High density lipoprotein medical therapy

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]


Since low HDL is associated with an increased risk of cardiovascular disease events, elevation of HDL concentration among subjects with low HDL is advised. The treatment of a patient with low HDL cholesterol should be individualized. Before the initiation of any medical treatment to elevate the HDL concentration, the initial treatment should aim to reduce the LDL and non-HDL lipoprotein concentrations if they are elevated. The management of low HDL should also begin with life style modification targeting diet, exercise, and smoking cessation. If HDL concentration remains high despite optimal LDL and non-HDL concentrations and life style modifications, then medical therapy with fibrates or niacin might be considered among patients with risk factors of coronary artery disease or its equivalent.


Who To Treat

The question on who to treat should be answered on a patient-by-patient basis. According to the ATP III guidelines, the treatment of low HDL cholesterol has become a tertiary target in the management of patients with low HDL, with the primary and secondary goals targeting LDL and non-HDL cholesterol, respectively.[1] There are several variables to be considered in a patient with low HDL such as serum triglyceride levels and metabolic abnormalities (diabetes mellitus, metabolic syndrome).

When To Treat

The National Cholesterol Education Program (NCEP) has not set a formal goal for HDL levels as a therapeutic target because of lack of evidence for decrease in primary CHD risk reduction with pharmacotherapy. Drug therapy for HDL can be considered in the presence of other risk factors for CHD such as hypertension, smoking, family history of premature coronary heart disease.

The following are the ATP III guidelines for low HDL management (i.e., HDL-C≤40 mg/dl):[2]

Among patients with low HDL, attempts towards a reduction in LDL and non-HDL concentration should be performed before the administration of medical therapy to raise HDL. Non-HDL-C represents the cholesterol content present in all the atherogenic lipoproteins i.e., a combination of LDL-C, VLDL-C, IDL-C, and lipoprotein(a) cholesterol.[2] Non-HDL-C is the difference between the total cholesterol and HDL cholesterol (Non-HDL-C = Total cholesterol minus HDL-C). Some studies have demonstrated that non-HDL cholesterol fraction may be a better predictor of future cardiovascular risk than LDL cholesterol.[3][4] The treatment goal for non-HDL-C is 30 mg/dL above the LDL-C treatment target.

Below is a table showing the non-HDL and LDL cholesterol goals to be achieved in the management of patients with a low HDL cholesterol according to the ATP III guidelines:

0 to 1 CHD risk factor <190 <160
Two or more CHD risk factors (10-year risk for CHD≤20%) <160 <130
Coronary heart disease (CHD) and CHD risk equivalent (10-year risk for CHD>20% ) <130 <100

Non-pharmacologic Therapies

Physical exercise[5] 5-30% increase
Weight reduction 5-20% increase[6]
Smoking cessation 5% increase[7]
Multivitamins 31% increase in HDL
DASH diet 21% increase in HDL[8]
Low carbohydrate diet 4.5mg/dl increase in HDL[9]
Soy protein with isoflavones 3% increase in HDL[10]
Fish oil (omega-3 fatty acid) Significant increase in HDL2 fraction[11]
Fish oil with exercise 8% increase in HDL[12]
Low fat diet 5-14% increase in HDL when combined with exercise[13]
Monounsaturated fat Increase in HDL
Moderate alcohol consumption 5-10% increase in HDL[14]

Significant increase in HDL was observed when a calorie restricted version of DASH diet was used. Liese et al found a lower level of HDL with DASH diet in diabetic patients.[15]

Pharmacologic Therapy

Nicotinic acid (Niacin) Decreases VLDL synthesis in the liver through diaglycerol acyl transferase-2 (DGAT-2),[16] decreases HDL-apo A-I catabolism[17] 15-30% increase Cutaneous flushing, hyperglycemia, hyperuricemia, hepatotoxicity
Fibrates Direct stimulation of apo-A1 and apo-AII synthesis via peroxisome proliferator-activated receptors,[18] 5-15% increase Increased risk of myopathy when combined with statins, gallstones, dyspepsia
HMG-CoA reductase inhibitor Increases synthesis of apo-A1 and HDL in the liver,[19] increases ABCA1 mRNA in hepG2 cells,[20] inhibits CETP mass and activities[21] 5-10% increase Myopathy, rhabdomyolysis
Ezetimibe Inhibits cholesterol absorption at intestine level 3% increase in HDL along with statins[22] Headache, diarrhea, hypersensitivity
Thiazolidinediones Increase in adiponectin which increases insulin resistance 14% increase in HDL[23] Fluid retention
Hormone replacement therapy Increases Apo-A1 and decreases activity of hepatic lipase 5 to 20% increase Increases risk of stroke and thromboembolic diseases
Bile acid sequestrants Increases apo A-1 production[24] 3-5% increase GI discomfort, constipation, reduces absorption of other medications


According to several studies, niacin therapy is associated with improved lipoprotein profile in general and increase in the level of HDL in particular, which has been associated with decrease in cardiovascular events, decrease in mortality and regression of atherosclerosis plaques. Increase in HDL level by niacin can be attributed to the direct effect of the drug itself as well as to the niacin-induced decrease in the triglycerides level. The link between increasing HDL and improving cardiovascular outcomes is difficult to interpret as niacin's effects are not only limited to HDL but also include decreasing LDL and triglyceride levels.[25]

Shown below is a table summarizing the trials that demonstrated a secondary preventive role of niacin for cardiovascular events along with the associated percent increase in HDL.

