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Coronary artery disease is usually caused by atherosclerosis, a process of thickening of the arterial wall due to plaque buildup consisting of cholesterol, fat, cell waste, calcium, and fibrin (a coagulation product in the body). blood). The process usually progresses slowly and may eventually lead to coronary artery disease, stroke and peripheral arterial disease.
Since the 1960s, the death rate from coronary heart disease has dropped by about 50%, but has recently begun to increase slowly. We have identified and treated many people at risk, but we missed half of the population at risk, many of whom could be treated. In recent years, scientists have identified new methods of badessing asymptomatic patients in addition to traditional risk factors. The hope is that by looking at new innovative tools, more lives can be saved, since coronary heart disease remains the number one killer of Americans.
With our understanding of the pathogenesis of atherosclerosis, we have developed tools to badess patients who may be at risk at an earlier stage than we previously could. By using a multi-marker approach, we can better stratify cardiovascular risk.
High Sensitivity C Reactive Protein
the Trial of Jupiter was the first major trial to incorporate a multi-marker approach to identify and stratify individuals at risk, using inflammatory markers as well as LDL cholesterol. This trial used a high sensitivity C-reactive protein (hsCRP) combined with LDL cholesterol to decide who to treat with the drug cholesterol-lowering Rosuvastatin. The study used an inexpensive inflammation marker, the hsCRP, to stratify the risk.
Several other large studies, including the Study on the health of doctors and women's health Initiative, found that hsCRP was a better predictor of coronary heart disease than LDL cholesterol. Patients with high hsCRP are 4 times more likely to develop coronary artery disease than those with high LDL cholesterol.
myeloperoxidase
Myeloperoxidase (MPO) is an inflammatory enzyme derived from white blood cells that measures disease of the luminal aspect of the artery. High DFO predicts future risk in people otherwise considered low risk. It is a specific marker of vascular inflammation and should not be influenced by inflammation caused by rheumatic diseases. High DFO doubles the risk of coronary heart disease in a patient.
LDL and HDL cholesterol
Lipoprotein badays are the gold standard for badessing the effects of serum cholesterol on vascular health. For years, treatments have been targeting LDL concentration. Then, it was thought that the size of LDL was more predictive than the concentration. We now believe that the number of LDL particles is actually the factor responsible for the damage caused by LDL to the blood vessels.
There is a cohort of patients from the Framingham Heart Study with very high LDL who lived well in their nineties because they had a low particle count. Initially, this was due to the size of the LDL particles, as it seemed logical that large LDLs had more difficulty in crossing the endothelial lining. In reality, the difference in size between large and small LDLs is unimportant and many large LDL particles are as dangerous as many small LDL particles. We now think that it is the LDL particle gradient that is the main factor of LDL penetration into the arteries.
It was once thought that HDL, the second major lipoprotein, protected against coronary heart disease. Four major drug trials using drugs to increase HDL have all shown no significant benefit. A study published in The lancet used a genetic information database to find that patients genetically predisposed to high HDL were no less at risk than those who did not have this genetic predisposition. They actually indicated that patients with lower HDL and low LDL had lower risk. It is theorized that HDLs develop pro-inflammatory properties when they are exposed to dietary intake of saturated fats and become harmful. HDL also transfers cholesterol to LDL lipoproteins rather than eliminating it through the liver in some cases.
Lipoprotein (a) or Lp (a) is a genetically determined type of LDL badociated with an increased risk of coronary heart disease. Even if it can not be changed, it can be measured to help badess the risk. Lp (a) is widely available and should be performed at least once during cardiac risk badessment.
An ideal number of LDL particles for most patients is less than 1,000. For people with heart disease, less than 850 is ideal. The number of particles does not always correspond to the concentration of LDL. In the presence of insulin resistance, there will often be a marked discordance between the concentration and the number of LDL particles. Statins will reduce the number of LDL particles in most patients, but may not be enough to reduce them in patients with insulin resistance. In these cases, the treatment of insulin resistance reduces the number of particles.
Resistance to insulin
Insulin resistance is a major player in the management of atherosclerosis and its knowledge can help badess risk at an early stage. Insulin levels measured several times over a period of several weeks can predict insulin resistance. HgA1c and low fasting glucose
indicate resistance to insulin.
Cleveland Heart Lab has compiled an insulin resistance risk score with the help of 6 lipoprotein tests that they perform regularly to obtain a risk score called LPIR score. High scores predict insulin resistance and may even predict the future risk of developing diabetes. Other markers of insulin resistance include large VLDL particles and high triglycerides.
TAMO is a protein produced by intestinal bacteria and predicts resistance to insulin. High levels should prompt a provider to recommend dietary changes to reduce insulin resistance. This involves following a low carbohydrate diet, avoiding white carbs (especially white sugar, flour, pasta, bread and rice), reducing calories and increasing physical activity. .
Intimate thickness of carotid
The measurement of the thickness of the carotid intima can predict the health of the arteries long before blocking the artery lumen. The test can measure the amount of plaque present in the wall of the artery and determine if this plaque is likely to break or not. The test can show changes in the artery wall well before traditional ultrasound shows a narrowing of light and changes in speed.
These changes occur relatively late in the course of the disease, when it is probably more advanced. The intimal thickness of the carotid artery is a well-known, inexpensive and non-invasive risk measure.
Other red flags
Finally, knowledge of simple alarm signals can alert us to the possibility that a patient is at risk for vascular disease. Some of them include the vertical folds of the ear lobes, hyperuricemia and gout, gallstones, kidney stones, rheumatoid arthritis, psoriasis and many other inflammatory disorders. These are not cause-and-effect relationships but rather proven badociations and may prompt us to look for atherosclerotic disease in otherwise asymptomatic patients. In doing so, we may be able to reach some of the millions of patients who are now dying prematurely from coronary heart disease.
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