DEVROEY D. Bad HDL-C Responders to Statins. In: Triglycerides and Cholesterol Research. Nova Science Publishers, Hauppauge, New York, 2006.
Eerste auteur: Devroey Dirk
Jaar: 2006
Type: Publicatie
Abstract:
Lowering high levels of low-density lipoprotein cholesterol (LDL-C) is the primary aim in the prevention of cardiac events. However, low levels of high-density lipoprotein cholesterol (HDL-C) are also associated with an increased risk of ischemic heart disease.
Lipid-lowering drugs are known to decrease LDL-C and to increase HDL-C slightly. However, not all patients benefit from this effect. Some patients have lower HDL-C during statin treatment than before the treatment.
These patients were first described in a case report in 2002 as ‘bad HDL-C responders to statins’. In the case of a man whose HDL-C and the ratios of total cholesterol (TC) to HDL-C and LDL-C to HDL-C worsened dramatically during pravastatin treatment. After 3 years, pravastatin was replaced by fenofibrate. The result was spectacular. The HDL-C increased to at least twice the level obtained during pravastatin.
Bad HDL-C responders are characterized by HDL-C levels which decrease below 40 mg/dl during the treatment, despite higher HDL-C levels before the treatment.
The existence of bad HDL-C responders to statins was confirmed by a prospective survey of 2259 patients treated with a statin or a fibrate for hyperlipidaemia. The proportion of bad HDL-C responders is higher for statins (6%) than for fibrates (4%).
In a review of the guidelines, almost all selected guidelines consider low HDL-C as a marker of increased risk for coronary heart disease. However, only few guidelines use the level of HDL-C as a threshold or target level for the treatment of dyslipidemia. The guidelines provide only little information on the management of patients with treatment-induced low HDL-C. Instead of using TC or LDL-C we consider the use of the ratios of TC to HDL-C or LDL-C to HDL-C as a threshold as well as a target for treatment.
Treatment with fibrates was studied in 14 bad HDL-C responders to statins. Far better levels for HDL-C, TC to HDL-C and LDL-C to HDL-C were obtained with fibrates compared to statins. For bad HDL-C responders to statins with low or normal LDL-C, treatment with fibrates instead of statins should be considered. For those with high LDL-C, fibrates should be added to statins.
Treatment for bad HDL-C responders should be studied in randomized controlled trials. Such a trial with simvastatin and fenofibrate has been initiated to corroborate our findings.