Background. Myocardial overload occurs in situations when one or another heart chamber receives excess blood during diastole. Most often it occurs as a result of insufficiency of aortic or atrioventricular valves. Changes in cardiomyocytes (CMs) are regarded as compensatory, and the way myocardial remodeling with volume overload passes into the stage of decompensation still remains unexplored. The aim. To determine the morphological signs of adaptation and maladaptation of the myocardium to its volume overload. Materials and methods. Four hearts obtained at autopsy from patients who died of heart failure due to mitral valve insufficiency were used for the microscopical examination. Histological specimens were stained with hematoxylin and eosin, picrofuxin according to Van Gieson, fuxelin according to Weigert, alizarin red S and MSB method modified by Zerbino-Lukasevich “orange-red-blue” (ORB). For the study by electron microscopy, the material was obtained during operations in 6 patients with dilated atria from the area of surgical access. Results and conclusions. The heart chambers volume overload is compensated by the increase in the size of their cavities due to the “longitudinal” hypertrophy of the CMs which is expressed by the increase in the number of sarcomeres in each myofibril. The compensation mechanism is limited by the ability of abruptly altered CMs to produce new sarcomeres. Decompensation of adaptive processes is manifested by: destruction of intermyocytic and interfiber connections in functional myocardial syncytium; desynchronization of CMs contraction; the effect of CMs “sliding” relative to each other with the damage of interstitial connective tissue; dilation of T-tubes of CMs with the subsequent calcium damage of cellular organelles; dissociation of CMs and myocardial fibrosis.
Цель работы -на основании данных современных источников научной литературы проанализировать морфологические особенности миокарда при гипертрофической кардиомиопатии.Обзор освещает современные взгляды на особенности структурного ремоделирования миокарда левого желудочка сердца у больных гипертрофической кардиомиопатией, приведены наиболее распространенные классификации данной патологии. Уделено внимание проблеме взаимосвязи фигур дизарея кардиомиоцитов и фиброза миокарда. Важное патогенетическое звено развития сердечной недостаточности, усиливающее связь между нарушениями гистоархитектоники миокарда и прогрессирующей ишемией сердца при гипертрофической кардиомиопатии -«болезнь малых сосудов».Выводы. Несмотря на большое количество исследований гипертрофической кардиомиопатии, в научной литературе нет единого мнения об этиологии и патогенезе гипертрофической кардиомиопатии. Противоречивые сведения о наличии взаимосвязи и последовательности развития фигур дизарея, гипертрофии кардиомиоцитов, интерстициального фиброза, изменений микроциркуляторного русла и митрального клапана при гипертрофической кардиомиопатии затрудняют поиски адекватного этиотропного лечения. Полиморфизм клинических и морфологических проявлений гипертрофической кардио миопатии требует от кардиологов и патогистологов совместных усилий по изучению данной болезни.A -research concept and design; B -collection and/or assembly of data; C -data analysis and interpretation; D -writing the article; E -critical revision of the article; F -final approval of the article The objective. Based on the modern sources of scientific data to analyze the morphological features of the myocardium in hypertrophic cardiomyopathy.The paper presents a literature review on current views on the features of structural remodeling of the left ventricular myocardium in patients with hypertrophic cardiomyopathy, as well as the most common classifications of this pathology. The emphasis is made on the problem of the interrelation of myocardial disarray and fibrosis.The "small vessel disease" is an important pathogenetic link in the development of heart failure, which enhances the relation between disorder of myocardial histoarchitectonics and progressive cardiac ischemia in hypertrophic cardiomyopathy. Conclusions.Notwithstanding the numerous research data on hypertrophic cardiomyopathy, no consensus among the authors regarding the etiology and pathogenesis of hypertrophic cardiomyopathy exists to date. Controversial data on the interrelation and sequence of disarray, myocardial hypertrophy, interstitial fibrosis, changes in the microvasculature and structural changes of the mitral valve in patients with hypertrophic cardiomyopathy hamper the search for adequate etiotropic treatment.Polymorphism of clinical and morphological manifestations of hypertrophic cardiomyopathy requires collaborative efforts to study the disease by cardiologists and pathologists.Морфологія міокарда при гіпертрофічній кардіоміопатії: сучасний стан проблеми А. А. Балабай Мета роботи -на підставі даних сучасни...
The aim. To study the morphological manifestations of the response of the myocardial capillaries to cardioplegia in patients with valvular defects and coronary heart disease. Materials and methods. Morphological research of operative and sectional material was carried out. Myocardium fragments for microscopical study were obtained from patients at different stages of an open-heart surgery and patients who died at the stage of conservative treatment without surgical intervention. Similar samples of the myocardium of a healthy young man who died from injuries incompatible with life were studied as a control. For electron microscopy study, samples of myocardium were taken from patients at the 185th minute of perfusion. Results. Histological preparations of the myocardium showed pronounced diffuse hypertrophy of cardiomyocytes (CMCs), sometimes at the stage of decompensation (perinuclear edema, loss of myofibrils, apoptosis). This transformation of CMCs was obviously related to their functional overload caused by combined defects of the mitral and aortic valves. Changes in muscle fibers were accompanied by interstitial and perinuclear fibrosis. In the pool of coronary arteries affected by atherosclerosis, signs of small focal coronary fibrosis were visible, as well as rough post-infarction scars in 3 patients. All the patients had signs of acute hypoxic damage to the myocardium in the form of CMCs shortening and interstitial edema. Conclusions. In patients with combined defects of the aortic and mitral valves of the heart with coronary artery disease, the phenomena of myocardial fibrosis prevail. Heart valve disease combined with coronary heart disease lead to the development of both alterative and compensatory-adaptiveprocesses in the vessels of the microcirculatory bed. The greatest loss of vital organelles in small vessels is observed at 185 min after administration of cardioplegic solution, irreversible changes develop 3 h after perfusion.
Мета. Вивчити ефективність застосування автоматичного режиму ендовенозного електрозварювання (ЕВЕЗ) в лікуванні варикозної хвороби нижніх кінцівок (ВХНК). Матеріали і методи. Автоматичний режим ЕВЕЗ досліджували на видалених сегментах великої підшкірної вени (ВПВ), визначаючи температуру, опір та морфологічні зміни. Проаналізовані результати застосування методу у 56 пацієнтів з ВХНК С2 - С5 класів (за класифікацією СЕАР - clinic, etiolody, anatоmy, pathogenesis): 21 чоловіка та 35 жінок у віці 18 - 63 років. Критерії оцінки: післяопераційний біль (ПБ), анатомічний результат, ускладнення. Втручання виконували під інфільтраційною анестезією 0,125% розчином бупівакаїну. Результати визначали під час ультразвукового ангіосканування через 14 діб, 3 і 6 міс. Результати. Протягом автоматичного циклу ЕВЕЗ (5 - 12 с) відбувалася оклюзія ВПВ при температурі 55 - 75 °С. Визначена альтерація вени на глибину ендотеліального та субендотеліального шарів без пошкодження паравазальної клітковини. ПБ був помірний. Фіброзну трансформацію (ФТ) ВПВ через 6 міс встановили у 55 (98,2%) пацієнтів. Екхімози та парестезію спостерігали у 4 (7,1%) та 2 (3,6%) пацієнтів. Висновки. Автоматичний режим ЕВЕЗ, який ґрунтується на взаємозв’язку електричних параметрів зварювання та опору тканин, забезпечує оклюзію ВПВ з подальшою ФТ, супроводжується низьким нагрівом вени та виключає вплив суб’єктивних факторів на результати операції.
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