Роль инфекционных заболеваний нижних дыхательных путей в патогенезе ишемического инсульта (обзор)

Цель: обоснование патогенеза ишемического инсульта при инфекционных заболеваниях нижних дыхательных путей.

Материал и методы. Провели поиск оригинальных исследований, клинических сообщений, обзорных и редакционных статей, комментариев и кратких сообщений, опубликованных до 25 июня 2025 г. в базе PubMed. Дополнительные источники, которые не выявили с помощью поиска в первичной базе данных, анализировали после изучения списков литературы по отобранным статьям. Статьи отбирали, исходя из соответствия названия и аннотации цели настоящего обзора. В анализ включили данные 160 источников.

Результаты. Выделили и подробно рассмотрели механизмы развития ишемического инсульта при респираторных инфекциях: 1) активацию свертывающей системы крови и нарушение естественных антикоагулянтных и фибринолитических механизмов; 2) взаимодействие системы гемостаза с врожденным иммунитетом; 3) воздействие возбудителей инфекции на прогрессирование атеросклероза и стабильность атеросклеротической бляшки; 4) формирование тромбоэмболов в легочных венах.

Заключение. Как бактериальная, так и вирусная инфекция могут инициировать прокоагулянтное состояние, опосредованное тканевым фактором, фактором фон Виллебранда, активацией тромбоцитов, нейтрофильных внеклеточных ловушек и снижением активности эндогенных антикоагулянтов. Инфекционный процесс, локализованный в легких, характеризующийся повреждениями эндотелия сосудов легких, альвеолоцитов, внутриальвеолярным отложением фибрина, отеком, клеточной инфильтрацией, в совокупности с нарушениями гемостаза создает условия для формирования тромбов в сосудах легких. Таким образом, легочные вены и венулы могут являться источником тромбоэмболии сосудов головного мозга. Этот механизм развития тромбоэмболического инсульта во многом объясняет случаи острых нарушений мозгового кровообращения у пациентов с инфекцией нижних дыхательных путей без сердечно-сосудистых факторов риска. Другой механизм ишемического инсульта связан с прямым или опосредованным воздействием патогенов на стабильность атеросклеротических бляшек в сосудах головного мозга, что в совокупности с системным прокоагулянтным дисбалансом, приводит к формированию атеротромбоза. Учитывая обоснованную патогенетическую связь острых инфекционных заболеваний легких с кардиоэмболическим и атеротромботическим инсультами, необходима клиническая настороженность относительно острых нарушений мозгового кровообращения в тактике ведения таких пациентов.

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