Trial Name Drug HDL Increase Follow up
ARBITER 2 Trial[26] Extended release Niacin in patients on statin 21% 12 months
ARBITER 3 Trial[27] Extended release Niacin in patients on statin 9.6 +/- 12.5 mg/dL 24 months
CLAS 1 Trial[28] Niacin and colestipol 37% 2 years
CLAS 2 TRIAL[28] Niacin and colestipol 37% 4 years
HATS Trial[29] Niacin and simvastatin +/- antioxidants 26% 3 years
Coronary Drug Project[30] Niacin or clofibrate - 6 years and 15 years
Stockholm Ischemic Heart Disease Study[31] Niacin + Clofibrate - 5 years
FATS[32] Lovastatin + colestipol
Niacin + Colestipol
2.5 years
FATS Extended follow-up Niacin + lovastatin + colestipol - 10 years
UCSF-SCOR[33] Niacin + colestipol +/- Lovastatin and diet 28% 2 years


Several studies on fibrates proved their efficacy in lowering cardiovascular events through improving the lipid profile in general and increasing the HDL level in particular. Shown below is a table summarizing the trials that showed a secondary preventive role of fibrates for cardiovascular events along with the associated percent increase in HDL.

Trial Name Drug HDL Increase Follow up
VA-HIT Trial[34] Gemfibrozil 6% 5 years
BECAIT Trial[35][36][37][38] Bezafibrate 9% 5 years
Helsinki Heart Study[39] Gemfibrozil 11% 5 years
LOCAT[40] Gemfibrozil 21% 3years
DAIS[41] Fenofibrate 8-9% 3 years

Challenging HDL-C Hypothesis

Studies have proven the inverse relationship between HDL levels and cardiovascular risks. Several therapies were designed to increase HDL levels aiming for secondary prevention of coronary heart diseases. While some trials succeeded to improve the cardiovascular outcomes by increasing HDL quantity, other trials failed to achieve this goal. The failure of these trials have raised questions regarding the efficacy of HDL-targeted therapies and the concept of improving HDL quality rather than quantity. The main trials that failed to improve cardiovascular outcomes by raising HDL levels are ILLUSTRATE, RADIANCE 1, RADIANCE 2, ILLUMINATE Trial and Dal-OUTCOMES Trial which investigated CETP inhibitors as well as AIM-HIGH Trial which investigated the combination of niacin and statin. The failure of the CETP inhibitors studies can be attributed to the associated increase in blood pressure or direct impairment of the HDL quality by the CETP inhibitor.[25]

Shown below is a table summarizing the trials that failed to show any secondary preventive role of CETP inhibitors, niacin or fibrates for cardiovascular events along with the associated percent increase in HDL.

Trial Name Drug HDL Increase Endpoints
ILLUSTRATE Torcetrapib 61% There was no significant decrease in coronary atherosclerosis.
There was increase in blood pressure.[42]
RADIANCE 1 Torcetrapib 24.5±0.4 mg/dL There was no significant relationship between HDL levels and carotid intima-media thickness.
There was increase in blood pressure.[43]
RADIANCE 2 Torcetrapib 63.4% There was no significant relationship between HDL levels and carotid intima-media thickness.
There was increase in blood pressure.[44]
ILLUMINATE Trial Torcetrapib 72.1% Hazard ratio for death was 1.58 in torcetrapib group at the end of the study (p=0.006).
Torcetrapib group had a 1.25 hazard ratio for primary outcomes (p=0.001), mostly significant for unstable angina (p=0.001) and least important for stroke (0.74).
Significant increase in adverse events in torcetrapib group was reported: Hypertension, peripheral edema, angina pectoris, dyspnea, and headache (p<0.001).[45]
Dal-OUTCOMES Trial Dalcetrapib 31-40% Dalcetrapib had no significant effect on primary end point or the frequency of any primary end point component with a hazard ratio of 1.04 only.[46]
AIM-HIGH Trial Niacin + Statin 25% There was no reduction in the rate of primary endpoint or all-cause mortality with niacin.
Moreover, there was a trend towards more ischemic strokes in the niacin group.[47]
BIP Trial Bezafibrate 18% There was no difference in fatal and non fatal MI.[48]
The FIELD study Fenofibrate 3% There was no difference in mortality and cardiovascular disease events.[49]


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