- ICH GCP
- Rejestr badań klinicznych w USA
- Badanie kliniczne NCT01944605
Intestinal Ischemia as a Stimulus for Systemic Inflammatory Response After Cardiac Arrest (TICA)
Out-of-hospital cardiac arrest (CA) is a leading public health problem causing nearly one third of a million deaths annually in the US, accounting for half of all cardiovascular deaths and surpassing deaths from stroke, heart failure, and breast and lung cancer combined. Twenty to fifty percent of CA patients (pts) can be resuscitated initially but many die before hospital discharge or suffer permanent neurologic damage. Therapeutic hypothermia (TH) improves survival and neurological outcomes. Despite aggressive, targeted post arrest management, including TH, approximately 50% of pts die before leaving the hospital due to global ischemia-reperfusion injury (IRI) known as the "post arrest syndrome", 1 which is a sepsis-like state characterized by elevated markers of cellular inflammation and injury. It is believed that TH works by decreasing the body's basal metabolic rate (BMR) and attenuating the systemic inflammatory response (SIR). However, specific triggers of the intense pro-inflammatory response are unclear. This "gap" in knowledge must be closed to identify targeted therapy to decrease IRI and improve outcomes.
Blood flow to the gut is decreased markedly and intestinal tissue becomes ischemic during CA and CPR, particularly when vasoconstrictor drugs such as epinephrine, are given. IRI of the intestine increases intestinal permeability leading to intestinal microbial translocation and endotoxin release that can stimulate and perpetuate systemic inflammation and cause subsequent multi-organ dysfunction. Endotoxin also increases body temperature and energy expenditure and may attenuate TH induced reductions in BMR and hence, decrease efficacy. The purpose of this novel pilot study is to detect systemic endotoxin release following CA in humans and determine association with cytokine activation, and BMR alterations during TH.
Przegląd badań
Status
Szczegółowy opis
Hypothesis 1 Intestinal ischemia during and following Caridac Arrest leads to increased gut permeability and endotoxin release that stimulates the Systemic Inflammatory Response that is responsible for subsequent death and disability after resuscitation.
Hypothesis 2: Different degrees of systemic endotoxin activity variably affect Basic Metabolic Rate during Therapeutic Hypothermia
Serial samples of blood, stool and expired gas will be measured at predetermined timepoints after ROSC from cardiac arrest.
Typ studiów
Zapisy (Rzeczywisty)
Kontakty i lokalizacje
Lokalizacje studiów
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Virginia
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Richmond, Virginia, Stany Zjednoczone, 23298
- Virginia Commonwealth University
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Kryteria uczestnictwa
Kryteria kwalifikacji
Wiek uprawniający do nauki
Akceptuje zdrowych ochotników
Płeć kwalifikująca się do nauki
Metoda próbkowania
Badana populacja
Opis
Inclusion Criteria:
Adult, Cardiac Arrest with ROSC receiving Therapeutic Hypothermia-
Exclusion Criteria:
- Age < 18
- Cardiac Arrest of traumatic etiology
- Known to be pregnant
- Prisoner
Plan studiów
Jak projektuje się badanie?
Szczegóły projektu
- Modele obserwacyjne: Kohorta
- Perspektywy czasowe: Spodziewany
Kohorty i interwencje
Grupa / Kohorta |
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Cardiac Arrest patients undergoing Therapeutic Hypothermia
Cardiac Arrest subjects with Return Of Spontaneous Circulation (ROSC) and undergoing treatment with Therapeutic Hypothermia will undergo sampling of blood, stool, and expired gas data at physiologically predetermined time points.
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Co mierzy badanie?
Podstawowe miary wyniku
Miara wyniku |
Opis środka |
Ramy czasowe |
---|---|---|
Detection of Endotoxin Activity
Ramy czasowe: 48 hours
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Endotoxin activity will be measured by the Endotoxin Activity Assay and values . of >0.4 EA units will be used as the "cut-off" for the presence of pathological endotoxin.
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48 hours
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Miary wyników drugorzędnych
Miara wyniku |
Opis środka |
Ramy czasowe |
---|---|---|
Detection of sCD14
Ramy czasowe: 48 hours
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To demonstrate activation of endotoxin by the immune system and "upstream" physiologic changes necessary for systemic endotoxemia to occur
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48 hours
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Detection of stool lactoferrin and stool α1-antitrypsin
Ramy czasowe: 48 hours
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To demonstrate evidence of intestinal inflammation and permeability that can lead to endotoxemia and "downstream" cellular inflammatory responses responsible for end organ damage
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48 hours
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Detection and quantification of inflammatory cytokines
Ramy czasowe: 48 hours
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To demonstrate an association with the primary outcome
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48 hours
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BMR measurement elevation
Ramy czasowe: 48 hours
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To determine its association with endotoxemia and cytokine.
BMR is being measured to determine if pts with higher levels of endotoxin and cytokines have higher BMR and therefore blunted therapeutic value of TH
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48 hours
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Współpracownicy i badacze
Sponsor
Współpracownicy
Śledczy
- Główny śledczy: Mary Ann Peberdy, M.D., Virginia Commonwealth University
Daty zapisu na studia
Główne daty studiów
Rozpoczęcie studiów
Zakończenie podstawowe (Rzeczywisty)
Ukończenie studiów (Rzeczywisty)
Daty rejestracji na studia
Pierwszy przesłany
Pierwszy przesłany, który spełnia kryteria kontroli jakości
Pierwszy wysłany (Oszacować)
Aktualizacje rekordów badań
Ostatnia wysłana aktualizacja (Rzeczywisty)
Ostatnia przesłana aktualizacja, która spełniała kryteria kontroli jakości
Ostatnia weryfikacja
Więcej informacji
Terminy związane z tym badaniem
Słowa kluczowe
Dodatkowe istotne warunki MeSH
Inne numery identyfikacyjne badania
- HM15326
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