A bidirectional link exists between atherosclerosis and pulse pressure, where increased pulse pressure may be both a cause and an effect of atherosclerosis.
Pulse pressure (PP) is traditionally believed to increase cardiovascular risk because of an increase in afterload leading to left ventricular hypertrophy. It has also been emphasized that low diastolic blood pressure, being in part responsible for high PP, leads to an impairment of myocardial perfusion with all its adverse consequences. More recently, however, a direct role of pulsatile blood pressure changes in the pathogenesis of atherosclerosis and its complications has become better known. Experimental studies indicate that there is a cause-and-effect type of relationship between the pulsatile component of blood pressure and atherosclerotic process. A significant relationship between the parameters of the pulsatile blood pressure component and the extent of coronary atherosclerosis was also demonstrated. Currently the presence of a bidirectional link between atherosclerosis and PP is commonly postulated, meaning that an increased PP may be both a cause and an effect of atherosclerosis. This may result in a vicious circle wherein the pulsatile blood pressure component induces/enhances the development of atherosclerosis, which in its turn reduces the arterial compliance and enhances pulse wave reflection, thereby leading to an increase in PP. Currently new drug classes are being investigated, which might reduce the pulsatile blood pressure component without changing mean blood pressure level. Their clinical usefulness should become known over the next few years.
Jankowski et al. (Mon,) conducted a review in Atherosclerosis. Pulse pressure was evaluated. A bidirectional link exists between atherosclerosis and pulse pressure, where increased pulse pressure may be both a cause and an effect of atherosclerosis.