eMedicine Specialties > Cardiology > Atherosclerosis and Risk Factors
Atherosclerosis: Treatment & Medication
Updated: Nov 17, 2009
- Overview
- Differential Diagnoses & Workup
- Treatment & Medication
- Follow-up
Treatment
Medical Care
The prevention and treatment of atherosclerosis requires control of the known modifiable risk factors for this disease. This includes the medical treatment of hypertension, hyperlipidemia, diabetes mellitus, and cigarette smoking.
Hypertension
Hypertension is a risk factor for the development of atherosclerosis, atherosclerotic cardiovascular disease, and stroke. See eMedicine article Hypertensive Heart Disease. The mechanism by which hypertension causes these effects is not known, and some uncertainty exists as to what the primary and secondary factors are in a typically multifactorial syndrome. These factors may include hyperlipidemia, hypertension, diabetes mellitus, obesity, and physical inactivity.
Dietary and pharmacological treatment of hypertension is associated with a decreased incidence of stroke and, to a lesser degree, atherosclerotic cardiovascular disease.
Hyperlipidemia and dyslipidemia
Convincing evidence exists that lowering serum cholesterol and treating dyslipidemia reduces the risk of subsequent coronary heart disease events and overall mortality.11
The HMG-CoA reductase inhibitors inhibit the rate-limiting step of cholesterol synthesis in the liver. HMG-CoA reductase inhibitors are effective in lowering the serum total cholesterol, LDL cholesterol, and triglyceride levels and in raising the serum HDL cholesterol level, and they have a low incidence of adverse effects, the most common being hepatotoxicity and myopathy.
The success of the HMG-CoA reductase inhibitors in reducing circulating lipid levels and improving the clinical and anatomic course of atherosclerosis has focused attention on the management of hyperlipidemia. In addition, an important role remains for other hypolipidemic agents that may be of particular benefit for patients with refractory LDL hypercholesterolemia, hypertriglyceridemia, low HDL cholesterol, and elevated lipoprotein(a).
Following a prespecified interim analysis conducted after 208 patients (mean age 65 y, 80% men) had completed the trial, the trial was terminated early on the basis of efficacy. The results are described for these 208 patients. In the niacin group, HDL cholesterol levels were increased by 18.4% to 50 mg/dL (P <0.001). Niacin also significantly reduced LDL cholesterol and triglyceride levels. The ezetimibe group showed a decrease of LDL cholesterol levels by 19.2% to 66 mg/dL (1.7 mmol/L) (P <0.001). Ezetimibe did not increase HDL cholesterol (HDL levels were actually reduced), but it did reduce triglycerides. Niacin had greater efficacy regarding the change in mean carotid intima–media thickness over 14 months compared with ezetimibe (P =0.003), leading to significant reduction of both mean (P =0.001) and maximal carotid intima–media thickness (P £0.001 for all comparisons).
