Treatment of Dyslipidemia
The treatment of hyperlipidemia requires two approaches:
Therapeutic lifestyle changes (TLC) and medications. To achieve target LDL levels, most patients need both approaches simultaneously.
a)Therapeutic Life Style Changes
TLCs encompasses increased physical activity, ideal weight maintenance, and a diet that encompasses a reduced intake of saturated fat (<7 per cent of total calories) and cholesterol (<200mg/day). Other TLCs are listed in table. It is essential to reduce saturated fat intake for patients with metabolic syndrome. A fat intake of 30 per cent to 35 per cent maybe optimal for reducing lipid and nonlipid risk factors. High carbohydrate diets may worsen the lipid abnormalities in these patients. Dietary carbohydrates should predominantly be derived from foods rich in complex carbohydrates, such as whole grains, fruits and vegetables. Daily intake of 5 to 10 G of viscous fiber reduces LDL levels by approximately 5 per cent and he use of plant stanols and Sterols (2 to 3 g/day) by another 6 per cent to 15 per cent. TLCs can achieve an almost 30 per cent reduction in LDL-C in highly motivated individuals and should form the cornerstone of all preventive activity LDL-C should be measured 6 weeks after initiating TLC diet, and if the goals are not met, intensification of TLCs and use of plant sterols or stanols should be considered. Referral to a dietitian for education and dietary counseling is often invaluable at this stage. If after 3 months of TLCs, adequate control is not achieved, drug therapy should be considered.
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| Components of Therapeutic Life Style |
b)Pharmacotherapy
The high efficacy of statins in lowering LDL-C and their demonstrated mortality benefits make them the agents of first choice for treatment of hyperlipidemia.HMG CoA reductase inhibitors: The third report of the NCEP Adult Treatment Panelnincluded HMG CoA reductase inhibitors among the first line alternatives in the management of hypercholesterolemia. The category includes five drugs lovastatin,simvastatin, pravastatin, fluvastatin, and atorvastatin.
i)Effectiveness: When dietary measures are inadequarte, HMG CoA reductase inhibitors effectively lower TC and LDL-C in patients with mixed hyperlipidemias HMG CoA reductase inhibitors are extremely effective in reducing LDL-C in most patients with primary hypercholesterolemia HMG CoA reductase inhibitors decrease TC by 15 per cent to 6 per cent and LDL-C by 20 per cent to mensurate with reductions in LDL have been demonstrated. Triglycerides levels have been reduced 10 per cent to 25 per cent.The HMG CoA reductase inhibitors appear to have minimal effects on apo AI apo AII, and lipoprotein (a) (Lpa).
ii) Lovastatin, simvastatin, pravastatin, and fluvastatin are well-tolerated, efficacious, and reasonably equivalent with respect to safety profiles.
iii) Adverse effects: Statins are remarkably safe drugs with a very low incidence of side effects. However, they are contraindicated in pregnancy.
iv) Minor side effects: The most common side effects are mild gastrointestinal disturbances. Headache, fatigue, pruritus, and myalgia are other minor side effects, but none of these complaints usually warrants discontinuation of therapy.
v) Liver function test abnormalities: Mild transient elevations in liver enzymes have been reported with all HMG CoA reductse inhibitors. Marked elevation of transaminases is rare; in the HPS trial, only 0.5 per cent of patients had to stop treatment because of elevated alanine aminotransferase levels. In general for each doubling of a statin dose, there is a 0.65 increase in risk for elevation of transaminase levels. Therapy should be discontinued when greater than three fold elevation occurs. Enzyme levels typically return to normal within 2 weeks. Lower doses of the same medication can be reinstituted, or a different HMG CoA reductase inhibitor can be tried.Monitoring of hepatic aminotransferase levels is recommended for those taking HMG CoA reductase inhibitors. Levels should be measured 6 weeks and 3 months after initiation of therapy and every 6 months thereafter. Because of the excellent safety profiles of pravastatin and simvastatin, the U. S Food and Drug Administration (FDA) recommends discontinuing hepatic enzyme monitoring after 3 months for pravastatin and after 6 months of continuous same dose therapy for simvastatin.
