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Myocardial Injury clinical trials

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NCT ID: NCT06000930 Enrolling by invitation - Clinical trials for Myocardial Infarction

Cardiac Troponin Fragmentation After Heavy Physical Exercise The MaraCat2 Study

MaraCat2
Start date: August 19, 2023
Phase:
Study type: Observational

Cardiac troponins are highly sensitive and specific biomarkers of cardiac injury and are in a key role in the diagnosis of acute myocardial infarction (MI). Minor troponin elevations are common after prolonged strenuous exercise without clinical symptoms of MI or myocardial injury. Importantly, currently used high-sensitivity troponin T (cTnT) test detects also smaller troponin fragments which may cause troponin elevation after exercise and lead to false diagnosis of MI. In the present study protocol, we compare the characteristics troponin release after marathon race and Type 1 MI with the improved version of our novel troponin fragmentation test (SuperTropo test) and the commercial cTnT test. A total of 65 recreational runners participating in the 2023 Paavo Nurmi Marathon in Turku are recruited. All participants give a blood sample during the post-race visit (within 30 min after finishing the marathon). A control group of 90 patients with acute Type 1 MI are recruited among patients admitted to Heart Centre of Turku University Hospital. Commercial cTnT and long troponin component of cTnT analyzed witha novel immunoassay are dtermined in all subjects to assess cTnT fragmentation. TYhe main aims of the study are: To assess how often cTnT is elevated after marathon running and which factors affect the cTnT rise? Is the fragmentation of troponin more common after marathon race compared with Type 1 MI and can the novel Supertropo test separate execise-induced troponin rise from those caused by MI ?

NCT ID: NCT03253835 Enrolling by invitation - Healthy Clinical Trials

Cardiac Blood Flow Patterns Associated With Left Ventricular Myocardial Damage

CMR-LHD
Start date: November 21, 2013
Phase:
Study type: Observational

Various factors affect the performance of the heart: The contractile properties of myocardial muscle cells are the fundamental devices for translating tension-generation and shortening of the cardiac muscle into pressure-generation and blood volume ejection from the heart into the body. On the other hand, the performance of heart can be analyzed with respect to input and output of blood to/from the hollow cardiac muscle and evaluated in terms of the performance of a pump: With every heartbeat blood is sucked from a low-pressure system (veins) and pumped to the arterial high-pressure system via one-way valves, whereas efficiency, ejected blood volume, blood flow and pressures are linked by hemodynamic laws. Cardiac magnetic resonance (CMR) is the "gold standard technique" to determine cardiac function and muscle mass, as well as for non-invasive diagnosis of myocardial necrosis/fibrosis. Furthermore, new CMR imaging techniques enabling the measurement of myocardial magnetic relaxation times for characterization of myocardial morphology and the acquisition of time-resolved, three-dimensional blood flow velocity fields in the heart and surrounding vessels, represent promising tools for the evaluation of the interaction between myocardial morphology and cardiac function. Aim of this explorative study is to 1. identify myocardial pathology-associated blood flow patterns in the heart and surrounding great vessels, and 2. correlate characteristic blood flow patterns in the heat (existence of vortices, vorticity, vortex formation, propagation dynamics …) with myocardial injuries.

NCT ID: NCT01020942 Enrolling by invitation - Myocardial Injury Clinical Trials

Cardioprotective Effects of Electroacupuncture Pretreatment Against Coronary Stenting

Start date: January 2010
Phase: N/A
Study type: Interventional

Myocyte necrosis as a result of elective percutaneous coronary intervention (PCI) occurs in approximately one third of cases and is associated with subsequent cardiovascular events. This study assesses the ability of electroacupuncture (EA) pretreatment to attenuate cardiac troponin I (cTnI) release after elective PCI.