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You are seeing for the first time a patient who was referred to you by his former physician. The patient is a 66-year-old former advertising executive who has a past medical history of hypertension. He has been maintained on metoprolol for the past 2 years and reports excellent medical compliance. The patient denies any chest pain syndrome with exertion and describes being able to œwalk for hours without any problems. Upon further questioning you learn the patient has a 40-pack-year history of smoking and currently has cut down to two to three cigarettes per day. The patient™s father died at age 52 from a œmassive heart attack. Vital signs are: temperature 37 C (98.6 F), blood pressure 170/85 mm Hg, pulse 80/min, respirations 12/min. Physical examination shows clear lungs and a laterally displaced point of maximum impulse. Screening lipid blood levels come back and show a total cholesterol of 195 mg/dL, LDL of 134 mg/dL, HDL of 34 mg/dL, and triglycerides at 140 mg/dL. Complete blood count, liver function tests, and serum electrolytes are normal. Which of the following is the most appropriate next step in managing this patient™s lipid profile?
A. Advise him to make therapeutic lifestyle changes including diet and exercise modification and recheck cholesterol levels in 1 year
B. Begin therapy with gemfibrozil in order to lower triglyceride levels
C. Begin therapy with an HMG-CoA reductase inhibitor and check liver function tests in 4 to 6 weeks
D. Begin therapy with nicotinic acid (niacin) therapy to preferentially raise HDL cholesterol
E. Concentrate on complete tobacco cessation because stopping smoking will likely have beneficial effects on lipid abnormalities
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no evidence of CHD, more than 2 CHD risk factors, LDL 130-159 --------diet. (A)
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I have read somewhere that if HDL is to low than the drug therapy has to be started .
even when LDL is not so high for drug therapy. Can someone check this?
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hi,
The answer could be controversial but please understand that i have just copied and posted the explanation as it appears on the qbank. Dispute if any will be dealt tomoro morning....yaaawwwwnnnn...too sleepy for a debate rght now.
chill
The correct answer is C. For patients with coronary heart disease or at increased risk for cardiac events, lipid-lowering therapy greatly reduces the risk for future coronary events and stroke. Recently the National Cholesterol Education Program (NCEP) released the Adult Treatment Panel (ATP)-3 guidelines for managing cholesterol, with a new focus on primary prevention in patients with multiple risk factors. The revised guidelines focus on identifying persons with a relatively high risk for coronary artery disease (CAD) by identifying multiple risk factors and starting more intensive lipid-lowering therapy.
In evaluating any patient for cholesterol modification you should begin with identifying an elevated LDL cholesterol as the primary target, and then assess a person™s risk status. Independent major risk factors include the presence of CAD, other clinical forms of atherosclerotic disease (peripheral vascular disease), diabetes, hypertension on antihypertensive medications, low HDL cholesterol (<40 mg/dl), family history of premature heart disease (CAD in male first-degree relative <55 years or CAD in female first-degree relative <65 years), and age of patient (men >45 or women >55). Although this patient does not have any history of CAD or CAD equivalents (diabetes, peripheral vascular disease) the patient does have multiple risk factors, including smoking, family history, high blood pressure on hypertensive medication, age >55, and low HDL cholesterol. At first glance the physician may categorize this patient as Intermediate Risk with an optimal LDL goal of 130, not necessarily requiring lipid-lowering drug therapy immediately. But if one were to calculate the 10-year risk of CAD (based on Framingham projections of 10-year absolute risk of coronary heart disease found in the ATP-3 guidelines), the treating physician would find an increased risk of >20%, which is equivalent to a patient with a prior history of heart disease or diabetes. Obviously, not all physicians are expected to be able to calculate this absolute 10-year risk for every patient, but it is important to be able to identify the presence of multiple risk factors. This patient has five separate risk factors, giving him the highest risk, and thus he should be treated aggressively with lipid-lowering agents for an LDL goal of <100 mg/dl.
HMG CoA reductase inhibitors (statins) are the most potent LDL-lowering agents, with an average of 18 to 55% in LDL lowering and a 5 to 15% HDL-raising effect. Statins have been shown to decrease mortality and coronary artery disease as well as stroke and should be considered first-line agents for LDL lowering. After starting a patient on statin therapy, liver function tests should be checked 4 to 6 weeks later to make sure there is no hepatotoxicity.
Therapeutic lifestyle changes such as diet modification or increased exercise (choice A) would be an appropriate recommendation for any patient with hyperlipidemia. This patient requires a substantial lowering in LDL cholesterol and would unlikely achieve this without additional therapy. A large proportion of the population whose short- or long-term risk for CAD is high will require LDL-lowering drugs in addition to therapeutic lifestyle modification.
Fibric acid preparations such as gemfibrozil or fenofibrate (choice B) are potent agents for lowering triglyceride levels (average of 20 to 50% reduction in triglyceride levels) but this patient has a normal triglyceride level of <150 mg/dL. Patients with extremely high triglyceride levels (>500 mg/dl) as found in the familial hypertriglyceridemia syndromes should be treated with a fibric acid derivative.
Nicotinic acid therapy (choice D) does provide the highest level of HDL raising, averaging a 15 to 35% increase in HDL levels, but does not lower LDL levels as effectively as statin therapy does.
Tobacco cessation (choice E) should be a priority in treating any patient who currently smokes, yet there is no evidence that smoking cessation would have any substantial impact on correcting lipid levels.