vi) Myopathy: A rare but potentially serious side effect of HMG CoA reductase inhibitors,occurs with muscle symptoms and elevations in serum creatine kinase (CK) level to more than 10 times the upper limit of normal. CK measurements are not needed unless symptoms occur. Muscle symptoms are common in the general population and were reported by at least one third of the patients in HPS trial at least once. No difference was observed in the incidence of myalgias or CK elevation in the two arms; about 0.5 per cent of patients in each arm had treatment stopped because of muscle symptoms. The risk of myopathy may be increased in the elderly, those with a low body
mass index, patients with multisystem disease such as chronic renal failure, in the perioperative period, and in those on multiple medications.
vii) Drug interactions: When statins are used in combination with certain pharmaceutical agents, such as erythromycin, gemfibrozil, azole antifungals, cimetidine, methotrexate,or cyclosporine, the risks for CK elevation and myositis increase. These drug combinations should be avoided or used judiciously with interval measurements of CK levels and liver function. Pravastatin and fluvastatin are safer in combination with other drugs do not use the cytochrome P450 3A4 microsomal pathways. Verapamil and amiodarone are two commonly used cardiovascular agents that inhibit this pathway, and the concurrent use of simvastatin, or lovastatin may therefore predispose to an increased risk of myositis.
c)Bile acid sequestrants
These are safe and free of systemic side effects. However, gastrointestinal side effects are common, and compliance is poor. The average LDL decreases by approximately 15 per cent to 30 per cent, HDL rises by 3 per cent to 5 per cent and TG levels shown no change or may rise. These agents maybe of particular benefit in patients with minor elevation LDL-C, for young patients, for women considering pregnancy, and in combination with a statin in those with very high LDL-C. In a pregnant patient, additional supplementation of iron and folate may be necessary because resins used over the long term can interfere with their absorption.
d)Nicotinic Acid or Niacin
Niacin affects all lipid parameters favorably. It is one of the only agents that reduces Lp (a) significantly (up to 30 per cent). Unfortunately, compliance is poor because of frequent side effects. Flushing and pruritus, gastrointestinal discomfort, glucose intolerance, and hyperuricemia often accompany use of niacin, hepatotoxicity is rare but is more commonly seen with the sustained released preparation. It is often heralded by a dramatic reduction in lipid levels. There are limited data on long-term therapy with this agent. Niacin may be particularly useful for patients who do not have substantial elevations in their LDL-C levels, and low doses may be used to treat diabetic dyslipidemia. High doses should be avoided in those with a history of gout, peptic ulcer disease, or active hepatic disease. Extended release preparations are to be used and not sustained release ones.
e)Fibrates are effective at lowering TG levels
Fibrates are effective at lowering TG levels by 20 per cent to 50 per cent and raising HDL by 10-35 per cent. LDL reduction varies with the agent used and may range from 5 per cent-20 per cent in patients who are not hypertriglyceridemic. Although a higher mortality rate was seen in the clofibrate arm of the World Health Organization study, such a finding was not seen in subsequent studies of gemfibrozil or bezafibrate. These agents have been demonstrated to impart reduction in risk of CAD events and are of use to treat mixed hyperlipidemia. Although these agents are often used in combination with statin therapy, there are no studies demonstrating reduction in clinical events with this approach. This combination increase the risk of myopathy. For patients with very high TG levels, fibrate therapy reduces the risk for pancreatitis.
f)Ezetimibe
It is a newer agent that inhibits cholesterol absorption by the enterocyte. It reduces cholesterol absorption by the enterocyte. It reduces cholesterol absorption by 23 per cent-50 per cent and LDL by 14 per cent-20 per cent when used in combination with a statin.Although large, long-term studies are lacking, this combination holds promise of a well- tolerated and efficacious regimen.
g)Choice of an Agent and Combination Therapy
The use of statin therapy for treatment of hyperlipidemia should be guided by the expected change in LDL-C levels. Most statins have a long linear dose response pattern, with each doubling of dose associated with a further 6 per cent reduction in LDL-C levels. Adverse effects of statins are also dose dependent and rise with the use of higher doses.
h)HMG CoA Reductase Inhibitors and Bile Acid Resins
In isolated forms of LDL elevation, this combination exhibits highly complementary mechanism of action. The combination of a statin with a bile acid sequestrant is ideal because of the lack of potentiation of side effects. The sequestrant provides little added toxicity and the LDL-C lowering needed may not necessitate a full sequestrant dosage.Unfortunately, patient compliance with the combination is poor because of the common side effects of resins. Although the combination may reduce LDL by as much as 70 per cent in some patients, there appears to be ceiling effect, with no LDL lowering occurring beyond the original level with an increase in dose of either agent.
