Raman did not smoke, his cholesterol levels were normal, he had no diabetes and he had none of the risk factors that conventional wisdom demanded for a heart attack. Despite it he suffered two heart attacks within the span of tree years.
Today there are answers at last to the mystery of why people with no obvious cardiac risks fall victim to heart disease.
ATHEROSCLEROSIS [narrowing of coronary arteries] the process starts when LDL [bad] cholesterol penetrates the wall of an artery. If all goes well HDL [good] cholesterol will reverse the process carrying cholesterol away from the artery for eventual disposal by the liver. But if LDL accumulates in the artery wall, it becomes a target for oxygen free radicals, which bombard cholesterol to turn it into oxidized LDL, much as free radicals turn fat rancid.
It's the oxidised cholesterol that gets atherosclerosis started. Now scientists have already identified inflammation and clot formation as the two basic processes that translate the initial effects of oxidized LDL Cholesrtol into the damage of a heart attack.
Now doctors have moved beyond cholesterol to identify new risk factors, many of which participate in inflammation or clotting. Below are some new risk factors responsible for heart ailments.
Homocystein
Homocystein and cholesterol both are natural substances that are present in many foods and are also synthesized by the body itself. In normal amounts, both are essential for health, but in high amounts they increase dramatically the risk of heart attack and stroke.
Cholesterol and homocystein are chemically distinct. Homocystein is not a fat but an amino acid.
It is one of the 20 nitrogen-rich compounds that are building block of all body proteins.
High level of homocystein accelerates the atherosclerosis in following ways:
As with the cholesterol levels, healthy people have a wide range of homocystein levels. The normal range is 5-15 micromoles per litre, but below 10 are safest,. In general, the levels for men are about one point higher than for women.
Infection
Although atherosclerosis has many causes, infection is emerging as new risk factor.the leading candidate is Chlamydia Pneumonia. It is an unusually small bacterium which such a primitive metabolism that it can survive only by living within the cells of the people it infects. But once it gets inside those cells, it tends to linger, causing low grade chronic inflammation.
Many people with the infection have no symptoms at all; others develop the flu, pneumonia, bronchitis, sinusitis etc.
From the respiratory passage C. Pneumonia enters the blood, where they are taken up by macrophages, these macrophages enter arteries with early atherosclerotic damage. Once in the arterial wall, C pneumonia stimulates inflammation, adding to the damage and weakling the plaque so that it ruptures and triggers clot formation.
Dental infection
There is a direct connection between periodontal diseases and the severity of coronary atherosclerosis, the worse the dental disease the worse the heart disease.
Inflammation
It is in prostatitis, appendicitis and bronchitis. Inflammation can show up in any part of the body because it's the most basic response to the injury. Infection is the most common trigger, but inflammation can also be set in motion by allergy, immunological reaction and even by trauma.
In arteries, oxidized LDL cholesterol produces injury and the body responds with the inflammation.
Macrophages and other white cells are the first to answer the call, in turn they produce CYTOKIN, tiny protein that injure endothelial cells, stimulates smooth muscle cells and recruit still more macrophages to perpetuate the process.
Liver also responds to cytokines by producing proteins of its own, including C reactive protein and Fibrinogen.
An elevated level of C reactive protein and fibrinogen is a reliable indicator of cardiac risk.
Blood lipids
Elevated blood cholesterol levels predicted increased cardiac risk. High LDL cholesterol increases risk but high HDL cholesterol decreases risk.
The other two important risk factors are TRIGLYCERIDES and LIPOPROTEIN (a).
High triglycerides levels do increase the cardiac risk, at least in those people who also have low HDL cholesterol levels. High lipoproteins (a) also increase risk.
BY
GEETA JHA
INDIA
Today there are answers at last to the mystery of why people with no obvious cardiac risks fall victim to heart disease.
ATHEROSCLEROSIS [narrowing of coronary arteries] the process starts when LDL [bad] cholesterol penetrates the wall of an artery. If all goes well HDL [good] cholesterol will reverse the process carrying cholesterol away from the artery for eventual disposal by the liver. But if LDL accumulates in the artery wall, it becomes a target for oxygen free radicals, which bombard cholesterol to turn it into oxidized LDL, much as free radicals turn fat rancid.
It's the oxidised cholesterol that gets atherosclerosis started. Now scientists have already identified inflammation and clot formation as the two basic processes that translate the initial effects of oxidized LDL Cholesrtol into the damage of a heart attack.
Now doctors have moved beyond cholesterol to identify new risk factors, many of which participate in inflammation or clotting. Below are some new risk factors responsible for heart ailments.
Homocystein
Homocystein and cholesterol both are natural substances that are present in many foods and are also synthesized by the body itself. In normal amounts, both are essential for health, but in high amounts they increase dramatically the risk of heart attack and stroke.
It is one of the 20 nitrogen-rich compounds that are building block of all body proteins.
High level of homocystein accelerates the atherosclerosis in following ways:
- By producing toxic damage to the endothelial cells that line the inner surface of arteries.
- By increasing the activity of oxygen free radicals.
- By stimulating the enlargement of smooth muscles cells in the middle layer of arterial walls
- By accelerating the clotting process.
As with the cholesterol levels, healthy people have a wide range of homocystein levels. The normal range is 5-15 micromoles per litre, but below 10 are safest,. In general, the levels for men are about one point higher than for women.
Infection
Although atherosclerosis has many causes, infection is emerging as new risk factor.the leading candidate is Chlamydia Pneumonia. It is an unusually small bacterium which such a primitive metabolism that it can survive only by living within the cells of the people it infects. But once it gets inside those cells, it tends to linger, causing low grade chronic inflammation.
Many people with the infection have no symptoms at all; others develop the flu, pneumonia, bronchitis, sinusitis etc.
Dental infection
Inflammation
It is in prostatitis, appendicitis and bronchitis. Inflammation can show up in any part of the body because it's the most basic response to the injury. Infection is the most common trigger, but inflammation can also be set in motion by allergy, immunological reaction and even by trauma.
In arteries, oxidized LDL cholesterol produces injury and the body responds with the inflammation.
Macrophages and other white cells are the first to answer the call, in turn they produce CYTOKIN, tiny protein that injure endothelial cells, stimulates smooth muscle cells and recruit still more macrophages to perpetuate the process.
The cytokines that causes such mischief in the artery wall also spill out into the bloodstream, travelling to other parts of the body.
Liver also responds to cytokines by producing proteins of its own, including C reactive protein and Fibrinogen.
An elevated level of C reactive protein and fibrinogen is a reliable indicator of cardiac risk.
Blood lipids
Elevated blood cholesterol levels predicted increased cardiac risk. High LDL cholesterol increases risk but high HDL cholesterol decreases risk.
High triglycerides levels do increase the cardiac risk, at least in those people who also have low HDL cholesterol levels. High lipoproteins (a) also increase risk.
BY
GEETA JHA
INDIA
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