The pathogenesis of the two main killers in
hypertension,
myocardial infarction (MI) and
stroke, differs. Prevention of
strokes, about a third of which result from haemorrhage, appears more immediately responsive to the level of blood pressure (BP). MI reflects the end stage of a slow underlying atheromatous process of the coronary arteries and lowering BP can, at best, hope only to slow this process and make less likely the eventual plaque
rupture and resultant occlusive
thrombosis and
infarction. Practically all the randomised trials have confirmed that the treatment of all grades of
hypertension, down to a treated diastolic BP level of perhaps about 95 mmHg, reduces the incidence of fatal and non-fatal
stroke by about 40-50%, though only two classes of
antihypertensive agent i.e.
diuretics (+/- other agents) and beta-blockers (+/-
diuretics), have actually demonstrated this benefit. It is possible, in the elderly, that excessive lowering of systolic BP (SBP) (to below about 140 mmHg) might increase the number of deaths from
stroke. Blood
lipid changes which constitute coronary risk factors in untreated hypertensive patients should not be regarded in the same light if beta-blocker induced. Animal data suggest that beta-blockers inhibit
catecholamine induced cardiovascular damage and modify coronary
atheroma formation in the presence of stress and/or high
cholesterol diets (in spite of blood
lipid changes). Evidence in the moderate to severely hypertensive man also suggests that in spite of beta-blocker induced increases in blood
triglyceride levels the incidence of deaths from MI markedly decreases over a ten year period in those whose SBP is well controlled.(ABSTRACT TRUNCATED AT 250 WORDS)