{"id":"97f17625cc1c","type":"article","url":"https://hartvaat.nl/2026/05/13/hypothese-falen-van-het-raas-verklaart-inappropriate-vasodilatatie-bij-cardiogen/","title":"Hypothese: falen van het RAAS verklaart inappropriate vasodilatatie bij cardiogene shock","title_en":"","category":"algemeen","category_label":"Algemeen","professions":["cardioloog","internist"],"tags":["acuut-hartfalen","bloeddrukbehandeling","cardiogene-shock","supraventriculaire-tachycardie","troponine"],"journal":"European heart journal","doi":"10.1093/eurheartj/ehag292","source_url":"https://doi.org/10.1093/eurheartj/ehag292","authors":["Adrien Picod","Susanna Price","Thomas Hanff"],"significance":6,"published":"2026-06-21","source_date":"2026-05-13","image":"","kennis":["https://hartvaat.nl/kennis/farmacologie/aldosteron-en-raas-farmacologie/","https://hartvaat.nl/kennis/coronairlijden/stemi/"],"congress":"","summary_en":"Conceptual paper in EHJ on an underappreciated aspect of cardiogenic shock (CS): a subgroup of patients — without concurrent sepsis — develop a mixed shock phenotype with unexpected vasodilation on top of the primary myocardial failure, which portends a worse prognosis. The authors propose that failure of the renin-angiotensin-aldosterone system (RAAS), analogous to recent findings in septic shock, plays a key role: through defective angiotensin II generation, enhanced peptide degradation, and/or receptor unavailability, angiotensin II signalling at the AT1 receptor becomes impaired. Recognising RAAS failure in CS could justify new therapeutic strategies to restore vascular tone and improve outcomes in mixed cardiogenic-vasodilatory shock.","created":"2026-07-03T10:33:05Z","updated":"2026-07-03T13:31:59Z","licence":"Citeer vrij, met bronvermelding en een link naar hartvaat.nl (de url van het record). Samenvattingen zijn redactioneel werk van HartVaat; de oorspronkelijke publicaties blijven van hun uitgevers (doi). Geen medisch advies.","body_markdown":"Conceptueel paper in EHJ over een onbegrepen aspect van cardiogene shock (CS): een subgroep patiënten ontwikkelt — zonder gelijktijdige sepsis — een gemengd shockfenotype met onverwachte vasodilatatie bovenop het primaire myocardiale falen, wat een slechtere prognose voorspelt. De auteurs stellen dat falen van het renine-angiotensine-aldosteron-systeem (RAAS), analoog aan recente bevindingen bij septische shock, hier een sleutelrol speelt: door defecte angiotensine-II-productie, versterkte peptide-afbraak en/of onvoldoende receptorbeschikbaarheid raakt angiotensine-II-signalering aan de AT1-receptor verstoord. Herkenning van RAAS-falen bij CS zou nieuwe therapeutische strategieën kunnen rechtvaardigen om de vaattonus te herstellen en uitkomsten bij gemengde cardiogene-vasodilatoire shock te verbeteren.","abstract_original":"Cardiogenic shock (CS) is a state of acute circulatory failure resulting from impaired myocardial function and reduced cardiac output, leading to inadequate tissue perfusion and subsequent organ dysfunction. In its early phase, CS is typically accompanied by systemic vasoconstriction as a compensatory response aimed at preserving mean arterial pressure and organ perfusion. However, an increasing body of evidence suggests that a subset of patients develop a mixed shock phenotype, characterized by superimposed vasodilation without evidence of concurrent sepsis, which portends a worse prognosis. Failure of the renin-angiotensin-aldosterone system (RAAS) may be a key driver of pathological vasodilation in CS, analogous to recent observations in septic shock. Specifically, RAAS dysfunction could lead to impaired angiotensin II signalling at the angiotensin II type 1 receptor level due to defective angiotensin II generation, enhanced peptide degradation, and/or receptor unavailability. Recognition of RAAS failure in CS could inform novel therapeutic strategies to restore vascular tone and improve outcomes in patients with mixed cardiogenic-vasodilatory shock."}