement of nodular components after IV infusion of contrast material. In the appropriate clinical setting, CT detection of lesions in the distribution of the mediastinal nerves strongly favors the diagnosis of plexiform neurofibromatosis.

Functional and anatomical variability of canine cardiac sympathetic efferent pathways: implications for regional denervation of the left ventricle.

To further elucidate the functional anatomy of canine cardiac innervation as well as to assess the feasibility of producing regional left ventricular sympathetic denervation, the chronotropic and (or) regional left ventricular inotropic responses produced by stellate or middle cervical ganglion stimulation were investigated in 22 dogs before and after sectioning of individual major cardiopulmonary or cardiac nerves. Sectioning the right or left subclavian ansae abolished all cardiac responses produced by ipsilateral stellate ganglion stimulation. Sectioning a major sympathetic cardiopulmonary nerve, other than the right interganglionic nerve, usually reduced, but seldom abolished, regional inotropic responses elicited by ipsilateral middle cervical ganglion stimulation. Sectioning the dorsal mediastinal cardiac nerves consistently abolished the left ventricular inotropic responses elicited by right middle cervical ganglion stimulation but minimally affected those elicited by left middle cervical ganglion stimulation. In contrast, cutting the left lateral cardiac nerve decreased the inotropic responses in lateral and posterior left ventricular segments elicited by left middle cervical ganglion stimulation but had little effect on the inotropic responses produced by right middle cervical ganglion stimulation. In addition, the ventral mediastinal cardiac nerve was found to be a significant sympathetic efferent pathway from the left-sided ganglia to the left ventricle. These results indicate that the stellate ganglia project axons to the heart via the subclavian ansae and thus effective sympathetic decentralization can be produced by cutting the subclavian ansae; the right-sided cardiac sympathetic efferent innervation of the left ventricle converges intrapericardially in the dorsal mediastinal cardiac nerves; and the left-sided cardiac sympathetic efferent innervation of the left ventricle diverges to innervate the left ventricle by a number of nerves including the dorsal mediastinal, ventral mediastinal, and left lateral cardiac nerves. Thus consistent denervation of a region of the left ventricle can not be accomplished by sectioning an individual cardiopulmonary or cardiac nerve because of the functional and anatomical variability of the neural components in each nerve, as well as the fact that overlapping regions of the left ventricle are innervated by these different nerves.

Functional anatomy of the canine mediastinal cardiac nerves located at the base of the heart.

The major canine cardiopulmonary nerves which arise from the middle cervical and stellate ganglia and the vagi course toward the heart in the dorsal mediastinum where they form, at the base of the heart dorsal to the pulmonary artery and aorta, the dorsal mediastinal cardiac nerves. In addition, the left caudal pole and interganglionic nerves project onto the left lateral side of the heart as the left lateral cardiac nerve. These nerves contain afferent and (or) efferent axons which, upon stimulation, modify specific cardiac regions and (or) systemic pressure. In addition, with the exception of the left lateral cardiac nerve, stimulation of each of these nerves produces compound action potentials in the cranial ends of the majority of the major cardiopulmonary nerves demonstrating that axons in each dorsal mediastinal cardiac nerve interconnect with axons in the majority of the cardiopulmonary nerves. Axons in the left lateral cardiac nerve connect primarily with axons in the left caudal pole and left interganglionic nerves. The dorsal mediastinal nerves project distally onto the heart as coronary nerves accompanying the right or left coronary arteries. These innervated the ventricular myocardium which is supplied by their respective vessels. The left lateral cardiac nerve projects directly onto the lateral epicardium of the left ventricle. The dorsal mediastinal and left lateral cardiac nerves are the major sympathetic cardiac nerves. Thus, the cardiac nerves located in the mediastinum at the base of the heart are not simple extensions of cardiopulmonary nerves, but rather have a unique anatomy and function of their own.

Cardioneuropathy and extracardiac neural disease

The pathology of cardiac innervation, both intrinsic and external to the heart (aortopulmonary glomera included), is scarcely known, yet it can be critical to life-threatening disorders in cardiac performance, or to reflexes discharging outside the heart, or both. Evidence has been supplied in cardiac neuroanatomy relevant to cardioneuropathy. The arrhythmogenic potential of imbalanced autonomic input in the heart has been corroborated by histopathologic findings in intrinsic plexuses. In turn, significant neurogenic substrates for cardiomyopathy have not been confirmed. Changes in the extrinsic sympathetic chain (left stellate ganglion) and in the prevailing vagal cardiac plexus were found in subjects with arrhythmias (with long QT interval and ventricular tachycardia/fibrillation, respectively). In myocardial infarction with sudden cardiac death, a complicating mediastinitis often presented and was seen to produce focal inflammation of mediastinal nerve plexus and paraganglia. This can worsen the imbalance in autonomic control of the performance of the heart and interfere with barochemoreflex regulation of the systemic or coronary circulation, or both. Such ill-understood sequelae of infarction as the shoulder-hand, chest pain and Dressler syndromes might also correlate with the newly described neuromediastinitis.

Arrhythmias induced by local cardiac nerve stimulation.

Arrhythmias induced by local cardiac nerve stimulation.