The high efficacy of statins in lowering LDL-C and their demonstrated mortality benefits make them the agents of first choice for treatment of hyperlipidemia.HMG CoA reductase inhibitors: The third report of the NCEP Adult Treatment Panelnincluded HMG CoA reductase inhibitors among the first line alternatives in the management of hypercholesterolemia. The category includes five drugs lovastatin,simvastatin, pravastatin, fluvastatin, and atorvastatin.
i)Effectiveness: When dietary measures are inadequarte, HMG CoA reductase inhibitors effectively lower TC and LDL-C in patients with mixed hyperlipidemias HMG CoA reductase inhibitors are extremely effective in reducing LDL-C in most patients with primary hypercholesterolemia HMG CoA reductase inhibitors decrease TC by 15 per cent to 6 per cent and LDL-C by 20 per cent to mensurate with reductions in LDL have been demonstrated. Triglycerides levels have been reduced 10 per cent to 25 per cent.The HMG CoA reductase inhibitors appear to have minimal effects on apo AI apo AII, and lipoprotein (a) (Lpa).
ii) Lovastatin, simvastatin, pravastatin, and fluvastatin are well-tolerated, efficacious, and reasonably equivalent with respect to safety profiles.
iii) Adverse effects: Statins are remarkably safe drugs with a very low incidence of side effects. However, they are contraindicated in pregnancy.
iv) Minor side effects: The most common side effects are mild gastrointestinal disturbances. Headache, fatigue, pruritus, and myalgia are other minor side effects, but none of these complaints usually warrants discontinuation of therapy.
v) Liver function test abnormalities: Mild transient elevations in liver enzymes have been reported with all HMG CoA reductse inhibitors. Marked elevation of transaminases is rare; in the HPS trial, only 0.5 per cent of patients had to stop treatment because of elevated alanine aminotransferase levels. In general for each doubling of a statin dose, there is a 0.65 increase in risk for elevation of transaminase levels. Therapy should be discontinued when greater than three fold elevation occurs. Enzyme levels typically return to normal within 2 weeks. Lower doses of the same medication can be reinstituted, or a different HMG CoA reductase inhibitor can be tried.Monitoring of hepatic aminotransferase levels is recommended for those taking HMG CoA reductase inhibitors. Levels should be measured 6 weeks and 3 months after initiation of therapy and every 6 months thereafter. Because of the excellent safety profiles of pravastatin and simvastatin, the U. S Food and Drug Administration (FDA) recommends discontinuing hepatic enzyme monitoring after 3 months for pravastatin and after 6 months of continuous same dose therapy for simvastatin.
vi) Myopathy: A rare but potentially serious side effect of HMG CoA reductase inhibitors,occurs with muscle symptoms and elevations in serum creatine kinase (CK) level to more than 10 times the upper limit of normal. CK measurements are not needed unless symptoms occur. Muscle symptoms are common in the general population and were reported by at least one third of the patients in HPS trial at least once. No difference was observed in the incidence of myalgias or CK elevation in the two arms; about 0.5 per cent of patients in each arm had treatment stopped because of muscle symptoms. The risk of myopathy may be increased in the elderly, those with a low body
mass index, patients with multisystem disease such as chronic renal failure, in the perioperative period, and in those on multiple medications.
vii) Drug interactions: When statins are used in combination with certain pharmaceutical agents, such as erythromycin, gemfibrozil, azole antifungals, cimetidine, methotrexate,or cyclosporine, the risks for CK elevation and myositis increase. These drug combinations should be avoided or used judiciously with interval measurements of CK levels and liver function. Pravastatin and fluvastatin are safer in combination with other drugs do not use the cytochrome P450 3A4 microsomal pathways. Verapamil and amiodarone are two commonly used cardiovascular agents that inhibit this pathway, and the concurrent use of simvastatin, or lovastatin may therefore predispose to an increased risk of myositis.
c)Bile acid sequestrants
These are safe and free of systemic side effects. However, gastrointestinal side effects are common, and compliance is poor. The average LDL decreases by approximately 15 per cent to 30 per cent, HDL rises by 3 per cent to 5 per cent and TG levels shown no change or may rise. These agents maybe of particular benefit in patients with minor elevation LDL-C, for young patients, for women considering pregnancy, and in combination with a statin in those with very high LDL-C. In a pregnant patient, additional supplementation of iron and folate may be necessary because resins used over the long term can interfere with their absorption.
