Description Module
The Description Module contains narrative descriptions of the clinical trial, including a brief summary and detailed description. These descriptions provide important information about the study's purpose, methodology, and key details in language accessible to both researchers and the general public.
Description Module path is as follows:
Study -> Protocol Section -> Description Module
Description Module
Ignite Creation Date:
2025-12-25 @ 12:44 AM
Ignite Modification Date:
2025-12-25 @ 12:44 AM
NCT ID:
NCT06491667
Brief Summary:
Acute myocardial infarction (AMI) is a serious and fatal cardiovascular emergency and considered the leading cause of mortality worldwide.
Atherosclerosis of coronary arteries which takes decades to manifest clinically, is the primary predisposing pathologic factor responsible for the development of coronary heart disease It has been shown that A complex immune and inflammatory pathophysiological process is thought to be crucial for in the initiation and progression of atherosclerotic plaques.
Inflammation is one of the main mechanisms in the pathogenesis of atherosclerosis , Destabilization of chronic artery plaques and development of thrombosis, which are the main mechanisms in the pathophysiology of ST-segment elevation myocardial infarction (STEMI).
, and the interest to the evaluation of inflammatory biomarkers in coronary artery disease (CAD) has been increasing over the last decade .
Although numerous inflammatory markers, including troponin T/I, lactate dehydrogenase (LDH), and creatine kinase (CK-MB), are linked to worsened clinical outcomes in both ST elevation and non-ST elevation myocardial infarction (NSTEMI), there is an unmet need for a cost-effective biomarker for impoverished countries of the world .
The neutrophil-to-lymphocyte ratio (NLR), and C-reactive protein (CRP) ; has emerged as an important inflammatory markers for cardiovascular risk stratification.
And are relatively cheap inflammatory markers, can act as a bridge to mitigate the gap in assessing the cardiovascular risk and outcomes
Detailed Description:
Acute myocardial infarction (AMI) is a serious and fatal cardiovascular emergency and considered the leading cause of mortality worldwide.
* Atherosclerosis of coronary arteries which takes decades to manifest clinically, is the primary predisposing pathologic factor responsible for the development of coronary heart disease
* It has been shown that A complex immune and inflammatory pathophysiological process is thought to be crucial for in the initiation and progression of atherosclerotic plaques
* Inflammation is one of the main mechanisms in the pathogenesis of atherosclerosis , Destabilization of chronic artery plaques and development of thrombosis, which are the main mechanisms in the pathophysiology of ST-segment elevation myocardial infarction (STEMI) .
, and the interest to the evaluation of inflammatory biomarkers in coronary artery disease (CAD) has been increasing over the last decade .
* Although numerous inflammatory markers, including troponin T/I, lactate dehydrogenase (LDH), and creatine kinase (CK-MB), are linked to worsened clinical outcomes in both ST elevation and non-ST elevation myocardial infarction (NSTEMI), there is an unmet need for a cost-effective biomarker for impoverished countries of the world
* The neutrophil-to-lymphocyte ratio (NLR), and C-reactive protein (CRP) ;
* has emerged as an important inflammatory markers for cardiovascular risk stratification.
* And are relatively cheap inflammatory markers, can act as a bridge to mitigate the gap in assessing the cardiovascular risk and outcomes In patients with acute myocardial infarction.
* Recent data indicates a strong independent relationship between increased complications after acute myocardial infarction in patients with a high NLR and high CRP level at admission and the initial post-hospitalization period.
* Accordingly, we designed this study to assess the predictive value and prognosis of NLR and CRP in ST-elevation myocardial infarction (STEMI).
Study:
NCT06491667
Study Brief:
Protocol Section:
NCT06491667