Rudy Bilous, MD, FRCP
Richard Donnelly, MD, PHD, FRCP, FRACP
Diabetes and hypertension have been termed the ‘bad companions’ for cardiovascular disease risk. Diabetes alone increases this risk 2 – 4-fold; in the presence of hypertension, the risk for coronary heart disease is further trebled and for stroke, doubled. There is also a close relationship with microvascular disease; in the UKPDS, for every 10 mmHg increase in systolic pressure, there was a 13% increase in the combined microvascular endpoint (with a 12% increase in myocardial infarction). Moreover, up to 50% of patients with type 2 diabetes are hypertensive or on antihypertensive therapy at diagnosis. In cross-sectional studies, up to 75% of adults with diabetes are hypertensive, increasing to 80% if they have microalbuminuria and over 90% if they have clinical nephropathy. For patients with type 1 diabetes, 30 – 43% of adults have hypertension but this is almost always in the presence of nephropathy….
Type 2 diabetes and hypertension are constituents of the so-called metabolic syndrome which is underpinned by insulin resistance. There are several plausible reasons why this might lead to hypertension as well as glucose intolerance (Box 19.1). However, not all epidemiological studies have demonstrated a positive link between fasting plasma insulin levels and blood pressure (or cardiovascular risk); moreover, patients with insulinomas, who have high circulating plasma insulin levels, do not have high blood pressure. There are also ethnic differences in estimates of insulin resistance and blood pressure levels.
Recently, the common role of oxidative stress for both hypertension and diabetes has been proposed (Box 19.2). Again, there are plausible mechanisms linking the two.
However, oxidative stress is hard to measure in humans, there are no data on the benefit or otherwise of antioxidant therapies, and the observed reduction in some measures of oxidative stress in response to antihypertensive therapy does not prove causality.
As can be seen from Box 19.2 and Figure 19.1, there is some overlap of potential mechanisms and it is possible that both insulin resistance and oxidative stress play a role, with a different predominance in individual patients.
For type 1 diabetes, hypertension is almost invariably a consequence of nephropathy and the processes that lead to it. Many of these will share potential mechanisms with insulin resistance and oxidative stress. Interestingly, the DCCT/EDIC 8-year follow-up showed a significantly lower number of patients with hypertension in the original intensively treated arm (29.9% versus 40.3%), almost certainly as a consequence of fewer cases of nephropathy in this cohort.
Definition of hypertension
With the increasing numbers of antihypertensive agents and large trials, the close relationship between level of blood pressure and cardiovascular disease risk has resulted in the definition being revised downwards, from 160/95 mmHg in the 1980s to 140/90 mmHg today.
For every 20/10 mmHg increase in blood pressure above 115/75, the risk for cardiovascular disease in the population doubles. For people with type 2 diabetes, there is an 18% increase in risk of myocardial infarction, and 29% for stroke for every 10 mmHg increase in blood pressure. However, intervention trials only show benefit for reduction of systolic and diastolic pressure to a level of about 130/80 mmHg (Figure 19.2).