d)Nicotinic Acid or Niacin
Niacin affects all lipid parameters favorably. It is one of the only agents that reduces Lp (a) significantly (up to 30 per cent). Unfortunately, compliance is poor because of frequent side effects. Flushing and pruritus, gastrointestinal discomfort, glucose intolerance, and hyperuricemia often accompany use of niacin, hepatotoxicity is rare but is more commonly seen with the sustained released preparation. It is often heralded by a dramatic reduction in lipid levels. There are limited data on long-term therapy with this agent. Niacin may be particularly useful for patients who do not have substantial elevations in their LDL-C levels, and low doses may be used to treat diabetic dyslipidemia. High doses should be avoided in those with a history of gout, peptic ulcer disease, or active hepatic disease. Extended release preparations are to be used and not sustained release ones.
e)Fibrates are effective at lowering TG levels
Fibrates are effective at lowering TG levels by 20 per cent to 50 per cent and raising HDL by 10-35 per cent. LDL reduction varies with the agent used and may range from 5 per cent-20 per cent in patients who are not hypertriglyceridemic. Although a higher mortality rate was seen in the clofibrate arm of the World Health Organization study, such a finding was not seen in subsequent studies of gemfibrozil or bezafibrate. These agents have been demonstrated to impart reduction in risk of CAD events and are of use to treat mixed hyperlipidemia. Although these agents are often used in combination with statin therapy, there are no studies demonstrating reduction in clinical events with this approach. This combination increase the risk of myopathy. For patients with very high TG levels, fibrate therapy reduces the risk for pancreatitis.
f)Ezetimibe
It is a newer agent that inhibits cholesterol absorption by the enterocyte. It reduces cholesterol absorption by the enterocyte. It reduces cholesterol absorption by 23 per cent-50 per cent and LDL by 14 per cent-20 per cent when used in combination with a statin.Although large, long-term studies are lacking, this combination holds promise of a well- tolerated and efficacious regimen.
g)Choice of an Agent and Combination Therapy
The use of statin therapy for treatment of hyperlipidemia should be guided by the expected change in LDL-C levels. Most statins have a long linear dose response pattern, with each doubling of dose associated with a further 6 per cent reduction in LDL-C levels. Adverse effects of statins are also dose dependent and rise with the use of higher doses.
h)HMG CoA Reductase Inhibitors and Bile Acid Resins
In isolated forms of LDL elevation, this combination exhibits highly complementary mechanism of action. The combination of a statin with a bile acid sequestrant is ideal because of the lack of potentiation of side effects. The sequestrant provides little added toxicity and the LDL-C lowering needed may not necessitate a full sequestrant dosage.Unfortunately, patient compliance with the combination is poor because of the common side effects of resins. Although the combination may reduce LDL by as much as 70 per cent in some patients, there appears to be ceiling effect, with no LDL lowering occurring beyond the original level with an increase in dose of either agent.
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| Average Reduction in LDL-C Associated with the Starting does of Statin Agents |
i)Combining a statin with niacin is attractive because it can favorably influence all lipid subfractions. The side effects of the combination are increased but not synergistic and the risk of myopathy may be lower than previously believed. The main serious side effect of the combination is hepatotoxicity, which maybe reduced by using extended 24release niacin. In small studies using this combination, the risk of hepatotoxicity at niacin doses of 2 g/day was about 1 per cent.
ii) The combination of a statin plus fibrate is highly effective at treating mixed hyperlipidemias. Although theoretically appealing no reduction in clinical events has been demonstrated with this approach. The combination is associated with an increased risk of myopathy. Although earlier work suggested a higher incidence later studies suggest this complication may be seen in approximately 1 per cent of patients with the currently used agents.
iii) The combination of a statin plus ezetimibe has been studied in small studies and has proved to be highly safe and effective at lowering LDL-C levels. Although the combination may become the standard for follow-up periods suggest that this combination should be reserved for the patients who fail maximal statin doses or a statin plus bile acid sequestrant combination.
i)Therapy of Specific Lipid Disorders
a)Very high LDL levels usually result from inherited disorders of lipoprotein metabolism and carry a high risk of premature atherosclerosis with attendant morbidity and mortality.Hypothyroidism may be associated with markedly elevated LDL levels and should be ruled out in any patient presenting with elevated LDL level. Most of these patients respond to high dose statin therapy in addition to dietary restrictions. The addition of a bile acid sequestrant with and additional third agent often is warranted to achieve target levels. Ezetimibe is another agent that may prove useful in this group. Therapy should be begun early, and family members should be screened for hyperlipidemia. Patients with homozygous familial hyperlipidemia are deficient in LDL receptors and measures that reduce cholesterol absorption or act by LDL receptor upregulation are largely ineffective. These patients are treated with LDL apheresis and should be managed in tertiary care centers only.
