The scientific and medical communities have over recent years lowered the threshold of raised blood pressure that defines hypertension. This has happened due to increasing evidence for even lesser degrees of increased blood pressure to be notably harmful over the long term. There is apparently no such thing as a safe rise in blood pressure over the course of aging - any increase is damaging, and the greater the increase the greater the damage. The high blood pressure of hypertension harms delicate tissues, such as those of the kidney and brain, through mechanisms such as the rupture of capillaries. It also acts to accelerate the progression of atherosclerosis, and thus raise the risk of cardiovascular mortality via stroke and heart attack. The research noted here should not be surprising in this context, as it reveals that even the a pre-hypertensive state of somewhat raised blood pressure correlates with increased organ damage and dysfunction.
Hypertension is exacerbated by the usual problems of excess weight and poor diet, and that contribution at least is well within our ability to control, but even the best lifestyle choice can only slow the progression of molecular damage that stiffens blood vessels. When blood vessels cannot respond to circumstances by contracting or dilating to the appropriate degree, the evolved system of pressure regulation runs awry. Cross-links that form in the extracellular matrix impair elasticity; the elastin required for that elasticity diminishes with age; calcification takes place in old blood vessel walls; the smooth muscle cells become dysfunction for a variety of reasons. Therapies to address these issues lie somewhere in our future. Once introduced, they will have a sizable impact on human life expectancy via the prevention and reversal of hypertension.
Hypertension is a well-known risk factor for a variety of cardiovascular and renal diseases. Nowadays, it is estimated that more than 1 billion people have hypertension around the world. Furthermore, the prevalence of pre-hypertension, which is defined by a systolic blood pressure (SBP) from 120 to 139 mm Hg or a diastolic blood pressure (DBP) from 80 to 89 mm Hg, has also been dramatically increasing in recent decades. The Prospective Studies Collaboration, which included data from 61 observational studies, shows that for every 20/10 mm Hg increase in SBP and DBP, the risk of cardiovascular disease and mortality is increased two-fold, and this relationship extends to a BP level of 115/75 mm Hg. These data together imply that treatment of pre-hypertension should be beneficial for reducing target organ damage and cardiovascular events.
Arterial stiffness is a pathophysiological process of vascular ageing, and prior observational studies suggest that arterial stiffness is highly prevalent in subjects with hypertension. Nevertheless, the prevalence of arterial stiffness in subjects with pre-hypertension is unclear, and whether arterial stiffness is associated with target organ damage in subjects with pre-hypertension is also less well studied. Using data from a cross-sectional study, we evaluated the prevalence of arterial stiffness in subjects with pre-hypertension and potential risk factors for pre-hypertension. Moreover, whether arterial stiffness was independently associated with the prevalence of target organ damage including left ventricular hypertrophy and albuminuria in pre-hypertensive subjects was also evaluated.
The principal findings of our current study include four aspects. First, the prevalence of pre-hypertension in patients who came to the outpatient clinic for screening potential hypertension is 17.5% and the prevalence of target organ damage including left ventricular hypertrophy and albuminuria in subjects with pre-hypertension is not low. Second, compared to subjects without arterial stiffness, those with arterial stiffness are more likely to have left ventricular hypertrophy and albuminuria. Third, ageing and presence of arterial stiffness are two major potential risk factors for pre-hypertension. Fourth, in subjects with pre-hypertension, increased carotid-femoral pulse wave velocity is associated with higher prevalence of target organ damage such as left ventricular hypertrophy and albuminuria.