This trial concluded that niacin is superior to ezetimibe for combination therapy in high-risk patients taking statin monotherapy. Two editorials stated the early termination, the small number of patients, and limited duration of follow-up do not yet merit changes in cholesterol therapy guidelines, but they did support niacin as the preferred agent for statin combination therapy until the completion of clinical trials with clinical end points can be completed.13,14 Two well-powered studies of clinical end points, AIM-HIGH (Atherothrombosis Intervention in Metabolic Syndrome with Low HDL/High Triglycerides and Impact on Global Health Outcomes; NCT00120289) and HPS2-THRIVE (Heart Protection Study 2: Treatment of HDL to Reduce the Incidence of Vascular Events; NCT00461630), will hopefully determine if adding niacin to statin therapy leads to a further risk reduction in patients with hypercholesterolemia.14
Secondary prevention of coronary artery disease
The Scandinavian Simvastatin Survival Study (4S) examined the effects of simvastatin on mortality in 4444 patients with established coronary heart disease and elevated total serum cholesterol. A statistically significant 29% reduction in the overall mortality rate (8.2% vs 11.5%) and a 42% reduction in the cardiac mortality rate (5% vs 8.5%) occurred after an average of 5.4 years of follow-up.15,16
The Cholesterol and Recurrent Events (CARE) study examined the effects of pravastatin on mortality rates and cardiac events in 1159 patients with established coronary heart disease and serum cholesterol concentrations that are within the reference range or are mildly elevated. A statistically significant 24% reduction in the incidence of fatal coronary heart disease or nonfatal myocardial infarction (9.9% vs 12.9%) occurred after an average of 5 years of follow-up. A lower total mortality rate (8.6% vs 9.4%) and coronary heart disease mortality rate (4.6% vs 5.7%) occurred in patients receiving pravastatin, although the results were not statistically significant.17
The Long-Term Intervention with Pravastatin in Ischaemic Disease (LIPID) trial examined the effects of 40 mg of pravastatin on the incidence of coronary events over a period of 6.1 years in 9014 patients with known coronary heart disease and a broad range of initial cholesterol levels. The following relative risk reductions occurred: 24% for death from coronary heart disease (P <0.001), 22% for the overall mortality rate (P <0.001), 29% for all cardiovascular outcomes (P <0.001), and 19% for stroke (P = 0.048). The effects were similar for all predefined subgroups.18
Primary prevention of coronary artery disease
The Justification for the Use of Statins in Primary Prevention: an Intervention Trial Evaluating Rosuvastatin (JUPITER Trial) was stopped early in 2008 when results showed a reduction in cardiovascular morbidity and mortality in patients treated with rosuvastatin compared with placebo. Notably, the patients studied had no evidence of cardiovascular disease and low to normal LDL-C. However, their C-reactive protein (CRP) levels were elevated, which the statin effectively lowered, suggesting that its effect on inflammation may be as important as lowering cholesterol.19,20
The West of Scotland Coronary Prevention Study (WOSCOPS) examined the effects of pravastatin on the incidence of nonfatal myocardial infarction and coronary mortality rates in 6595 men with moderate hypercholesterolemia and no prior history of coronary heart disease. A statistically significant 29% reduction in nonfatal myocardial infarction (4.6% vs 6.5%) and a 30% reduction in death from all cardiovascular causes (1.6% vs 2.3%) occurred after an average of 4.9 years of follow-up.21
The Air Force/Texas Coronary Atherosclerosis Prevention Study (AFCAPS/TexCAPS) examined the effects of lovastatin on the incidence of a first major coronary event in 5608 men and 997 women with average total cholesterol and LDL cholesterol and below-average HDL cholesterol levels. A statistically significant 37% reduction in the incidence of the first major coronary event (4% vs 6.8%) occurred after an average of 5.2 years.22
Therapy with lipid-lowering agents should be a component of multiple risk factor intervention and is indicated in primary prevention as an adjunct to diet therapy when the response to a diet restricted in saturated fat and cholesterol has been inadequate. The NCEP guidelines recommend aggressive lipid-lowering therapy for patients at high risk for coronary heart disease and for anyone with LDL-C over 160 mg/dL.{Ref6} More than 50 million individuals in the United States are candidates for some form of dietary and/or pharmacological intervention to modify their lipid profile. Pharmacoeconomic studies of implementation of the NCEP guidelines confirm the cost-effectiveness of primary and secondary prevention.
Diabetes mellitus
For patients with diabetes mellitus, strict control of comorbid risk factors is especially important, and ample evidence exists that this reduces the incidence of the clinical complications of microvascular and macrovascular disease.
- Cholesterol lowering with the HMG-CoA reductase inhibitors has yielded important reductions in coronary heart disease events in patients with diabetes mellitus.
- The benefit of strict glycemic control in the prevention of macrovascular disease has been difficult to confirm, although this intuitively is beneficial and is known to retard the progression of microvascular disease.