b) Elevated TG levels may be caused by many factors, and more than one cause may be active in a given patient.Minor elevations in TG levels (150 to 299mg/dL) usually are caused by obesity, sedentary lifestyle smoking, excess alcohol intake, and high carbohydrate diets. In other patients, secondary, causes such as diabetes, renal failure, Cushing’s disease, nephrotic syndrome, or medications, may be responsible, and genetic causes maybe pertinent to others. The therapy for this group of patients involves identification and treatment of secondary cause change in medication and lifestyle changes. These patients benefit from total caloric restriction and switching from a very high carbohydrate diet to a more balanced diet. Very high TG levels ( > 500 mg/dl) usually result from genetic defects of lipoprotein metabolism. In some patients, there is a combination of factors at play.These patients are at risk for acute pancreatitis and treatment is directed to prevention of this condition. This is achieved with a combination of dietary measures increasing physical activity, maintaining optimal weight, and initiating fibrates or niacin therapy.
Fibrates are especially efficacious in this group. Statins are not especially effective agents for TG reduction and should be considered after the other two agents. Patients with an in intermediate rise in TG levels (200mg/dL) are a more heterogenous group with a wide array of underlying pathogenetic mechanisms at play. This pattern often is a result of an intersection of poor lifestyle secondary causes and genetic factors. These patients often have other markers of increased atherogenic risk such as increased small LDL low HDL or elevated VLDL remnants. They need to be treated aggressively to bring the LDL level to the target statins with their ability to lower non HDL cholesterol are the preferred agents. After the LDL target has been achieved, the secondary goal is
non HDL-C. These patients also need aggressive TLCs High dose statins often suffice to achieve the LDL-C and non HDL-C goals, but for most patients a second agent becomes necessary. The choices are niacin or fibrates in addition to a statin these combinations carry an increased risk for hepatotoxicity or myopathy and careful monitoring for these is essential. Fish oils used in combination with a statin is another option that is relatively free of major organ toxicity but patients often are unable to tolerate current preparations. Weight loss by obese patients should be encouraged. It is associated with an improvement in the lipid profile and facilitates pharmacologic therapy if still necessary.
c)Low HDL cholesterol levels often accompany minor or modest elevations in TG levels and should be addressed as previously discussed. In patients goal is to identify and modify lifestyle factors and medications the next step encompasses calculation of 10- years risk and treating LDL-C with a statin when appropriate. The AFCAPS/Tex CAPS study found a clear benefit for statin therapy inpatients with low HDL-C levels. In patients who are not able to tolerate statins, pharmacologic intervention for primary therapy has no defined role. Gemfibrozil may be a reasonable alternative because of its success in reducing cardiovascular events in the Department of Veterans Affairs HDL Intervention Trial.
d) Patients with Diabetic dyslipidemia are at an increased risk for cardiovascular events and fare poorly after CAD manifests. Diabetes is associated with an increase in small LDL particles and often is associated with high TG and low HDL levels Hyperglycemia is an independent risk factor for CAD. Primay prevention is important in this group and was demonstrated to be efficacious in the HPS trial. All diabetic patients (irrespective of LDL-C) should be considered for statin therapy and TLCs. Secondary goals include improved non HDL-C levels and treatment for elevated TG levels. Blood sugar control and insulin therapy often facilitate the former, but fibrates or low dose niacin may be necessary in some patients. Diabetes patients also often have coexisting hypertension. Blood pressure control and smoking cessation are essential because both interventions are highly effective at reducing cardiovascular events in this population.
ii) The combination of a statin plus fibrate is highly effective at treating mixed hyperlipidemias. Although theoretically appealing no reduction in clinical events has been demonstrated with this approach. The combination is associated with an increased risk of myopathy. Although earlier work suggested a higher incidence later studies suggest this complication may be seen in approximately 1 per cent of patients with the currently used agents.
iii) The combination of a statin plus ezetimibe has been studied in small studies and has proved to be highly safe and effective at lowering LDL-C levels. Although the combination may become the standard for follow-up periods suggest that this combination should be reserved for the patients who fail maximal statin doses or a statin plus bile acid sequestrant combination.
