AN ELECTRONIC DEVICE FOR ACCURATE IDENTIFICATION OF THE CARDIAC CONDUCTION SYSTEM. ITS DEVELOPMENT AND USE IN OPEN HEART SURGERY.
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The distributing artery of the conducting system of the heart is occasionally injured in cardiac surgery. The aim of this study was to define the anatomic characteristics of the principal arterial source of the sinu-atrial node and atrioventricular node. Furthermore, the morphology of the tendon of Todaro was clarified. Thirty hearts were studied by gross anatomic methods, and the exact area of the conducting system was supported by histologic observations of four hearts. The sinu-atrial node was supplied by the right coronary artery more frequently (73% of cases) than by the left (3%), and in 23% of cases this node was supplied by both coronary arteries. The atrioventricular node was supplied by the right coronary artery (80% of cases) more than by the left (10%), and in 10% of the cases this node was supplied by both coronary arteries. The atrioventricular bundle branch arose from the right coronary artery in 10% of cases, the left coronary artery in 73%, and both coronary arteries in 17%. Most of the blood to the right bundle (the moderator band) was supplied by the interventricular septal branches of the anterior interventricular branch from the left coronary artery. Finally, all the arteries of the right bundle and left bundle were defined to be derived from left coronary arteries.
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Working and specialized cardiac myocytes and their intercalated disks (ID) in the mammalian heart were examined by transmission and scanning electron microscopy. The NaOH/ultrasonication treatment of cardiac tissues resulted in the digestion of collagen fibers and separation of intercellular junctions. Auricular and ventricular myocytes were cylindrical in shape, bifurcated, and connected end-to-end at the ID. The ID in the working myocardium showed a stair-like profile, consisting of steps (plicate segments) and corresponding risers (interplicate segments). The ventricular myocytes had many steps and risers. The steps were filled with numerous finger-like microprojections, including desmosomes, fasciae adherentes, and small gap junctions. The risers showed the smooth surface, including desmosomes and large gap junctions. The cell strands of the sinoatrial node were oriented linearly, while those of the atrioventricular node formed a reticular network. The ID in both nodal cells was underdeveloped, having few microprojections. Myocytes in the His bundle and its branches were arranged in parallel, and Purkinje cell strands formed reticular networks. The ID in the His-Purkinje system was irregular in appearance, and the microprojections were larger in size and smaller in number than those of working myocytes. There were few microprojections in the sheep Purkinje cells. The gap junctions in the conduction system were few or small in size in the nodal tissue, but large in the His-Purkinje system.
The principles of a quantitative determination of characteristics concerning the types of anatomical correspondence between the conduction system and the heart at its congenital malformations are presented. This makes it possible to establish that the topographoanatomical type of the conduction system depends on the peculiarities of the heart structure at its congenital malformations rather than from changes in the structure and position of the parts of the conduction system, or the conduction system as a whole according to the types of congenital heart malformations. The mechanism of the left-sided position of the atrioventricular bundle (His bundle) in some congenital malformations of the heart is explained.
This article reviews the cardiovascular effects of the standard tricyclic antidepressants and what is known of the cardiovascular effects of the newer antidepressants. The cardiovascular effects of the standard tricyclics are orthostatic hypotension, conduction delay and a potent antiarrhythmic effect. Patients who have congestive heart failure and are on cardiac medications are at greatly increased risk for orthostatic hypotension, while patients who have pre-existing conduction delay are at risk for heart block.
The development of the heart-conducting system has been controversially discussed. The common opinion that these specialized myocytes originate from mesodermal precursors has been challenged when nerve-specific antigens (Leu-7, NF, GIN2) were demonstrated in embryonic hearts of various species, suggesting a neural crest contribution to the embryonic conducting tissue. Anti-Leu-7 (HNK-1) antibodies were reported to reliably mark the conducting system in developing rat, chicken and human hearts. The present investigation was carried out on the hearts of 15 camel fetuses at 35, 45, 60, 75 and 100 cm crown-rump length (three specimens for each stage), in addition to three adult hearts. We investigated the antigenicity of cardiac structures for Leu-7, NSE (Neurone specific Enolase) and PGP (Protein Gene Peptide) 9.5. In all specimens investigated, both NSE and PGP 9.5 were expressed by cardiac nerves and conducting system components. The sinuatrial and atrioventricular nodes, the atrioventricular bundle as well as subendocardial and intramyocardial Purkinje fibers were stained. In contrast, the developing conducting system did not react with anti-Leu-7 antibody, although Leu-7 antigenicity was strongly expressed by the developing cardiac nerves. In adult camel hearts, the same pattern of immunoreactivity for the markers studied was still retained. Our results show that the expression of marker proteins for the developing conducting system is species-specific. Therefore, these markers are of little significance in discussions on the possible neurogenic nature of the heart conducting tissue.
