Sudden unexpected death due to coronary heart disease. Postmortem coronary angiography and histological investigation of the heart conduction system.
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Electrophysiological examination of hearts were performed in 35 women and 25 men aged 18-63 years (mean age 38 years) without any concurrent heart diseases, divided into two groups: with PMVP (group I--40 subjects) and patients without this valvular anomaly (group II--20 subjects). In the patients with PMVP the examination revealed a significantly more frequent occurrence of the so-called "electrophysiological anomalies" (in 67.5%). The following appeared most frequently: sinus automatism disorders (32.5%), accessory a-v pathways (32.5%), longitudinal a-v node dissection (20%), and disorders of intracardiac conduction in segments: proximal (15%), distal (7.5%) and in both (5%). The implementation of pharmacological tests (with ajmalin, propranolol and atropine) made it possible to detect, in group with PMVP, the existence of occult conduction disturbances, particularly in distal segments of the conduction system (10%), and also to estimate exactly the character of the sinus node dysfunction (the background being in 7 patients functional, in 6 organic). During the programmed heart stimulation supraventricular dysrhythmias were evoked in 17 patients with PMVP. This is a proof that there is increased predisposition for paroxysmal supraventricular arrhythmias to occur in patients with mitral valve anomaly.
The distribution of nerve fibers showing neuropeptide Y-like immunoreactivity (NPY-LI) was compared with the distribution of the sympathetic nerve fibers in all parts of the conduction system and adjacent atrial and ventricular tissue of the bovine heart. Tyrosine hydroxylase (TH) and dopamine-beta-hydroxylase (DBH) served as markers for the sympathetic nerve fibers. NPY-LI was detected in most of the sympathetic nerve fibers that were present in nerve fascicles and that were associated with conduction cells and arterial walls in all regions examined. This phenomenon was more apparent when staining for NPY was compared with staining for DBH than with staining for TH. It was also found that some nerve varicosities exhibiting NPY-LI in association with arterial walls and local ganglia did not show DBH-LI. Furthermore, some of the ganglionic cells located in the regions of the conduction system showed NPY-LI but not DBH- or TH-LI. The observations are discussed in relation to what is known of the subcellular localization of NPY, TH and DBH. It is furthermore concluded that an NPY-like peptide is present in the sympathetic innervation of all parts of the conduction system and ordinary myocardial tissue, but that this peptide is also present in nerve fibers in the heart that do not represent sympathetic fibers. The observations raise important questions for further research aimed at determining the effects of NPY in relation to the function of the conduction system and in relation to the functions of not only sympathetic but also non-sympathetic nerve fibers in the heart.
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Intracardiac electrophysiologic studies were carried out in 9 patients with progressive muscular dystrophy. Diagnostic stimulation of the heart demonstrated no sinus mode dysfunction. The intra-atrial conduction time increased to 72 +/- 7.1 ms (p less than 0.05), and the interatrial conduction time, to 97 +/- 12.5 ms (p greater than 0.05) in response to shortened testing stimulus delay in 3 patients. All 9 patients showed great variation in the duration of effective refractory atrial and atrioventricular periods (97.0 +/- 12.5 ms). The H-V interval increased from 43.9 +/- 4.3 to 73.9 +/- 7.6 ms (p less than 0.01) in response to shortened delay in 7 of 9 patients. Atrial pre-excitation resulted in a block of the right and left limbs of the His bundle in 5 of 7 patients. Third-degree atrioventricular block was recorded by continuous ECG monitoring in 7 patient. It is suggested that an apparent or latent intraventricular conductivity disorder may be present in most cases of progressive muscular dystrophy.
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