However, both elevated triglycerides and elevated cholesterol, before they become coronary heart disease or heart failure, are “silent”, giving no symptoms, so as to lead sufferers to the doctor.
However, their early diagnosis can save lives, because only this will lead to hypolipidemic treatment, which will mitigate or prevent the risk.
Cholesterol & triglycerides
High levels of cholesterol and / or triglycerides cause premature atherosclerosis and consequently myocardial infarction, stroke, peripheral artery disease, generalized atherosclerosis and possibly pancreatitis. All of these diseases, if not treated in time, can even lead to death.
“Multi-year studies of people with elevated cholesterol levels who have been given hypolipidemic drugs have shown that lowering cholesterol has led to fewer cardiovascular events and fewer cardiovascular deaths. “Also, there was a slowdown in the progression of coronary heart disease or even a remission of the stenoses created in the blood vessels”, points out Ms. Genoveva Kolovou, Director of Preventive Cardiology at the Metropolitan Hospital.
What is cholesterol?
Cholesterol, commonly known as “cholesterol”, belongs to the group of lipids, and is produced mainly in the liver and to a lesser extent, comes from food. Cholesterol circulates in the blood in four forms. Its two forms, low density lipoprotein cholesterol (LDL cholesterol) and high density lipoprotein cholesterol (HDL cholesterol) are the best known. The other two are very low density lipoprotein (VLDL) and lipoprotein (a).
LDL cholesterol is called “bad” because its elevated levels in the blood (hypercholesterolemia) are responsible for the development of coronary heart disease. HDL cholesterol is called “good” because it inhibits the development of atherosclerosis.
What are triglycerides?
In addition to cholesterol, triglycerides also belong to the group of lipids. The main mass of food lipids consists of triglycerides, however they are also synthesized by our body.
Diet
Dietary cholesterol is derived from animal products. The largest amount of cholesterol is contained in animal organs (inside the brain, pancreas, kidneys, liver). Meat does not contain a large amount of cholesterol, but because its daily consumption is high, it contributes significantly to the daily intake of cholesterol. Saturated fatty acids as well as dietary cholesterol increase the levels of total cholesterol and triglycerides.
Hypolipidemic treatment
Hypolipidemic treatment is administered in dyslipidemias (hypercholesterolemia and / or hypertriglyceridemia), in patients with coronary heart disease, stroke, carotid disease, peripheral arterial disease, diabetes, etc.
Interventional treatment
Interventional treatment of dyslipidemias is applied only in extreme cases, especially in patients with severe hypercholesterolemia and / or severe hypertriglyceridemia. The most common intervention is lipoprotein removal.
Therapeutic goals for lowering LDL cholesterol
“How much we need to lower LDL cholesterol depends on the condition of the person being examined. In people at very high risk LDL cholesterol should be below 55 mg / dL, in people at high risk it should be below 70 mg / dL and in people without risk factors (eg obesity, hypertension, smoking, diabetes ) must be below 100 mg / dL. “Triglycerides should be below 150 mg / dL,” explains the doctor.
Medicate
The administration of a drug is based on the clinical condition of the patient. There is no age limit. Hypolipidemic drugs can also be given to children if they have severe hypercholesterolemia.
Dyslipidemias
Dyslipidemias are divided into primary (inherited) and secondary (disorders that are due to known diseases or syndromes beyond the lipids that affect them).
Primary dyslipidemias
Primary dyslipidemias include familial hypercholesterolemia, familial combined dyslipidemia, type III dyslipidemia, and familial hypertriglyceridemia.
Familial hypercholesterolemia
Familial hypercholesterolemia is mainly caused by a mutation in the LDL particle receptor gene. More than 2,000 mutations (genetic abnormalities) of the LDL receptor have been described. These mutations lead to the accumulation of cholesterol in the plasma. Familial hypercholesterolemia occurs either as a heterozygous or as a homozygous form. The heterozygous form (adverse effect of mutation by 50%) occurs with a frequency of one child in 200-500 births and the homozygous form (adverse effect of mutation by 100%) occurs with a frequency of one child in 400,000-600,000 births.
People with heterozygous familial hypercholesterolemia present with early coronary heart disease, carotid stenosis and / or peripheral arterial disease. People with homozygosity experienced myocardial infarction, carotid artery stenosis or severe aortic valve stenosis in childhood.
Familial combined dyslipidemia
Familial combined dyslipidemia does not manifest clinically in the same way in all patients. Xanthomas are rare and there is a moderate increase in cholesterol and a moderate or large increase in triglycerides in the plasma.
Often the disease manifests itself when other diseases are added such as diabetes, obesity, hypothyroidism, etc.
People with familial combined dyslipidemia often have early coronary heart disease, peripheral arterial disease, and rarely pancreatitis.
Familial hypertriglyceridemia
“Familial hypertriglyceridemia is caused by a genetic defect, which is still unknown. It is monogenic dyslipidemia. It can remain asymptomatic and appear only with the addition of another condition such as obesity, alcoholism, hypothyroidism, diabetes. It appears in children after the age of 16. “The clinical signs of familial hypertriglyceridemia are rash xanthomas, hepatomegaly (swollen liver seen on palpation or ultrasound), elevated plasma triglycerides, and normal / marginally elevated cholesterol.”
Secondary dyslipidemias
Diseases that can cause secondary dyslipidemias are:
a. Kidney disease (high cholesterol, high triglycerides)
b. Thyroid disease (very high cholesterol)
c. Obesity (high cholesterol, high triglycerides)
d. Diabetes mellitus (high cholesterol, high triglycerides and low HDL cholesterol)
e. Metabolic syndrome (elevated triglycerides, low HDL cholesterol)
Postprandial lipemia
We spend most of our lives in the afternoon. Postprandial lipoproteins rich in triglycerides and their residues, constitute a population of complexes of different origin and composition. They also differ in their interaction with cellular receptors, and as a result have the potential to cause atherosclerosis.
Triglyceride-rich lipoproteins from the liver or intestine cause the normal postprandial increase in triglycerides (up to 220 mg / dL), which occurs 3 to 7 hours after a high-fat meal.
“Patients with coronary heart disease, even without significant fasting lipid disorders (8-12 hours without food intake), have elevated levels and reduced catabolism of chylomicrous residues for more than 8 hours after fat loading, which may be a potential important causal mechanism for the development of atherosclerosis.
The link between postprandial lipemia and coronary heart disease has been known since 1950.
A fat curve is recommended to determine postprandial lipemia.
The fat curve consists of 2 measurements of triglycerides (one before and one 4 hours after taking a special meal rich in saturated fats) “, concludes Ms. Genoveva Kolovou.
Writes:
Mrs. Genoveva Kolovou, Director of Preventive Cardiology at the Metropolitan Hospital
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