Why has the primary prevention of @entity583 in the treatment of XXXX been so elusive?

@entity1 @entity64 @entity101 @entity548 @entity301 @entity397 @entity1188 @entity412 @entity2922 @entity65 @entity1856 @entity583 @entity715 @entity165
The pathogenesis of the two main killers in @entity101 , @entity583 ( @entity583 ) and @entity64 , differs. Prevention of @entity64 , about a third of which result from @entity548 , appears more immediately responsive to the level of blood pressure (BP). @entity583 reflects the end stage of a slow underlying @entity1856 process of the coronary arteries and lowering BP can, at best, hope only to slow this process and make less likely the eventual @entity397 and resultant occlusive @entity715 and @entity1188 . Practically all the randomised trials have confirmed that the treatment of all grades of @entity101 , down to a treated diastolic BP level of perhaps about 95 mmHg, reduces the incidence of fatal and non-fatal @entity64 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 @entity64 . Blood lipid changes which constitute coronary risk factors in untreated @entity101 @entity1 should not be regarded in the same light if beta-blocker induced. Animal data suggest that beta-blockers inhibit @entity2922 induced @entity65 and modify @entity301 formation in the presence of stress and/or high @entity165 diets (in spite of blood lipid changes). Evidence in the moderate to severely @entity101 @entity1 also suggests that in spite of beta-blocker induced increases in blood @entity412 levels the incidence of deaths from @entity583 markedly decreases over a ten year period in those whose SBP is well controlled.(ABSTRACT TRUNCATED AT 250 WORDS)
