Течение ишемической болезни сердца при метаболическом синдроме тема диссертации и автореферата по ВАК РФ 14.01.05, кандидат медицинских наук Фирова, Эльвира Михайловна
- Специальность ВАК РФ14.01.05
- Количество страниц 139
Оглавление диссертации кандидат медицинских наук Фирова, Эльвира Михайловна
ИСПОЛЬЗОВАННЫЕ СОКРАЩЕНИЯ.
1. ВВЕДЕНИЕ.
1.1. Актуальность.
1.2. Цель и задачи исследования.
1.3. Основные положения, выносимые на защиту.
1.4. Научная новизна работы.
1.5. Теоретическое и практическое значение работы.
1.6. Апробация работы.
1.7. Личный вклад.
2. ОБЗОР ЛИТЕРАТУРЫ.
2.1. Метаболический синдром: концепция и критерии диагностики
2.2. Патогенетические факторы, способствующие развитию метаболического синдрома.
2.2.1. Неэстерифицированные жирные кислоты.
Роль различных типов жировой ткани в повышении уровня НЭЖК.
Роль НЭЖК в развитии инсулинорезистентности.
Роль НЭЖК в развитии атерогенной дислипидемии.
2.2.2. Адипокины.
2.3. Влияние метаболического синдрома и его проявлений на течение ИБС.
2.3.1. Метаболический синдром и клиническое течение ИБС.
Роль неэстерифицированных жирных кислот.
Роль адипонектина.
Роль лептина.
2.3.2. Метаболический синдром и структурно-функциональные нарушения миокарда.
2.3.2.1. Артериальная гипертензия.
2.3.2.2. Ожирение.
2.3.2.3. Инсулинорезистентность и нарушение углеводного обмена.
Влияние гипергликемии.
Влияние гиперинсулинемии.
2.3.2.4. Дислипидемия.
2.3.2.5. Роль адипокинов.
Адипонектин.
Лептин.
3. МАТЕРИАЛЫ И МЕТОДЫ.
3.1. Пациенты.
3.2. Определение биохимических показателей в образцах плазмы пациентов.
3.3. Оценка функционального состояния сердечно-сосудистой системы и морфофункционалъного состояния миокарда.
3.4. Статистическая обработка результатов.
4. РЕЗУЛЬТАТЫ И ИХ ОБСУЖДЕНИЕ.
4.1. Толерантность к физической нагрузке и морфофункциональные параметры миокарда у пациентов с метаболическим синдромом.
4.2. Роль адипокинов и метаболических факторов в формировании морфофункциональных нарушений миокарда при ИБС.
4.3. Роль адипокинов и метаболических факторов в понижении функционального резерва миокарда и толерантности к физической нагрузке у пациентов с ИБС.
4.4. Адипокины: влияние на метаболические пути, ответственные за развитие нарушений структуры и функции миокарда при ИБС.
5. ВЫВОДЫ.
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1.1. Актуальность
В последнее десятилетие значительно возрос интерес исследователей к проблеме метаболического синдрома (МС). Это обусловлено как широким распространением его в популяции, так и значительным увеличением риска развития сердечно-сосудистых заболеваний (ССЗ) и, прежде всего, ишемиче-ской болезни сердца (ИБС) у пациентов, страдающих МС. Вплоть до настоящего времени недостаточно изученным остается вопрос о влиянии МС и его проявлений на течение ИБС. В частности, не выяснено, в какой степени при МС усугубляются такие сопутствующие ИБС нарушения со стороны сердца, как снижение функционального резерва миокарда, гипертрофия и ремодели-рование левого желудочка (ЛЖ), систолическая и диастолическая дисфункция миокарда ЛЖ.
Механизмы развития метаболического синдрома остаются окончательно не выясненными. Согласно современным представлениям, одним из ведущих патогенетических факторов развития МС, а также структурно-функциональных нарушений миокарда и снижения толерантности к физической нагрузке, является ожирение и/или абдоминальный тип распределения жировой ткани. Предполагается, что патогенное влияние ожирения на формирование МС опосредуется за счет повышения секреции в кровь жировой тканью неэстерифицированных жирных кислот (НЭЖК) и изменения продукции жировой тканью биологически активных белков - адипокинов. Но если участие НЭЖК и адипокинов в патогенезе МС более или менее известно, то влияние данных факторов на клиническое течение ИБС остается менее изученным.
Оценка значения клинико-биохимических проявлений МС в течении ИБС, с учетом влияния НЭЖК и адипокинов, позволит приблизиться к пониманию механизмов ухудшения течения ИБС, выявить наиболее неблагоприятные прогностические факторы, осложняющие течение ИБС, что будет способствовать разработке новых методов диагностики, профилактики и лечения данного заболевания.
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5. ВЫВОДЫ
1. У пациентов с метаболическим синдромом ИБС протекает на фоне повышения массы миокарда левого желудочка, снижения его функционального резерва и ухудшения толерантности к физической нагрузке, проявляющейся в виде снижения времени и объема выполненной работы и повышения частоты ишемических реакций при велоэргометрической пробе.
2. Ведущими факторами, способствующими формированию гипертрофии и ремоделирования миокарда ЛЖ у пациентов с ИБС, являются артериальная гипертензия, инсулинорезистентность и ожирение. Систолическая функция ЛЖ обратно взаимосвязана со степенью инсулинорезистентности и абдоминального распределения жировой ткани. При этом в формировании указанных морфофункциональных нарушений миокарда прямой роли НЭЖК и адипокинов не выявлено.
3. Важным фактором, определяющим снижение толерантности к физической нагрузке и функционального резерва миокарда у пациентов с ИБС, является инсулинорезистентность. Уменьшению функционального резерва миокарда также способствует гипоальфахолестеринемия. НЭЖК и адипокины в снижении толераностности к физической нагрузке и функционального резерва миокарда прямого участия не принимают.
4. Концентрации в крови адипонектина, лептина и НЭЖК у женщин являются независимыми детерминантами индекса инсулинорезистентности НОМА; у мужчин при этом данный показатель определяется уровнем НЭЖК. В свою очередь, на концентрацию НЭЖК у них оказывает независимое влияние уровень адипонектина.
5. Концентрации в крови адипонектина и лептина не оказывают прямого воздействия на уровень в крови ТГ и ХС ЛВП. При этом адипонектин влияет на содержание указанных липидов, воздействуя на метаболизм НЭЖК и глюкозы.
6. ПРАКТИЧЕСКИЕ РЕКОМЕНДАЦИИ
1. У пациентов с ИБС следует учитывать наличие метаболического синдрома в процессе лечения.
2. В целях оптимизации терапевтических мероприятий у пациентов с ИБС с сопутствующим метаболическим синдромом необходимо оценивать индекс инсулинорезистентности НОМА, уровень инсулина и глюкозы крови.
3. Для прогноза течения ИБС у пациентов с метаболическим синдромом использовать в практике определение уровня адипонектина, лептина.
4. Артериальную гипертензию, инсулинорезистентность, ожирение необходимо учитывать в прогнозировании течения ИБС у больных с метаболическим синдромом как факторы развития гипертрофии, ремодели-рования миокарда, изменения систолической функции.
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