A study of the prevalence of thick intimas and of obstructive lesions in the vessels supplying the conduction system of the heart (first septal artery, sinus node artery, atrioventricular node artery, posterior descending artery) was carried out on both non-hospitalized and hospitalized subjects. A total of 932 cases aged 6 to 55 years were investigated. The age period of the onset of both intimal thickenings and atherosclerotic plaques, the percent of cases with intimal thickenings and atherosclerotic plaques in successive age groups and the highest value of the intima thickness/media thickness ratio, were recorded. Comparative data are presented between apparently healthy subjects who died of accidental causes and patients of similar age and sex, who died of coronary heart disease. Sudden cardiac death cases are presented showing as the most important lesion the obstruction of the sinus node and atrioventricular node arteries. The results point to a need for a more frequent routine examination of the vessels supplying the conduction tissue of the heart.
Intravenous injection of T-2 toxin or roridin-A (2 mg/kg) into pentobarbital-anesthetized (30 mg/kg) dogs produced, respectively, decreased systolic pressure within 30 min and atrio-ventricular block within 60 min. Within 45 +/- 15 min after injection of each toxin heart rate increased and remained elevated for at least 4 hr. The increase in sinus rate was reduced by 50% when dogs were pretreated with i.v. propranolol--HCl (5 mg/kg); pretreatment with atropine sulphate (5 mg/kg) did not alter the effect of the trichothecenes. Upon administration of T-2 toxin or roridin-A (30 mg/l) to isolated arterially perfused canine right atria, sinus rate decreased by 12% and 28%, respectively, and sinus node cell diastolic potentials became more negative by 7% and 10%, respectively. Sino-atrial block observed in 50% of the isolated atrial preparations perfused with roridin-A disappeared when toxin perfusion was discontinued. Perfusion with T-2 toxin or roridin-A produced no significant effects on atrial muscle cell action potentials. The cardiovascular response to systemic trichothecenes was hypotension followed by propranolol-sensitive tachycardia. The direct effects on conduction system cells may contribute to the overall deleterious action on the cardiovascular system.
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This study has been performed applying postmortem coronary angiography and histological investigation of the conduction system of the heart in 21 persons who died suddenly and unexpectedly because of coronary sclerosis. This "coronary group" is compared with a sex and age matched control group of 24 persons. Acute vascular lesions were found in 20 persons (95.2%), fresh infarctions in 10 (45%), heart rupture in 2 (9.5%) and old infarctions (indicated by localized fibrosis) in 7 (33.3%). The coronary arteries were graded using WHO's recommendations from 1958. Arteriosclerosis of the major coronary arteries was significantly more extensive in the "coronary group". The origin and course of the arteries to the conduction system were located by postmortem coronary angiography. The right coronary artery supplied these arteries in the majority of cases (sinus node artery 77%, a.-v. node artery 85%). A significantly greater degree of arteriosclerosis could be demonstrated histologically in the sinus node artery in the "coronary group". In both groups the degree of arteriosclerosis was greater in the a.-v. node artery than in the sinus node artery. The conduction system was investigated using Hudson's method. There were only 3 cases of infarction in the conduction system, possibly due to its greater resistance to damage from anoxia. In all patients "non-specific changes" (hemorrhage, small cellular infiltrations and/or degeneration) were found and these changes can, therefore, be of no pathophysiological importance in this group of patients. The degree of fibrosis and the amount of fat was semiquantified. Six patients in the "coronary group" had moderate fibrosis around the left sided fibres of the bundle of His. This leads to the conclusion that these changes might play a role in the fatal course, and that some cases of sudden, unexpected cardiac death can be explained by pre-existing fibrosis in the conduction system.
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