View clinical trials related to Death, Sudden, Cardiac.
Filter by:The purpose of the study is to determine the myocardial function and vascular adaptation after strenuous exercise in association with genotype/polymorphisms. We aim to investigate the effects of extreme endurance exercise on the cardiovascular system. Furthermore, the role of the inflammatory response and adaptive mechanisms of the vasculature are examined. Subclinical injuries to the myocardium and vascular wall are being investigated.
Rationale: Despite spontaneous cardiac activity recovery, a shock occurs in more than half of patients after resuscitation for cardiac arrest. This acute circulatory insufficiency presents similar characteristics with septic shock and is responsible of most early deaths. Most frequently, usual treatments are unable to control this shock and to avoid the appearance of multiple organ failure. Aim of the study: In addition to conventional therapeutics, an early plasma epuration of inflammatory mediators (HDHP) could be able to improve hemodynamic parameters and to reduce the shock duration. This improvement could have an impact on multiple organ dysfunctions and also on early mortality.
Sudden death is a natural death occurring within one hour after the onset of symptoms. It remains a major public health problem and accounts for 5 to 10 % of the annual total mortality ie about 300.000 in the United States. Despite community-based interventions, overall survival remains below 5%. Better understanding of the mechanisms causing sudden death could allow early identification of high risk subjects and implementation of specific prevention strategies. The cause of more than 90% of sudden deaths is cardiac with ventricular fibrillation or fast ventricular tachycardia complicating an underlying heart disease. Coronary heart disease and its consequences account for at least 80% of sudden cardiac deaths. Several risk factors associated with sudden death and not with myocardial infarction have been identified in population-based studies. However, the relationship between the occurrence of a coronary artery occlusion and the onset of arrhythmia is unclear. In particular, coronary artery occlusion can be rapidly followed by chest pain, which acts as a signal and allows identification of patients for emergency reperfusion. However, in some cases, the coronary artery occlusion is followed by a sudden onset of arrhythmia and sudden death. Recent data suggest that acute coronary occlusion is caused by plaque erosion or rupture and is followed by an intense local inflammation and rapid thrombus formation. Our hypothesis is that the speed of thrombus formation and coronary occlusion determines the clinical symptoms. Slow and progressive thrombus formation is likely to induce myocardial pre-conditioning thereby reducing the occurrence of ventricular arrhythmia. In contrast, rapid thrombus formation followed by acute coronary artery occlusion and ischemia is more likely to trigger fatal ventricular arrhythmia. During angioplasty procedures, coronary artery thrombus are aspirated, providing the opportunity for pathological studies. The aim of the TIDE study (Thrombus and Inflammation in Sudden Death) is therefore to compare the composition and age of thrombus collected at the site of coronary occlusion in patients with sudden death due to acute coronary artery occlusion and patients with an acute myocardial infarction without ventricular arrhythmia. The following hypothesis will be tested : fresh thrombus is more frequent in patients with sudden cardiac death versus patients with acute myocardial infarction without ventricular arrhythmia.
The overall hypothesis of this study is that subtle interactions between structural (substrate) and functional (trigger) abnormalities of the heart, some of which are genetically-determined, can be used to identify patients at high risk of sudden cardiac death (SCD). Such information may be used to better define patients most likely to benefit from replacement of an internal defibrillator (ICD). The prospective, observational study to enroll, categorize and follow patients who receive an ICD pulse generator replacement for primary prevention of SCD (PROSe-ICD) was established to : 1. to gain a better understanding of the biological mechanisms that predispose to SCD 2. to develop readily determined clinical, electrocardiographic, genetic and blood protein markers identify patients with an increased risk of dying suddenly
Doctors use magnetic resonance imaging (MRI) to obtain detailed pictures of the inside of the body. This study will evaluate a new MRI technique in people who have recently had a heart attack. Researchers will also examine the effect of fish oil supplementation on heart health in study participants.
To generate a list of potential genetic markers that correlate with an increased risk of life-threatening arrhythmias. To evaluate ECG-based risk markers such as heart rate variability and T-wave Alternans for their association with arrhythmic events.
Sudden cardiac arrest (SCA) is a sudden, unexpected loss of heart function. It is a leading cause of death, and more than 400,000 people in the United States die each year as a result of SCA. This study will analyze genetic samples of people who have experienced SCA and people who have not experienced SCA to determine if there is a genetic basis for SCA.
The aim of this prospective observational study is to evaluate the safety, over a follow-up of 2 years, of two strategies, consisting in performing or not performing defibrillation testing(DT) during first implant of implantable cardioverter defibrillator
Boston Scientific CRM's Longitudinal Surveillance Registry (LSR) will serve as an active ongoing source of updated information on the long-term reliability and performance of BSC commercially available leads and LATITUDE-enabled (wireless or wanded) pulse generators (PGs).
The purpose of this prospective study is to evaluate the effect of cardiac resynchronization therapy (CRT) on the defibrillation threshold (DFT) estimates in cardiac resynchronization therapy defibrillators (CRT-D) patients. The hypothesis of the study is that defibrillation threshold (DFT) will decrease with 6 months of cardiac resynchronization therapy (CRT).