Cigarette smoking
Some evidence suggest that cardiovascular risk subsides within about 5 years after smoking cessation.23
Diet
- The National Cholesterol Education Program (NCEP) and the American Heart Association (AHA) made specific recommendations for dietary therapy for coronary heart disease prevention.
- Moderate alcohol intake (20 g/day or less) in men is associated with a reduced incidence of coronary heart disease events.24 The mechanism(s) of this benefit is not well understood. It should be noted that although alcohol may have cardiovascular benefits for women,25 even moderate intake of alcohol in women has been associated with a significantly increased risk for breast cancer.26 Heavy alcohol intake is associated with an increased incidence of coronary heart disease events, as well as cardiomyopathy, arrhythmia, and other adverse health effects and obviously should be discouraged.
- Sinha and colleagues concluded that high intakes of red or processed meat were associated with modest increases in total mortality, cancer mortality, and cardiovascular disease mortality. The baseline population was a cohort of half a million people aged 50-71 years from the National Institutes of Health-AARP (formerly known as the American Association of Retired Persons) Diet and Health Study.27
Activity
Physical inactivity is another modifiable risk factor for coronary heart disease, and regular exercise has been shown to reduce the risk of coronary heart disease in a number of observational epidemiological studies. The mechanisms for this apparent benefit may include an increase in HDL cholesterol and nitric oxide release and a decrease in body weight, insulin resistance, and blood pressure. Most health benefits occur with at least 150 minutes a week of moderate-intensity physical activity, such as brisk walking. Additional benefits occur with more physical activity.28
Medication
Prevention and treatment of atherosclerosis requires risk factor control, including the medical treatment of hypertension, diabetes mellitus, and cigarette habituation.
Advances in the understanding of the vascular biology of atherosclerosis raises the possibility of novel therapies that may address more directly the various aspects of endothelial dysfunction and the role of endothelial dysfunction in atherogenesis. Potential cellular targets include vascular smooth muscle cells, monocyte/macrophage cell lines, platelets, and endothelial cells. Evidence exists that antiplatelet agents, antioxidant therapies, amino acid supplementation, angiotensin-converting enzyme inhibitors, and angiotensin receptor blockers may prove to prevent or slow the progression of the disease.
Combination therapy in the future may allow for even greater achievement of greater LDL-C lowering with associated cardiovascular benefit. As one example, however, Vytorin, which combines ezetimibe (decreases small intestinal absorption of cholesterol) with simvastatin, has shown no incremental benefit on cardiovascular morbidity and mortality over and above that demonstrated for simvastatin alone.
HMG-CoA reductase inhibitors
These agents are competitive inhibitors of 3-hydroxy-3-methyl Co-A reductase, an enzyme that catalyzes the rate-limiting step in cholesterol biosynthesis, resulting in up-regulation of LDL receptors in response to the decrease in intracellular cholesterol. The HMG-CoA reductase inhibitors are indicated for the secondary prevention of cardiovascular events and for the treatment of hypercholesterolemia and mixed dyslipidemia.
A number of HMG-CoA reductase inhibitors are indicated for patients with homozygous familial hypercholesterolemia as an adjunct to other lipid-lowering treatments. However, these agents may be less effective in patients with rare homozygous familial hypercholesterolemia, possibly because these patients are lacking functional LDL receptors, making it more likely to raise serum transaminases.
Pravastatin (Pravachol)
Effective in reducing circulating lipid levels and improving the clinical and anatomic course of atherosclerosis.
Adult
10-40 mg/d PO hs
Pediatric
Not established
Immunosuppressive agents, gemfibrozil, clofibrate, cholestyramine, niacin, and erythromycin increase toxicity; may increase the PT when coadministered with warfarin; coadministration with either niacin or erythromycin has been associated with rhabdomyolysis
Documented hypersensitivity; active liver disease; unexplained elevations in liver function tests; pregnancy; breast-feeding
Pregnancy
X - Contraindicated in pregnancy
Precautions
May elevate creatine kinase and transaminase levels; caution in liver disease and ethanol abuse
Simvastatin (Zocor)
Inhibits cholesterol synthesis and increases cholesterol metabolism.
