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About Heart Disease
Heart disease is the leading cause of death in the United States. Coronary artery disease (CAD) is the most common form of heart disease.
Like all the cells and muscles in the body, the heart muscle itself needs oxygen. With the rest of the body that life-sustaining oxygen is carried to the individual cells of the heart and the arteries. These are called the coronary arteries. If the coronary arteries are blocked and unable to do their job, then the heart is left without oxygen and unable to do its job. Depriving the heart of oxygen for even a brief period of time will result in the death of some of the heart muscle—otherwise known as a heart attack.
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Surprising, about 80% of individuals who are destined to have heart attacks have the same blood cholesterol values as those who do not develop CAD. Only 50% of cases of coronary artery disease are associated with high cholesterol or any of six additional classic risk factors: advanced age, male gender, positive family history, high blood pressure, diabetes, and smoking. In addition, treatments that improve these disorders may fail to prevent the progression of CAD, as shown by x-ray visualization of the arteries (coronary artheriography) or prevent the occurrence of heart attacks and other CAD-related cardiac events.
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Beyond the basics: Cholesterol Subclasses
We now know that cholesterol can be broken down beyond just LDL and HDL. Within both LDL and HDL, there exist particles that vary in their characteristics and therefore in their risk (in the case of LDL) and protective (in the case of HDL) factors for CAD. A much better assessment of CAD risk is achieved by enlarging the spectrum of testing to include additional disorders, such as a predominance of small particles within the LDL family (small LDL trait), and low levels of HDL2b, the most heart-protective type of HDL.
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This more comprehensive approach can point to treatment that differs from traditional therapy and is more effective in slowing, halting, or reversing the progression of CAD.
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LDL particles contribute to the harmful buildup of fat inside artery walls, a process called atherosclerosis. The LDL particles contribute to atherosclerosis partly by slipping through the spaces between the cells of the artery0-wall lining and unloading their cargoes of cholesterol inside the wall. LDL particles floating in the blood of the same person vary in size and small particles penetrate the artery wall with relative ease! Making matters worse, they are also more susceptible to oxidation, a chemical process that intensifies the atherosclerotic activity of LDL.
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People with a predominance of small LDL particles have an increased risk of developing CAD and suffering a heart attack. The small LDL trait is found in 50% of men and postmenopausal women, and in 30% of pre-menopausal women with CAD. The small LDL trait is also present in 50% of their first-degree relatives, who may or may not have CAD symptoms.
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HDL particles, on the other hand, inhibit atherosclerosis in part by carrying cholesterol out of the arterial wall and, the liver, via the circulation, which can dispose of it. The process is called reverse cholesterol transport. HDL2b is the most active of all the HDL particles in such transport. The more HDL2b you have the better!
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