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.
D001145:Arrhythmias, Cardiac / Q000473:pathology; D009202:Cardiomyopathies / Q000473:pathology; D005260:Female; D006325:Heart Atria / Q000294:innervation / Q000473:pathology; D006329:Heart Conduction System / Q000033:anatomy & histology / Q000473:pathology*; D006352:Heart Ventricles / Q000294:innervation / Q000473:pathology; D006801:Humans; D008297:Male; D008480:Mediastinitis / Q000473:pathology; D009203:Myocardial Infarction / Q000473:pathology; D009206:Myocardium / Q000473:pathology*; D009443:Neuritis / Q000473:pathology; D010233:Paraganglia, Chromaffin / Q000473:pathology; D013610:Tachycardia / Q000473:pathology