The raised blood pressure of old age is known as hypertension, and it is predominantly caused by dysfunction in blood vessel walls: cross-links, calcification, and loss of elastin cause reduced elasticity, while smooth muscle cells lose their capacity to act for a variety of other reasons. When blood vessels can no longer correctly react to circumstances by contracting and dilating to an appropriate degree, then the whole system of pressure control is thrown off, and higher blood pressure is the result.
Atherosclerosis, on the other hand, is the progressive formation of fatty plaques in blood vessel walls. This narrows and weakens blood vessels. Atherosclerosis interacts with hypertension in the obvious way: weakened blood vessels and fragile plaques are more likely to suffer catastrophic structural failure in a high pressure environment, leading to a fatal stroke or heart attack. Just considering this interaction, it is clear that hypertension raises the risk of death and shortens life expectancy. This isn’t the only interaction, however, just the most direct one. In addition, hypertension accelerates the growth of atherosclerotic plaques, and the reasons for this are not fully understood.
In the research materials noted here, the authors report