Adult
5-80 mg/d PO hs
Pediatric
Not established
Mibefradil, cyclosporine, itraconazole, ketoconazole, gemfibrozil, niacin, erythromycin, clarithromycin, and nefazodone increase toxicity; coadministration with warfarin may increase PT; rifampin and nicotinic acid may decrease effects; coadministration with either niacin or erythromycin has been associated with rhabdomyolysis
Documented hypersensitivity; active liver disease; unexplained elevation of liver enzymes; pregnancy; breastfeeding
Pregnancy
X - Contraindicated in pregnancy
Precautions
May elevate creatine kinase and transaminase levels; discontinue therapy if symptoms of myopathy or renal failure develop; caution in patients with a history of liver disease and in those who consume excessive amounts of alcohol
Lovastatin (Mevacor, Altocor)
Adjunct to dietary therapy in reducing serum cholesterol. Immediate-release (Mevacor) and extended-release (Altocor) are available.
Adult
Immediate-release: 10-80 mg/d PO qd or divided bid
Sustained-release: 10-20 mg PO hs initially; may increase dose q4wk, not to exceed 60 mg/d
Pediatric
Not established
Mibefradil, cyclosporine, itraconazole, ketoconazole, gemfibrozil, niacin, erythromycin, clarithromycin, and nefazodone increase toxicity; coadministration with warfarin may increase PT; increases effects of levothyroxine; rifampin, nicotinic acid, bile acid sequestrants, and propranolol may decrease effects
Documented hypersensitivity; active liver disease; unexplained elevations in liver function tests; pregnancy; breastfeeding
Pregnancy
X - Contraindicated in pregnancy
Precautions
May elevate creatine kinase and transaminase levels; discontinue therapy if symptoms of myopathy or renal failure develop; caution in patients with a history of liver disease and in those who consume excessive amounts of alcohol
Fluvastatin (Lescol)
Used as an adjunct to dietary therapy in decreasing cholesterol levels.
Adult
20-80 mg/d PO qd or divided bid
Pediatric
Not established
Toxicity increases when coadministered with triazole antifungals, CNS depressants, macrolide antibiotics, mibefradil, immunosuppressive agents, gemfibrozil, and niacin; coadministration with warfarin may increase PT; rifampin, nicotinic acid, bile acid sequestrants, and propranolol may decrease effects
Documented hypersensitivity; active liver disease; unexplained elevations in liver function tests; pregnancy; breastfeeding
Pregnancy
X - Contraindicated in pregnancy
Precautions
May elevate creatine kinase and transaminase levels; photosensitivity may occur with prolonged exposure to sunlight or tanning equipment
Atorvastatin (Lipitor)
Adjunct to dietary therapy in reducing serum cholesterol.
Adult
10 mg PO qd; titrate to maximum 80 mg/d
Pediatric
Not established
Toxicity increases when coadministered with triazole antifungals, CNS depressants, macrolide antibiotics, mibefradil, cyclosporine, fibric acid derivatives, and niacin; increases toxicity of levothyroxine; coadministration with warfarin may increase the PT
Documented hypersensitivity; significant hepatic impairment; pregnancy; breastfeeding
Pregnancy
X - Contraindicated in pregnancy
Precautions
May elevate creatine kinase and transaminase levels; caution in patients receiving drugs that prolong QRS or QT interval; discontinue therapy if symptoms of myopathy or renal failure develop; caution in patients with a history of liver disease and in those who consume excessive amounts of alcohol
Rosuvastatin (Crestor)
HMG-CoA reductase inhibitor that in turn decreases cholesterol synthesis and increases cholesterol metabolism. Reduces total-C, LDL-C, and TG levels and increases HDL-C level. Used adjunctively with diet and exercise to treat hypercholesterolemia.
