PPARγ Variant Influences Angiographic Outcome and 10-Year Cardiovascular Risk in Male Symptomatic Coronary Artery Disease Patients
Response to Schneider et al.
- Jakub J. Regieli, MD1,2,
- J. Wouter Jukema, MD3,4,5,
- Pieter A. Doevendans, MD2,
- Aeilko H. Zwinderman, PHD6,
- Yolanda van der Graaf, MD1,
- John J. Kastelein, MD7 and
- Diederick E. Grobbee, MD1
- 1Julius Center for Health Sciences and Primary Care, University Medical Center Utrecht, Utrecht, the Netherlands;
- 2Department of Cardiology, University Medical Center Utrecht, Utrecht, the Netherlands;
- 3Department of Cardiology and Einthoven Laboratory of Experimental Vascular Medicine, Leiden University Medical Center, Leiden, the Netherlands;
- 4Interuniversity Cardiology Institute of the Netherlands, Utrecht, the Netherlands;
- 5Durrer Institute for Cardiogenetic Research, Amsterdam, the Netherlands;
- 6Department of Clinical Epidemiology and Biostatistics, Academic Medical Center, Amsterdam, the Netherlands;
- 7Department of Vascular Medicine, Academic Medical Center, Amsterdam, the Netherlands.
- Corresponding author: Diederick E. Grobbee, d.e.grobbee{at}umcutrecht.nl.
The effects of peroxisome proliferator–activated receptor (PPAR)γ are largely unknown, and studies of genetic variation are one approach to confirm and estimate its impact on disease in humans. Vasculoprotective effects have been observed preclinically with small-molecule stimulation of the PPARγ pathway. Therefore, it constitutes a potential target of secondary prevention to further reduce cardiovascular risk in patients with manifest vascular disease. Other than our current report, there is no evidence on the impact of genetic variation in PPARγ on cardiovascular prognosis in a secondary prevention setting. Hence, we fully share the opinion of Schneider et al. (1) that the current data are not generalizable and only pertain …
