Pathophysiology of Coronary Vascular Remodeling

The relationship between cardiovascular risk factors and vascular remodeling is a relatively new area of investigation. We discuss the various mechanisms by which cardiovascular risk factors cause vascular remodeling. Endothelial dysfunction, lipoprotein alterations, inflammation, and platelet activation are the mechanisms by which remodeling occurs. Plaque composition also plays an important role in directing remodeling. Plaque with extensive calcification is more likely to undergo constrictive remodeling. Positive and negative remodeling is based on how these factors coordinate and determine the direction of remodeling. Matrix metalloproteinases perform a crucial role in vascular remodeling. Advanced glycation end-products are key substances involved in the negative remodeling associated with diabetes. Remodeling in hypertension can be either eutrophic or hypertrophic. Endothelial dysfunction and low-grade inflammation lead to negative remodeling in hypertension. Dyslipidemia can be associated with either positive or negative remodeling. High high-density lipoprotein is associated with positive remodeling and high low-density lipoprotein with negative remodeling. Smoking causes endothelial dysfunction, increased oxidative stress, and decreased nitric oxide synthesis leading to inward remodeling. Aging also causes endothelial dysfunction and predisposes to negative remodeling. Knowledge of these associations can elucidate various clinical presentations and guide therapeutic choices in the future.