Author + information
- Received February 10, 2009
- Accepted February 25, 2009
- Published online June 9, 2009.
- Fadi G. Hage, MD⁎,†,⁎ (, )
- Rajesh Venkataraman, MD⁎,
- Gilbert J. Zoghbi, MD⁎,†,
- Gilbert J. Perry, MD⁎,
- Angelo M. DeMattos, MD‡ and
- Ami E. Iskandrian, MD⁎
- ↵⁎Reprint requests and correspondence:
Dr. Fadi G. Hage, Zeigler Research Building 1024, 1530 3rd Avenue South, Birmingham, Alabama 35294-0006
Chronic kidney disease (CKD) affects approximately 13% of the U.S. population and is associated with increased risk of cardiovascular complications. Once renal replacement therapy became available, it became apparent that the mode of death of patients with advanced CKD was more likely than not related to cardiovascular compromise. Further observation revealed that such compromise was related to myocardial disease (related to hypertension, stiff vessels, coronary heart disease, or uremic toxins). Early on, the excess of cardiovascular events was attributed to accelerated atherosclerosis, inadequate control of blood pressure, lipids, or inflammatory cytokines, or perhaps poor glycemia control. In more recent times, outcome research has given us further information that relates even lesser degrees of renal compromise to an excess of cardiovascular events in the general population and in those with already present atherosclerotic disease. As renal function deteriorates, certain physiologic changes occur (perhaps due to hemodynamic, inflammatory, or metabolic changes) that decrease oxygen-carrying capacity of the blood by virtue of anemia, make blood vessels stiffer by altering collagen or through medial calcinosis, raise the blood pressure, increase shearing stresses, or alter the constituents of atherosclerotic plaque or the balance of thrombogenesis and thrombolysis. At further levels of renal dysfunction, tangible metabolic perturbations are recognized as requiring specific therapy to reduce complications (such as for anemia and hyperparathyroidism), although outcome research to support some of our current guidelines is sorely lacking. Understanding the process by which renal dysfunction alters the prognosis of cardiac disease might lead to further methods of treatment. This review will outline the relationship of CKD to coronary heart disease with respect to the current understanding of the traditional and nontraditional risk factors, the role of various imaging modalities, and the impact of coronary revascularization on outcome.
Dr. Iskandrian has served as consultant for Astellas, CV Therapeutics and received research grants from Astellas, CV Therapeutics, and Molecular Imaging. The data reported here have been supplied by the United States Renal Data System (USRDS). The interpretation and reporting of these data are the responsibility of the authors and in no way should be seen as an official policy or interpretation of the U.S. government. Drs. Hage, Venkataraman, and Zoghbi contributed equally to this report.
- Received February 10, 2009.
- Accepted February 25, 2009.
- American College of Cardiology Foundation