Clinical Trials Directory

Trials / Unknown

UnknownNCT03179137

Mitochondrial Bioenergetics and Role in Cellular Damage in Ischemic Myocardium

Pathophysiological Mechanisms Elicited by Ischemia and Metabolic Co-morbidities in Myocardium of Patients With Coronary Artery Disease

Status
Unknown
Phase
Study type
Observational
Enrollment
80 (estimated)
Sponsor
University of Split, School of Medicine · Academic / Other
Sex
All
Age
50 Years – 85 Years
Healthy volunteers
Not accepted

Summary

Cardiac ischemia is a common pathological condition, known to elicit multiple pathological processes at the cellular level. One of the most affected is thought to be cellular metabolism, key for the adequate cardiac function. The aim is to study mitochondrial bioenergetic function, interaction with other cellular systems and influence of several co-morbidities in myocardium of the affected patients.

Detailed description

Coronary artery disease, one of the most common pathologies in the developed world, causes hypoperfusion of myocardial tissue, usually evident by the presence of anginal pain. This myocardial ischemia elicits alterations in normal cardiomyocyte physiology, which gradually deteriorate cellular function, affecting the performance of the entire organ. The condition is frequently further complicated (and aggravated) by the presence of various co-morbidities, such as diabetes mellitus. The primary aim of this study is to investigate the cardiomyocyte bioenergetics and the consequences of potentially reduced mitochondrial metabolic function in ischemic heart, and evaluate the potential contribution of other conditions, primarily ones affecting metabolic homeostasis.

Conditions

Interventions

TypeNameDescription
OTHERStandard therapyPatients with therapy prescribed independent of the study

Timeline

Start date
2016-10-01
Primary completion
2021-04-01
Completion
2021-10-01
First posted
2017-06-07
Last updated
2020-06-19

Locations

1 site across 1 country: Croatia

Source: ClinicalTrials.gov record NCT03179137. Inclusion in this directory is not an endorsement.