In the United States, the residual lifetime risk of developing hypertension is greater than 90% in both men and women. Figures currently indicate that approximately 30% of the population suffer from hypertension. Long-term sustained hypertension increases morbidity and mortality from myocardial infarction, stroke, atherosclerosis, and renal failure. Large-artery stiffening is a comorbidity associated with all of these cardiovascular disorders, but is reported to be accelerated in patients with uncontrolled blood pressure. In addition, increased vascular stiffness is believed to amplify the pathogenesis of hypertension by increasing the penetration of pressure throughout the cardiovascular system. Based on the results of recent Framingham studies, it appears that aortic increased stiffness may actually precede hypertension suggesting that controlling arterial stiffness may provide a new strategy for pharmacological treatments of large artery disease. Of importance is the observation that an increase in aortic stiffness is also characteristic of the normal aging process. Clinically, elderly hypertensive patients harbor stiffness levels above that of age-matched normotensive older patients. This has suggested an additive or synergistic effect of hypertension and aging such that the disease process accelerates the aging process. At present, no specific therapeutic targets are emerging leading us to conclude that the underlying causes of increased vascular stiffness and its role in the large artery disease process are incompletely understood and that its causes remain controversial. Prior studies on vascular stiffness in hypertension have largely focused on extracellular matrix (ECM), endothelial cell contributions or inflammatory mechanisms. However, recent data are indicating that the intrinsic mechanical and adhesive properties of vascular smooth muscle cells (VSMCs) are playing a role. The overall goal of this research topic is, at a minimum, to bring together leaders in this field of investigation to provide a summary of their concepts, identify current controversies and identify gaps in our knowledge, even more significantly, to suggest directions for new therapeutic approaches.
In the United States, the residual lifetime risk of developing hypertension is greater than 90% in both men and women. Figures currently indicate that approximately 30% of the population suffer from hypertension. Long-term sustained hypertension increases morbidity and mortality from myocardial infarction, stroke, atherosclerosis, and renal failure. Large-artery stiffening is a comorbidity associated with all of these cardiovascular disorders, but is reported to be accelerated in patients with uncontrolled blood pressure. In addition, increased vascular stiffness is believed to amplify the pathogenesis of hypertension by increasing the penetration of pressure throughout the cardiovascular system. Based on the results of recent Framingham studies, it appears that aortic increased stiffness may actually precede hypertension suggesting that controlling arterial stiffness may provide a new strategy for pharmacological treatments of large artery disease. Of importance is the observation that an increase in aortic stiffness is also characteristic of the normal aging process. Clinically, elderly hypertensive patients harbor stiffness levels above that of age-matched normotensive older patients. This has suggested an additive or synergistic effect of hypertension and aging such that the disease process accelerates the aging process. At present, no specific therapeutic targets are emerging leading us to conclude that the underlying causes of increased vascular stiffness and its role in the large artery disease process are incompletely understood and that its causes remain controversial. Prior studies on vascular stiffness in hypertension have largely focused on extracellular matrix (ECM), endothelial cell contributions or inflammatory mechanisms. However, recent data are indicating that the intrinsic mechanical and adhesive properties of vascular smooth muscle cells (VSMCs) are playing a role. The overall goal of this research topic is, at a minimum, to bring together leaders in this field of investigation to provide a summary of their concepts, identify current controversies and identify gaps in our knowledge, even more significantly, to suggest directions for new therapeutic approaches.
