q12.35 - sami2004

[ArchivalUser]

A 55-year-old postmenopausal woman who had a myocardial infarction 1 year ago is seen for a routine office visit. She has an intact uterus, and menstrual periods stopped at age 52. Her lipid values prior to the myocardial infarction (while she was not on any specific lipid-lowering treatment) were:

Plasma total cholesterol 266 mg/dL
Plasma low-density lipoprotein cholesterol 175 mg/dL
Plasma high-density lipoprotein cholesterol 28 mg/dL
Serum triglycerides 315 mg/dL

The patient is a former cigarette smoker. She exercises three times per week, follows a Step II fat reduction diet carefully, and takes simvastatin, 20 mg daily. She currently takes no other medications. Her body mass index is 28. Her present lipid values are:

Plasma total cholesterol 232 mg/dL
Plasma low-density lipoprotein cholesterol 140 mg/dL
Plasma high-density lipoprotein cholesterol 32 mg/dL
Serum triglycerides 300 mg/dL

Which of the following is most appropriate at this time?

(A) Change from simvastatin to fluvastatin in maximal doses.
(B) Change from simvastatin to gemfibrozil.
© Continue simvastatin, 20 mg daily.
(D) Continue simvastatin, 20 mg daily, and add cholestyramine.
(E) Increase simvastatin to 40 mg daily and measure lipid levels in 4 to 8 weeks

[ArchivalUser]

E,

http://simvastatin.me/simvastatin-dosage/

[ArchivalUser]

eeee

[ArchivalUser]

e.

[ArchivalUser]

(D) Continue simvastatin, 20 mg daily, and add cholestyramine.

[ArchivalUser]

dddd

[ArchivalUser]

eeeeee

[ArchivalUser]

I remember they always recommend to max your first drug before you add another one unless medically necessary

[ArchivalUser]

ANSWER IS E

Compelling evidence supports the need to minimize risk factors for recurrent cardiac events in patients with coronary artery disease. Cardiovascular event rates are five to seven times higher in patients with existing coronary artery disease than in previously healthy individuals. Based on strong clinical trial evidence, the low-density lipoprotein cholesterol (LDL-C) goal in a patient with coronary artery disease (such as the patient described here) is less than 100 mg/dL. This patient has responded to drug treatment and lifestyle alterations by lowering her total cholesterol level by 13% and her LDL-C level by 20%; however, it is appropriate to lower LDL-C to 100 mg/dL or less in this high-risk patient.

Simvastatin is a proven secondary agent for improving lipid levels. Its dosage range is wide (5 mg to 80 mg), and it has expected beneficial effects on lowering LDL-C, increasing high-density lipoprotein cholesterol (HDL-C), and lowering triglycerides. A dose higher than the current 20 mg daily would be expected to lower LDL-C to 100 mg/dL in this high-risk patient. An acceptable alternative (not given in the options) would be to use one of the other potent statin preparations in an appropriate dosage.

Fluvastatin is less potent than simvastatin and is unlikely to achieve the required LDL-C reduction (total of 42% from baseline). Gemfibrozil is incorrect because the primary target of lipid modification in the patient with coronary artery disease is lowering LDL-C, and gemfibrozil is not an LDL-C-lowering drug. Based on data from a Veterans Administration trial in men using gemfibrozil to increase HDL-C levels in patients who had had a myocardial infarction, gemfibrozil should be used in patients with primary low HDL-C levels, with or without accompanying features such as hypertriglyceridemia. However, gemfibrozil is unlikely to decrease LDL-C.

Maintaining simvastatin at the current dose is incorrect because the goal of reducing LDL -C to 100 mg/dL has not yet been reached despite an adequate trial. Clearly, a higher dose of simvastatin is preferred to continuation of the current dose. Cholestyramine tends to raise triglyceride levels, especially in patients with baseline triglyceride elevations. Although cholestyramine can be very helpful in lowering LDL-C further in combination with a statin preparation, its use in this patient would be inappropriate