fgummett
10-01-2009, 07:05 AM
I found this article on Medscape... not sure if you can view it without registration...
Small LDL and Its Clinical Importance as a New CAD Risk Factor: A Female Case Study
H. Robert Superko, MD, Mary Nejedly, MS, ANP, Brenda Garrett, RN
Abstract
The underlying metabolic cause of coronary heart disease in many patients is not high blood cholesterol. In fact, the Framingham study has reported that 80% of individuals who go on to have coronary artery disease have the same total blood cholesterol values as those who do not go on to have a cardiovascular event. The most common metabolic contributor to coronary artery disease is the atherogenic lipoprotein profile, characterized by an abundance of highly atherogenic small, dense low-density lipoprotein particles and a deficiency of the high-density lipoprotein (HDL) subtype most associated with coronary artery disease protection (HDL2b). This trait is present in 50% of men with coronary artery disease and is not reflected by total or low-density lipoprotein cholesterol values. While fasting triglycerides tend to he higher, and HDL cholesterol lower in patients with the atherogenic lipoprotein profile, the majority have triglyceride and HDL cholesterol values generally accepted to be in the "normal" range. An abundance of basic science and clinical trial evidence convincingly indicates that the presence of an atherogenic lipoprotein profile signifies a three-fold increased risk for a cardiovascular event and rapid arteriographic progression, but it also identifies a group of patients who respond particularly well to specific therapeutic interventions. Often the most effective interventions are the least expensive.
Treatment of the small LDL trait involves diets that restrict simple carbohydrates, loss of excess body fat, and appropriate exercise. Pharmacologic treatment involves medications that tend to reduce triglycerides, such as nicotinic acid and the fibric acid derivatives. Many medications have a differential response based on LDL subclass distribution.
In summary, the small LDL trait is a common metabolic disorder that contributes to CAD risk and disease progression and at the American Cardiovascular Research Institute, is present in 57.4% of patients with established CAD despite standard LDL-C-lowering therapies. It is powerfully impacted by a gene-environment interaction. Accurate identification of this trait allows determination of CAD risk that contributes information independent of the standard CAD risk factors and allows identification of first-degree relatives who may benefit from identification and early treatment of this disorder. Lack of treatment in the CAD population with ALP results in a significantly greater rate of arteriographic progression but appropriate treatment can result in significant arteriographic benefit. Treatments such as diet, exercise, loss of body fat, and niacin, are often effective and the least expensive treatments.
In short, it echoes what I have posted before... that the current concentration on just the LDL volume is far from the answer to preventing CVD... as in this PDF Beyond Routine Cholesterol Testing... (http://www.centerforpreventivemedicine.com/04114med_messenger.pdf)
Small LDL and Its Clinical Importance as a New CAD Risk Factor: A Female Case Study
H. Robert Superko, MD, Mary Nejedly, MS, ANP, Brenda Garrett, RN
Abstract
The underlying metabolic cause of coronary heart disease in many patients is not high blood cholesterol. In fact, the Framingham study has reported that 80% of individuals who go on to have coronary artery disease have the same total blood cholesterol values as those who do not go on to have a cardiovascular event. The most common metabolic contributor to coronary artery disease is the atherogenic lipoprotein profile, characterized by an abundance of highly atherogenic small, dense low-density lipoprotein particles and a deficiency of the high-density lipoprotein (HDL) subtype most associated with coronary artery disease protection (HDL2b). This trait is present in 50% of men with coronary artery disease and is not reflected by total or low-density lipoprotein cholesterol values. While fasting triglycerides tend to he higher, and HDL cholesterol lower in patients with the atherogenic lipoprotein profile, the majority have triglyceride and HDL cholesterol values generally accepted to be in the "normal" range. An abundance of basic science and clinical trial evidence convincingly indicates that the presence of an atherogenic lipoprotein profile signifies a three-fold increased risk for a cardiovascular event and rapid arteriographic progression, but it also identifies a group of patients who respond particularly well to specific therapeutic interventions. Often the most effective interventions are the least expensive.
Treatment of the small LDL trait involves diets that restrict simple carbohydrates, loss of excess body fat, and appropriate exercise. Pharmacologic treatment involves medications that tend to reduce triglycerides, such as nicotinic acid and the fibric acid derivatives. Many medications have a differential response based on LDL subclass distribution.
In summary, the small LDL trait is a common metabolic disorder that contributes to CAD risk and disease progression and at the American Cardiovascular Research Institute, is present in 57.4% of patients with established CAD despite standard LDL-C-lowering therapies. It is powerfully impacted by a gene-environment interaction. Accurate identification of this trait allows determination of CAD risk that contributes information independent of the standard CAD risk factors and allows identification of first-degree relatives who may benefit from identification and early treatment of this disorder. Lack of treatment in the CAD population with ALP results in a significantly greater rate of arteriographic progression but appropriate treatment can result in significant arteriographic benefit. Treatments such as diet, exercise, loss of body fat, and niacin, are often effective and the least expensive treatments.
In short, it echoes what I have posted before... that the current concentration on just the LDL volume is far from the answer to preventing CVD... as in this PDF Beyond Routine Cholesterol Testing... (http://www.centerforpreventivemedicine.com/04114med_messenger.pdf)