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Published on: January 28, 2020
Association of body mass index with coronary plaque regression: 6-month prospective study
Shigemasa Tani1, Ken Nagao, Takeo Anazawa
1Department of Cardiology, Nihon University Surugadai Hospital, Tokyo 101-8309, Japan. tanishigem@yahoo.co.jp
Insights
Higher body mass index (BMI) in patients with coronary artery disease (CAD) reduces the effectiveness of pravastatin in treating atherosclerosis. This suggests personalized treatment strategies for obese CAD patients are needed.
Area of Science:
- Cardiology
- Metabolic Syndrome
- Pharmacology
Background:
- Obesity is a significant risk factor for coronary artery disease (CAD).
- Understanding how body mass index (BMI) impacts treatment efficacy is crucial for managing CAD patients.
Purpose of the Study:
- To investigate the influence of BMI on the effectiveness of pravastatin in reducing coronary atherosclerosis.
- To explore the relationship between BMI and changes in plaque volume during statin therapy.
Main Methods:
- Prospective study involving 56 patients with stable CAD.
- 3D intravascular ultrasound used to assess coronary plaque volume at baseline and after 6 months of pravastatin treatment.
Main Results:
- Pravastatin treatment significantly reduced plaque volume by 11% (p<0.001).
- Baseline BMI positively correlated with percent plaque volume (r=0.37, p<0.001).
- BMI independently predicted changes in plaque volume, indicating reduced treatment efficacy in higher BMI individuals.
Conclusions:
- Increased BMI attenuates the plaque-reducing effects of pravastatin in CAD patients.
- Results highlight the need for tailored treatment approaches for obese individuals with coronary artery disease.
Aim:
Obesity is a well known strong risk factor for coronary artery disease (CAD). We prospectively investigated the influence of body mass index (BMI) on the inhibitory effects of pravastatin against the development of coronary atherosclerosis.
Methods:
In 56 patients with stable CAD, 3-dimensional intravascular ultrasound was performed in matched coronary segments at the baseline and after 6-month treatment with pravastatin.
Results:
The plaque volume was significantly reduced by 11% after treatment (p<0.001 vs. baseline). The percent plaque volume was positively correlated with the baseline BMI (r=0.37, p<0.001), and negatively correlated with the serum total cholesterol / high-density lipoprotein cholesterol ratio (r=0.27, p<0.05) and total leukocyte count (r=0.27, p<0.05). Multivariate regression analysis showed that BMI was an independent predictor of the change in plaque volume (beta coefficient: 0.326; 95% CI: 0.003 to 0.037; p<0.05). No correlations were found between BMI and changes in the serum levels of any other lipids, apolipoproteins, or hs-CRP.
Conclusion:
The present study demonstrated that an increase in BMI attenuated pravastatin-induced coronary atherosclerosis regression. The results may provide new insight into the framework for the treatment of obese patients with CAD.
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