Poor Response to Statins May Signify Atherosclerosis
By HospiMedica International staff writers Posted on 08 Mar 2015 |
A substantial proportion of patients with coronary artery disease (CAD) fail to achieve effective reductions in low-density lipoprotein cholesterol (LDL-C), according to a new study.
Researchers at the University of Adelaide (Australia) conducted a review of seven clinical studies involving 647 patients diagnosed with CAD who were prescribed statin therapy to help lower their cholesterol levels. The patients underwent serial imaging of vessel lumen with intravascular ultrasound, and disease progression was compared in responders (517 patients) and hyporesponders (130 patients); responders were defined as a percentage reduction in LDL-C higher than 15%. The patients were followed for 18–24 months.
The results showed that the statin hyporesponders were younger, more likely to be male (79% versus 66%), and obese, and less likely to have a history of dyslipidemia; baseline levels of systolic blood pressure and LDL-C were lower in statin hyporesponders. While baseline atheroma levels were similar among groups, a greater progression of percent atheroma volume was observed in statin hyporesponders, which remained after adjustment for clinical characteristics and measures of plaque burden. The study was published on February 26, 2015, in Arteriosclerosis, Thrombosis and Vascular Biology.
“A substantial proportion of patients with coronary artery disease fail to achieve effective reductions in LDL-C, despite prescription of statin therapy. Greater progression of atherosclerosis is observed in these patients,” concluded lead author professor of cardiology Stephen Nicholls, PhD. “Our current study underscores monitoring LDL-C level after the commencement of statin to ensure adequate response to statin therapy.”
LDL-C, one of the five major groups of lipoproteins, is considered the “bad” cholesterol. Increasing concentrations of LDL-C particles are strongly associated with atherosclerosis, eventually resulting in sudden plaque ruptures that trigger clotting within the artery opening, resulting in CAD, stroke, and other vascular complications. In contrast to LDL-C, high-density lipoprotein cholesterol (HDL-C) particles are often called good cholesterol or healthy cholesterol, because they can remove fat molecules from macrophages in the wall of arteries.
Related Links:
University of Adelaide
Researchers at the University of Adelaide (Australia) conducted a review of seven clinical studies involving 647 patients diagnosed with CAD who were prescribed statin therapy to help lower their cholesterol levels. The patients underwent serial imaging of vessel lumen with intravascular ultrasound, and disease progression was compared in responders (517 patients) and hyporesponders (130 patients); responders were defined as a percentage reduction in LDL-C higher than 15%. The patients were followed for 18–24 months.
The results showed that the statin hyporesponders were younger, more likely to be male (79% versus 66%), and obese, and less likely to have a history of dyslipidemia; baseline levels of systolic blood pressure and LDL-C were lower in statin hyporesponders. While baseline atheroma levels were similar among groups, a greater progression of percent atheroma volume was observed in statin hyporesponders, which remained after adjustment for clinical characteristics and measures of plaque burden. The study was published on February 26, 2015, in Arteriosclerosis, Thrombosis and Vascular Biology.
“A substantial proportion of patients with coronary artery disease fail to achieve effective reductions in LDL-C, despite prescription of statin therapy. Greater progression of atherosclerosis is observed in these patients,” concluded lead author professor of cardiology Stephen Nicholls, PhD. “Our current study underscores monitoring LDL-C level after the commencement of statin to ensure adequate response to statin therapy.”
LDL-C, one of the five major groups of lipoproteins, is considered the “bad” cholesterol. Increasing concentrations of LDL-C particles are strongly associated with atherosclerosis, eventually resulting in sudden plaque ruptures that trigger clotting within the artery opening, resulting in CAD, stroke, and other vascular complications. In contrast to LDL-C, high-density lipoprotein cholesterol (HDL-C) particles are often called good cholesterol or healthy cholesterol, because they can remove fat molecules from macrophages in the wall of arteries.
Related Links:
University of Adelaide
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