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Published on: January 28, 2020
Association of circulating leukocyte count with coronary atherosclerosis regression after pravastatin treatment
Shigemasa Tani1, Ken Nagao, Takeo Anazawa
1Department of Cardiology, Nihon University Surugadai Hospital, Tokyo, Japan. tanishigem@yahoo.co.jp
Insights
Pravastatin treatment reduced coronary atherosclerosis plaque volume and peripheral blood leukocyte count in patients with coronary artery disease. Decreased leukocyte count independently predicted plaque reduction, suggesting a novel non-lipid marker for atherosclerosis regression.
Area of Science:
- Cardiology
- Immunology
- Pharmacology
Background:
- Peripheral blood leukocyte count is a marker for atherosclerosis progression.
- Limited data exist on statins' anti-inflammatory effects and leukocyte count in coronary artery disease (CAD).
Purpose of the Study:
- To investigate the relationship between pravastatin treatment, leukocyte count, and coronary atherosclerosis progression in CAD patients.
Main Methods:
- A 6-month prospective study involving 50 patients with coronary artery disease treated with pravastatin.
- Intravascular ultrasound assessed plaque volume; leukocyte counts and lipid levels were monitored.
Main Results:
- Pravastatin significantly reduced plaque volume (14%) and leukocyte count (8.9%).
- No correlation was found between changes in leukocyte count and lipid levels.
- Decreased leukocyte count was an independent predictor of coronary atherosclerosis inhibition.
Conclusions:
- Leukocyte count reduction is a non-lipid-lowering effect of pravastatin.
- This reduction may serve as a novel marker for coronary atherosclerosis regression.
Abstract:
Epidemiological studies have demonstrated that the peripheral blood leukocyte count could be used as a marker of the progression of atherosclerosis. Few data exist regarding the relationship between inhibition of the progression of coronary atherosclerosis and the anti-inflammatory effects of statins, especially the drugs' effects on the leukocyte count in patients with coronary artery disease. A 6-month prospective study was, therefore, conducted in 50 patients treated with pravastatin. The plaque volume, as assessed by volumetric analysis using intravascular ultrasound, reduced significantly by 14% (p<0.0001, vs. baseline) following the treatment, furthermore, a corresponding decrease of the leukocyte count (8.9%, p<0.01, vs. baseline) was also seen. No correlation was found between the change in the leukocyte count and any of the changes in the lipid levels; changes in either of these are known to be associated with the rate of progression of atherosclerosis. A multivariate regression analysis using other traditional risk factors and medications as covariates revealed that the decrease in the leukocyte count was an independent predictor of inhibition of the progression of coronary atherosclerosis. In conclusion, a reduction of the leukocyte count as one of the non-lipid-lowering effects of pravastatin may be a novel marker of regression of coronary atherosclerosis.
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