Adult
5-10 mg PO qd initially; may increase dose if needed, not to exceed 40 mg/d; for marked hypercholesterolemia (ie, LDL-C >190 mg/dL), initiate with 20 mg/d PO
Pediatric
Not established
Cyclosporine or gemfibrozil significantly increase Cmax and AUC, thereby increasing myopathy and rhabdomyolysis risk; limit dose to 5 mg/d when coadministered with cyclosporine and 10 mg/d when coadministered with gemfibrozil; coadministration with aluminum and magnesium hydroxide antacids decreases plasma concentrations (administer antacids 2 h after rosuvastatin); may increase oral contraceptive plasma concentrations; alcohol may increase hepatotoxic risk
Documented hypersensitivity; active liver disease; unexplained serum transaminase elevation
Pregnancy
X - Contraindicated in pregnancy
Precautions
Common adverse effects include muscle aches, stomach pain, constipation, nausea, and weakness; may cause myopathy, rhabdomyolysis, and kidney failure; monitor LFTs (ie, baseline, 12 wk after drug initiation and any dose elevation, and semiannually), discontinue if elevation persists; decrease dose with CrCl <30 mL/min; doses 40 mg or greater associated with hematuria and proteinuria
Pitavastatin (Livalo)
HMG-CoA reductase inhibitor (statin) indicated for primary or mixed hyperlipidemia. In clinical trials, 2 mg/d reduced total cholesterol and LDL cholesterol similar to atorvastatin 10 mg/d and simvastatin 20 mg/d.
Adult
2 mg PO qd; not to exceed 4 mg/d
Pediatric
Not established
Data limited; CYP2C9 substrate; OATP1B1 transporter substrate; 4-fold increase in AUC when coadministered with cyclosporine (an OATP1B1 inhibitor); coadministration with other drugs that cause myopathy (eg, gemfibrozil) may increase risk; CYP2C9 inhibitors (eg, fluconazole, gemfibrozil, nevirapine, sulfisoxazole) may decrease metabolism and thereby increase serum concentration
Documented hypersensitivity; active liver disease; pregnancy
Pregnancy
X - Contraindicated; benefit does not outweigh risk
Precautions
Common adverse effects include myalgias and myopathy, joint pain, back pain, and constipation; caution with history of liver/renal impairment
Fibric acid derivatives
The precise mechanism of action of this class of drugs is complex and incompletely understood. They increase the activity of lipoprotein lipase and enhance the catabolism of triglyceride-rich lipoproteins, which is responsible for an increase in the HDL cholesterol fraction. A decrease in hepatic very low-density lipoprotein (VLDL) synthesis and an increase in cholesterol excretion into bile also appear to occur. The fibrates typically reduce triglyceride levels by 20-50% and increase HDL cholesterol levels by 10-15%.
The effect on LDL cholesterol is variable. Levels may be expected to decrease by 10-15%. In patients with marked hypertriglyceridemia, LDL cholesterol levels may increase, which likely reflects the ability of the LDL receptor to clear the increased LDL generated by increased VLDL catabolism. Fibrate therapy may also be responsible for a decrease in the clotting ability of platelets and fibrinogen levels, which may account for some of the reported clinical benefits.
These agents can enhance the synthesis of lipoprotein lipase, which can cause triglycerides and very low density lipoprotein levels to decrease.
Fenofibrate (Tricor)
Adjunct to dietary therapy in treating hyperlipidemias associated with hypertriglyceridemia, including type IV and type V. Not proven to be of use in prevention of coronary artery disease.
