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45 active trials for Out of Hospital Cardiac Arrest

Direct or Subacute Coronary Angiography in Out-of-hospital Cardiac Arrest

The overall aim of this prospective, randomized study is to investigate whether acute coronary angiography (within 120 minutes) with a predefined strategy for revascularization, will improve 30-day survival in patients with out of hospital cardiac arrest with no signs of ST-elevation on ECG after Restoration of Spontaneous Circulation (ROSC). The patients will be randomized to a strategy of immediate coronary angiography within 120 minutes or to a strategy of delayed angiography that may be performed three days after the cardiac arrest.

Start: December 2014

Early Initiation of Extracorporeal Life Support in Refractory OHCA

Despite adequate conventional cardiopulmonary resuscitation (CCPR) and attempted defibrillation, a considerable number of patients in cardiac arrest fail to achieve sustained return of spontaneous circulation. The INCEPTION trial is a multicenter, randomized controlled trial that will explore extracorporeal cardiopulmonary resuscitation (ECPR) in patients in refractory out-of-hospital cardiac arrest (OHCA) presenting with ventricular fibrillation or tachycardia. It aims to determine the effect on survival and neurological outcome. Additionally, it will evaluate the feasibility and cost-effectiveness of ECPR.

Start: May 2017

Cardiac Arrest Registry of the Lombardia Region (Lombardia CARe)

The registry enroll all the patients who suffered an out-of-hospital cardiac arrest in the Lombardia Region with a follow-up up to five years after the event.

Start: October 2014

Hypothermia After Cardiac Arrest - Effects on Myocardial Function and Inflammatory Response.

The on-going randomized clinical trial TTM2 (Target Hypothermia Versus Targeted Normothermia After Out-of-hospital Cardiac Arrest, NCT02908308) investigates if there is a difference in mortality, neurological function or quality of life in comatose survivors after out-of-hospital cardiac arrest if treated (Group A) at target temperature of 33 oC or (Group B) by avoiding fever during the first 24 h. In this sub study, the effect of different target temperatures on cardiac and circulatory physiology is evaluated by echocardiography and pulmonary artery catheter. Tissue damage after cardiac arrest in part is caused by an activation of different parts of the inflammatory system (reperfusion injury). This study investigates the effect of temperature management on inflammation and the link to the circulatory effects.

Start: November 2018

DIagnostics, Fatty Acids and Vitamin D in SCA

Sudden cardiac death (SCD) is a major cause of mortality in industrialized countries and represents a major health issue. The survival rate after out-of-hospital cardiac arrest (OHCA) is only 10-15%, regardless of first recorded rhythm. Prior heart disease is a major risk factor for sudden cardiac arrest (SCA), and coronary artery disease (CAD) is the most common underlying cause. A better understanding of pathophysiological mechanisms occurring during cardiac arrest (CA), earlier diagnosis of underlying cause as well as identification of risk factors related to CA may improve patient treatment and increase survival. In our out-of-hospital cardiac arrest (OHCA)-study, we intend to investigate whether biomarkers, such as copeptin, hs-cTnT and NT-proBNP in addition to clinical evaluation may improve risk stratification and supply information related to pathophysiology. Furthermore, we intend to gather additional pathophysiological information related to coagulation activation in CA and cardiopulmonary resuscitation (CPR), as intravascular thrombosis may impair microcirculation and reduce end-organ blood flow which is associated with a poor prognosis. We intend to study coagulation activation during and immediately after SCA with regard to outcome, and assess the contribution of the intrinsic system, measured together with that of the extrinsic system. Low levels of n-3 fatty acids (FA) are reported as a risk factor for SCD. Red blood cell eicosapentaenoic acid (EPA) + docosahexaenoic acid (DHA) may serve as a useful surrogate of cardiac omega-3 fatty acid status. The exact mechanism by which FAs might protect against serious cardiac arrhythmias is not known, but they are expected to exert a membrane stabilizing effect during an ischemic episode. In our study we intend to evaluate the association between ventricular fibrillation (VF) and the content of EPA and DHA in red blood cells. Furthermore, as vitamin D is associated with n-3 FAs in the diet, we also aim at investigating the association between 25-hydroxy (OH)-vitamin D and VF.

Start: January 2007