Keywords
cholecystocardial syndrome
right coronary artery
How to Cite
Abstract
The aim of our investigation was to estimate the modern condition of problem of cholecystocardial interrelations’ mechanisms. We organized the literature review and analyzed data of 98 patients with ischemic heart disease (IHD), which underwent coronary bypass surgery. Patients were divided into two groups in dependence of GB condition (intact; sludge and cholesterosis; bent GB body; neck deformations and cholecystitis; cholelithiasis; cholecystectomy in past). According to our results, prevalence of atrial fibrillation varied from (7.7±7.4)% (bent GB body) and (7.7±5.2)% (neck deformations and cholecystitis) to (50.0±15.8)% in cholelithiasis. Any rhythm disorders were the most often seen in patients with cholelithiasis (34.6%), twice more rarely – in patients with sludge (15.4%) and GB neck deformations together with chronic cholecystitis (18.5%). In all patients left atrium size was bigger than normal values: the biggest – in case of bent GB body and cholelithiasis (4.04 and 4.03 cm), minimally – in case of GB neck deformations and cholecystitis (3.82 cm). Progress of GB disorders is associated with arterial hypertension, which was diagnosed in all patients with IDH and bent GB body, GB neck deformation, cholelithiasis and past cholecystectomy. In literature we found description of significant correlation between GB width and right coronary artery diameter,which was proven by own data. One of the links which unite cholelithiasis and coronary atherosclerosis is blood cholesterol (Ch) increase. Ch concentration was maximal in case of bent GB body and minimal in patients with sludge. Taking into account literature data and own investigation, it can be stated that in patients with GB disorders takes place autonomous viscera-visceral cardioneuropathy, which progresses simultaneously with atherosclerosis and leads to more significant problems in coronary arteries. Leading mechanisms of it include reflectory influences of afferent pathologic impulsation form GB and autonomous nervous system dysfunction. Additional mechanisms comprise stimulation of metabolic disorders, inflammatory response and oxidative stress by GB pathology.References
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