Adult
67 mg/d PO
Pediatric
Not established
May increase effects of warfarin; the benefits and risks of administration with immunosuppressants and other nephrotoxic drugs should be considered carefully and the lowest possible dose used; a theoretical risk of severe myositis, rhabdomyolysis, and renal failure exists if combined with the HMG-CoA reductase inhibitors, and close monitoring of serum creatine kinase is appropriate
Documented hypersensitivity; hepatic or renal dysfunction, including primary biliary cirrhosis; unexplained persistent liver function abnormalities; gallbladder disease; caution in hypothyroidism
Pregnancy
C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus
Precautions
May cause cholelithiasis or cholecystitis; associated with myositis and elevated creatine kinase levels, particularly when used with HMG-CoA reductase inhibitors; increased incidence of malignancy
Gemfibrozil (Lopid)
Adjunct to dietary therapy in adult patients with type IV and V hyperlipidemias presenting at risk for pancreatitis. Adjunctive therapy in coronary heart disease prevention in patients with type IIb hyperlipidemia (low HDL, elevated LDL and triglycerides) not responding to other agents or diet modifications.
Adult
1200 mg/d PO divided bid 30 min before breakfast and dinner
Pediatric
Not established
May potentiate effects of warfarin; closely monitor if coadministered with lovastatin
Documented hypersensitivity; gallbladder disease; renal or hepatic insufficiencies
Pregnancy
B - Fetal risk not confirmed in studies in humans but has been shown in some studies in animals
Precautions
Discontinue if reduction in triglyceride levels is not observed after 3 mo of therapy; monitor for abnormal elevation of ALT, AST, LDH, bilirubin, and alkaline phosphatase serum levels; may increase cholesterol excretion into bile, leading to cholelithiasis; incidence of myositis is higher among patients with renal impairment; caution in diabetes and hypothyroidism
Bile acid sequestrants
The bile acid sequestrants block enterohepatic circulation of bile acids and increase the fecal loss of cholesterol. This results in a decrease in intrahepatic levels of cholesterol. The liver compensates by up-regulating hepatocyte LDL receptor activity. The net effect is a 10-25% reduction in LDL cholesterol, but no consistent effect on triglycerides or HDL cholesterol exists.
Cholestyramine (Questran, LoCholest, Prevalite)
May use as adjunct in primary hypercholesterolemia. Forms a nonabsorbable complex with bile acids in the intestine, which, in turn, inhibits enterohepatic reuptake of intestinal bile salts.
Adult
4-24 g PO ac divided bid; not to exceed 24 g/d or 6 doses per d
Pediatric
Not established; suggested dosing is 240 mg/kg/d PO divided bid/tid; not to exceed 8 g/d
Inhibits absorption of many drugs, including warfarin, thyroid hormone, amiodarone, NSAIDs, methotrexate, digitalis glycosides, glipizide, phenytoin, imipramine, niacin, methyldopa, tetracyclines, clofibrate, hydrocortisone, and penicillin G
Documented hypersensitivity; biliary obstruction
Pregnancy
C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus
Precautions
Patients may require fat-soluble vitamins and folic acid replacement with long-term therapy; caution in constipation and phenylketonuria; administer 1-2 h before or 4-6 h after bile acid sequestrant
Colestipol (Colestid)
Forms a soluble complex after binding to bile acid, increasing fecal loss of bile acid-bound LDL cholesterol.
Adult
Granules: 5-30 g/d PO qd or divided bid mixed with liquid
Pediatric
Not established
Decreases absorption of methotrexate, glipizide, imipramine, phenytoin, tolbutamide, niacin, clindamycin, NSAIDs, gemfibrozil, ursodiol, clofibrate, phenobarbital, warfarin, digitalis glycosides, propranolol, phenobarbital, hydrocortisone, and other drugs by inhibiting their absorption in the intestine
Documented hypersensitivity; complete biliary obstruction
Pregnancy
C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus
Precautions
Patients may require fat-soluble vitamins and folic acid replacement with long-term therapy; may be associated with increase in bleeding tendencies due to hypoprothrombinemia resulting from a decrease in vitamin K absorption; administer 1-2 h before or 4-6 h after bile acid sequestrant
Vitamin E (Vita-Plus E, Softgels, Aquasol E)
Protects polyunsaturated fatty acids in membranes from attack by free radicals.
