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NCT Number: NCT02633358

Anti-inflammatory Effect of Therapeutic Hypothermia in Out-hospital Cardiac Arrest Patients With Cardiogenic Shock

Acute myocardial infarction complicated with cardiogenic shock trigger IL-6, the strong inflammatory response, result in multiple organ failure, even death.

While therapeutic hypothermia,to expect the possibility of anti-inflammatory effect via IL-6 bi-phasic effect and IL-10 , to improve the multiple organ failure, to increase survival rate and well cerebral performance.

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Key information

Conditions

Cardiac Arrest Cardiovascular Diseases Heart Arrest Heart Diseases Infarction Ischemia Myocardial Infarction Myocardial Ischemia Necrosis Pathologic Processes Pathological Conditions, Signs and Symptoms Shock Shock, Cardiogenic Vascular Diseases

Age range

18 year–100 year

Sex eligibility

All sexes

Study type

Interventional

Phase

Not applicable

Primary location

China Medical University Hospital

Taichung, Taiwan

About this study

Despite emergency coronary revascularization coupled with medical stabilization, intra-aortic balloon pump have significantly improved survival in patients with cardiogenic shock complicating acute myocardial infarction, mortality still remains excessively high, being actually about 30-50%. Future research should focus on new therapeutic strategies, aimed to further decrease mortality rate of these patients or improve possible hospitalization and prognosis.

Heart pumping failure result in cardiogenic shock. Increased LA filling pressure result in acute pulmonary edema, hypoxemic respiratory failure, even congestive kidney and congestive liver. Decreased stroke volume result in hypoperfusion obviously direct induce acute renal failure, disturbance consciousness and lactate accumulation, even, shock liver. Multiple organ failure is the major mortality in the patients suffered from cardiogenic shock after acute myocardial infarction.

Cardiogenic shock remains the leading cause of death in patients hospitalized for myocardial infarction . Systemic inflammation , especially endovascular Interleukin-6, triggered by Tumor necrosis factor-alfa and Interleukin-1 beta result in inappropriate vasodilatation is observed in many patients with cardiogenic shock and may contribute to an excess mortality rate. In recent study, interleukin-6 represented a reliable independent early prognostic marker of 30-day mortality.

Therapeutic hypothermia (34℃) increase stroke volume, reduce muscle oxygen consumption and enhance anti-inflammatory action . The mechanism of anti-inflammatory effect for therapeutic hypothermia in cardiogenic shock is still unclear, need to further study in clinical trial. Furthermore, this study will provide new strategy to increase survival rate in cardiogenic shock.

Who can participate

Healthy volunteers accepted: Yes

Only the study team can determine whether someone qualifies for participation.

Inclusion criteria

  • Age between 18-100 years
  • Cardiogenic sock including initial lactate level >18 mg/dL, necessary of vasopressor to keep mean artery pressure >65mmHg after adequate fluid supply, and signs of reduced cardiac output including disturbance consciousness, cold limbs, decreased urine output, acute pulmonary congestion and so on.

Exclusion criteria

  • Patient or family refuse
  • Metastatic cancer
  • Pregnancy

Treatment and study plan

Therapeutic hypothermia group

Device

Therapeutic hypothermia

Primary outcomes

  1. Survival Rate - Number of Participants Alive

    Time frame: 90 days after enrollment

    Survival rate according to the number of participants alive in the 90 days after enrollment.

Secondary outcomes

  1. Neurologic Outcome - Number of Participants

    Time frame: 90 days after enrollment

    Neurological outcome according to Cerebral performance Category scales: scales 1-2 in favor of favorable neurological outcome; scales 3-5 in favor of poor neurological outcome including severe cerebral disability, coma or vegetative state, brain death.

Other outcomes

  1. Interleukin-6 - the Plasma Level of Participants

    Time frame: between 6 and 24 hours after enrollment.

    IL-6 level change

  2. Interleukin-6/Soluble Interleukin-6 Receptor Complex - the Plasma Level of Participants

    Time frame: between 6 and 24 hours after enrollment

    Interleukin-6/soluble Interleukin-6 receptor complex plasma level hint the pro-inflammatory pathway via Interleukin-6 trans-signaling

  3. Soluble Interleukin-6 Receptor - the Plasma Level of Participants

    Time frame: between 6 and 24 hours after enrollment

    Check the soluble Interleukin-6 plasma level at 6 hours and 24 hours after enrollment

Sponsors and collaborators

Lead sponsor

China Medical University Hospital

Other

Registry information

Official study title

Anti-inflammatory Effect of Therapeutic Hypothermia in Out-hospital Cardiac Arrest Patients With Cardiogenic Shock Via Interleukin-6 Trans-signaling

Important dates

Study start
2015
Primary completion
2018
Study completion
2018
First posted
Dec 17, 2015
Registry last updated
Aug 7, 2019

OpenTrials presents study information sourced from ClinicalTrials.gov. The official registry record should be consulted for the latest information.

View the official ClinicalTrials.gov record (opens in a new tab)

This listing is for discovery and informational purposes only. It is not medical advice, does not guarantee that a study is recruiting, and does not determine eligibility. Contact the study team and a qualified healthcare professional when considering participation.

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