i)Therapy of Specific Lipid Disorders
a)Very high LDL levels usually result from inherited disorders of lipoprotein metabolism and carry a high risk of premature atherosclerosis with attendant morbidity and mortality.Hypothyroidism may be associated with markedly elevated LDL levels and should be ruled out in any patient presenting with elevated LDL level. Most of these patients respond to high dose statin therapy in addition to dietary restrictions. The addition of a bile acid sequestrant with and additional third agent often is warranted to achieve target levels. Ezetimibe is another agent that may prove useful in this group. Therapy should be begun early, and family members should be screened for hyperlipidemia. Patients with homozygous familial hyperlipidemia are deficient in LDL receptors and measures that reduce cholesterol absorption or act by LDL receptor upregulation are largely ineffective. These patients are treated with LDL apheresis and should be managed in tertiary care centers only.
b) Elevated TG levels may be caused by many factors, and more than one cause may be active in a given patient.Minor elevations in TG levels (150 to 299mg/dL) usually are caused by obesity, sedentary lifestyle smoking, excess alcohol intake, and high carbohydrate diets. In other patients, secondary, causes such as diabetes, renal failure, Cushing’s disease, nephrotic syndrome, or medications, may be responsible, and genetic causes maybe pertinent to others. The therapy for this group of patients involves identification and treatment of secondary cause change in medication and lifestyle changes. These patients benefit from total caloric restriction and switching from a very high carbohydrate diet to a more balanced diet. Very high TG levels ( > 500 mg/dl) usually result from genetic defects of lipoprotein metabolism. In some patients, there is a combination of factors at play.These patients are at risk for acute pancreatitis and treatment is directed to prevention of this condition. This is achieved with a combination of dietary measures increasing physical activity, maintaining optimal weight, and initiating fibrates or niacin therapy.
Fibrates are especially efficacious in this group. Statins are not especially effective agents for TG reduction and should be considered after the other two agents. Patients with an in intermediate rise in TG levels (200mg/dL) are a more heterogenous group with a wide array of underlying pathogenetic mechanisms at play. This pattern often is a result of an intersection of poor lifestyle secondary causes and genetic factors. These patients often have other markers of increased atherogenic risk such as increased small LDL low HDL or elevated VLDL remnants. They need to be treated aggressively to bring the LDL level to the target statins with their ability to lower non HDL cholesterol are the preferred agents. After the LDL target has been achieved, the secondary goal is
non HDL-C. These patients also need aggressive TLCs High dose statins often suffice to achieve the LDL-C and non HDL-C goals, but for most patients a second agent becomes necessary. The choices are niacin or fibrates in addition to a statin these combinations carry an increased risk for hepatotoxicity or myopathy and careful monitoring for these is essential. Fish oils used in combination with a statin is another option that is relatively free of major organ toxicity but patients often are unable to tolerate current preparations. Weight loss by obese patients should be encouraged. It is associated with an improvement in the lipid profile and facilitates pharmacologic therapy if still necessary.
c)Low HDL cholesterol levels often accompany minor or modest elevations in TG levels and should be addressed as previously discussed. In patients goal is to identify and modify lifestyle factors and medications the next step encompasses calculation of 10- years risk and treating LDL-C with a statin when appropriate. The AFCAPS/Tex CAPS study found a clear benefit for statin therapy inpatients with low HDL-C levels. In patients who are not able to tolerate statins, pharmacologic intervention for primary therapy has no defined role. Gemfibrozil may be a reasonable alternative because of its success in reducing cardiovascular events in the Department of Veterans Affairs HDL Intervention Trial.
d) Patients with Diabetic dyslipidemia are at an increased risk for cardiovascular events and fare poorly after CAD manifests. Diabetes is associated with an increase in small LDL particles and often is associated with high TG and low HDL levels Hyperglycemia is an independent risk factor for CAD. Primay prevention is important in this group and was demonstrated to be efficacious in the HPS trial. All diabetic patients (irrespective of LDL-C) should be considered for statin therapy and TLCs. Secondary goals include improved non HDL-C levels and treatment for elevated TG levels. Blood sugar control and insulin therapy often facilitate the former, but fibrates or low dose niacin may be necessary in some patients. Diabetes patients also often have coexisting hypertension. Blood pressure control and smoking cessation are essential because both interventions are highly effective at reducing cardiovascular events in this population.
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