Clinical Trial Details
— Status: Completed
Administrative data
NCT number |
NCT04243876 |
Other study ID # |
20/9 |
Secondary ID |
|
Status |
Completed |
Phase |
|
First received |
|
Last updated |
|
Start date |
December 30, 2019 |
Est. completion date |
May 27, 2022 |
Study information
Verified date |
May 2022 |
Source |
Bezmialem Vakif University |
Contact |
n/a |
Is FDA regulated |
No |
Health authority |
|
Study type |
Observational
|
Clinical Trial Summary
Myocardial infarction is a polygenic disease that may occur due to various environmental risk
factors. Mortality risk of the disease; sex, age, smoking, systolic blood pressure, total
cholesterol, and high-density lipoprotein levels. The paraoxonase-1 phenotype is expressed as
the paraoxonase/arylesterase ratio and is closely related to high-density lipoprotein, acting
as an endogenous defense mechanism against vascular oxidative stress, thus contributing to
the prevention of atherosclerosis. Serum concentration and activity depend on environmental
factors as well as genetic polymorphism. This decrease in enzyme concentration causes changes
in gene expression (1). Numerous data on Paraoxonase-1 levels have been found in studies,
especially with decreasing serum paraoxonase and arylesterase activities with age, associated
with increased risk of systemic oxidative stress and atherosclerosis in humans. Many studies
have shown that serum Paraoxonase-1 activity is significantly reduced in people with
myocardial infarction, dyslipidemia, atherosclerosis, and chronic kidney disease. The most
important risk factor for these and similar diseases is aging. Diversity of conditions such
as genetic predisposition, malnutrition, stress, and smoking, which increases vascular
dysfunction due to oxidative stress, classify individuals with acute myocardial infarction
according to age groups and investigate whether there is a relationship between serum
Paraoxonase-1 activity and severity of coronary artery disease in young patients. The
paraoxonase-1 enzyme, which is known to decrease blood levels with age, is found to be
significantly lower in patients with myocardial infarction at a young age compared to the
healthy control group.
Description:
High-density lipoprotein (HDL), known as good cholesterol, is named because of its protective
effects on the cardiovascular system. in order to summarize the mechanism of the event,
cholesterol is transported from the liver to the cells and from the cells back to the liver
via blood. Cholesterol and other fats are carried in packets called lipoprotein to dissolve
in the blood. Those with these are two kinds of cholesterol, these low-density lipoproteins
and good cholesterol can help to lower the cholesterol as well. LDL cholesterol is the main
package that carries cholesterol in the blood. When the blood is high, it sticks to the
inside of the veins and forms plaques around here. With the addition of cholesterol, a blood
clot that formed in cracks that occur on these plaques grow the arteries and clogs them. If
the blockage occurs in the heart vessels, it can cause a heart attack and stroke. Cholesterol
in the blood is a part of a package called HDL-cholesterol is carried in. HDL-cholesterol
prevents the accumulation of cholesterol in the veins.
It collects the cholesterol circulating in the blood and brings it to the liver to get rid of
it from the body. Thus, it reduces the exposure of blood vessels to the harmful effects of
cholesterol. All these effects of HDL cholesterol in the paraoxonase enzyme owes. This may be
the reason why Dolat may even use another nomenclature instead of HDL in future years. A
paraoxonase-1 enzyme, which is known to decrease blood level with age, is found to be
significantly lower in patients with myocardial infarction at a young age compared with the
healthy control group in this study, and the measurement of this enzyme level can be used as
a screening test in people with risk factors.