Adult
60-75 IU/d PO/IM; study doses for the prevention of coronary artery disease have ranged from 400-800 IU/d PO
Pediatric
Not established
Mineral oil decreases absorption of vitamin E; vitamin E delays absorption of iron and increases effects of anticoagulants
Documented hypersensitivity; iron deficiency anemia
Pregnancy
B - Fetal risk not confirmed in studies in humans but has been shown in some studies in animals
Precautions
Large doses of vitamin E may result in vitamin K deficiency, enhancing the anticoagulant activity of warfarin and increasing the risk of major and minor bleeding complications, especially in patients who are also taking antiplatelet medication; necrotizing enterocolitis may occur
Nicotinic acid derivatives
Niacin (vitamin B-3) inhibits the hepatic secretion of VLDL cholesterol. Niacin is effective in most categories of hyperlipidemia. Niacin has been demonstrated to lower LDL cholesterol and triglyceride levels by 32% and 20-50%, respectively, and to raise the HDL cholesterol level by 43%. Niacin lowers lipoprotein (a) levels, which may be of some clinical importance because lipoprotein (a) levels have been associated with coronary heart disease in numerous epidemiological studies. The clinical benefit of lowering lipoprotein (a) levels has not been determined.
Niacin (Niaspan, Niacor, Slo-Niacin)
Used in tissue respiration, lipid metabolism, and glycogenolysis. Available in immediate- and extended-release formulations. Extended-release formulation may reduce flushing, an unpleasant adverse effect that causes 30-40% of patients to discontinue therapy.
Adult
2-6 g/d PO with food divided tid
Pediatric
Not established
HMG-CoA reductase inhibitors increase the risk of rhabdomyolysis; cutaneous vasodilation may be a problem if high dose is used with peripheral dilators such as nitroglycerine; taking aspirin 30-60 min before first dose of the day may help alleviate prostaglandin-mediated adverse effects (eg, flushing, itching); clonidine may inhibit niacin-induced flushing; separate dosing of bile acid sequestrants by at least 4-6 h; may increase PT when coadministered with warfarin
Documented hypersensitivity; active liver disease or unexplained significant increases in AST and ALT; substantial alcohol consumption; active peptic ulcer disease; active gout; hyperuricemia
Pregnancy
A - Fetal risk not revealed in controlled studies in humans
C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus
Precautions
Caution in patients with gallbladder disease or diabetes in those predisposed to gout; monitor blood glucose; may elevate uric acid levels and lower blood phosphate levels
Nutritional Agent
Omega-3 polyunsaturated fatty acid
Possible benefits in the treatment of atherosclerosis include effects on lipoprotein metabolism, hemostatic function, platelet/vessel wall interactions, anti-arrhythmic actions and also inhibition of proliferation of smooth muscle cells and therefore growth of the atherosclerotic plaque. Fish oil feeding has also been found to result in moderate reductions in blood pressure and to modify vascular neuroeffector mechanisms.
Adult
4-12 g/d PO in divided doses as directed
Pediatric
Not established
May increase effects of antiplatelet agents; concomitant use of other oils (eg, olive oil) may reduce effects
Documented hypersensitivity
Pregnancy
C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus
Precautions
May cause fishy odor, diarrhea, hyperglycemia, and bleeding due to decreased platelet aggregation; caution in bleeding disorders or diabetes
More on Atherosclerosis |
| Overview: Atherosclerosis |
| Differential Diagnoses & Workup: Atherosclerosis |
 Treatment & Medication: Atherosclerosis |
| Follow-up: Atherosclerosis |
| References |
| « Previous Page | Next Page » |
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Further Reading
Keywords
myocardial infarction, transient ischemic attack, TIA, stroke, atheroembolism, coronary heart disease, coronary artery atherosclerosis, peripheral vascular disease, ischemia, atherosclerosis, hyperlipidemia, coronary artery disease, cerebrovascular disease, sudden cardiac death, hypertension, hypotension, atherosclerotic cardiovascular disease, diabetes mellitus
