Tom 17, Nr 2 (2020)
Nadciśnienie tętnicze
Opublikowany online: 2020-10-14
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Eksport do Mediów Społecznościowych

Eksport do Mediów Społecznościowych

Nowoczesna protekcja w nadciśnieniu tętniczym i przewlekłym zespole wieńcowym

Stefan Grajek1
Choroby Serca i Naczyń 2020;17(2):84-95.

Streszczenie

Obraz kliniczny nadciśnienia tętniczego jest wynikiem współdziałania dwóch mechanizmów: presyjnego (następstwa wzrostu ciśnienia przezściennego) oraz miażdżycy (przyspieszony rozwój blaszek miażdżycowych). Pierwszy z mechanizmów prowadzi do udaru krwotocznego mózgu, przerostu mięśnia sercowego z rozwojem niewydolności serca czy tętniaka/rozwarstwienia aorty, drugi — do udaru niedokrwiennego mózgu, ostrego (ACS) i przewlekłego zespołu wieńcowego (CCS), obwodowych zmian miażdżycowych. W nowych badaniach genetycznych potwierdzono udział obu mechanizmów w rozwoju zdarzeń sercowo-naczyniowych. Osoby z wariantem genetycznym umożliwiającym niższe wartości cholesterolu frakcji LDL (LDL-C) i niższe wartości ciśnienia tętniczego są istotnie rzadziej narażone na powikłania sercowo-naczyniowe. W licznych randomizowanych badaniach dowiedziono, że u chorych z nadciśnieniem tętniczym łączne stosowanie leków hipotensyjnych i hipolipemizujących (polypill) przynosi większe korzyści kliniczne niż monoterapia hipotensyjna. Obserwacje epidemiologiczne potwierdzają słuszność obecnie obowiązującego paradygmatu terapeutycznego.

Prewencyjnym celem optymalnego leczenia farmakologicznego (OMT) CCS jest zapobieganie wystąpieniu pierwszego i kolejnych epizodów ACS. Istota choroby miażdżycowej tętnic wieńcowych to rozwój blaszki miażdżycowej (kumulacja lipidów) z jej gromadzeniem się na zerodowanej powierzchni płytkowych zakrzepów (atherothrombosis). Farmakoterapia winna być oparta przede wszystkim na „twardym jądrze leczenia przeciwmiażdżycowego” (zawierającego statyny oraz inhibitory konwertazy angiotensyny [ACE-I]). Obie grupy leków w odmienny sposób korzystnie wpływają na blaszkę miażdżycową. Statyny zmniejszają jej objętość i tłumią proces zapalny, jednakże warunkiem koniecznym jest obniżenie stężenia LDL-C poniżej 55 mg/dl (70 mg/dl). Inhibitory konwertazy angiotensyny, hamując aktywność układu renina–angiotensyna–aldosteron (działanie antyzapalne), prowadzą do jej włóknienia i stabilizacji blaszki. Nowe połączenia leków obniżających stężenie LDL-C z ACE-I, na przykład atorwastatyna z peryndoprylem, umożliwiają skuteczne leczenie za pomocą jednej tabletki. Drugim niezbędnym elementem optymalnego leczenia farmakologicznego jest „twarde jądro leczenia przeciwkrzepliwego” zawierające kwas acetylosalicylowy i jeden z leków z grupy inhibitorów P2Y12 lub riwaroksaban. Pozostałe leki, takie jak beta-adrenolityki, antagoniści wapnia, nitraty o przedłużonym działaniu, iwabradyna, leki cytoprotekcyjne, stosuje się w zależności od indywidualnych wskazań.

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