The risk for the primary outcome, all-cause death, and MI, but not stroke, progressively increased with low diastolic blood pressure. Excessive reduction in diastolic pressure should be avoided in patients with CAD who are being treated for hypertension.

Among CAD patients with hypertension, RHR predicts adverse outcomes, and on-treatment RHR is more predictive than baseline RHR. A Ve strategy is less effective than an At strategy for lowering RHR but has a similar effect on adverse outcomes.

Blood pressure responses to 1 week of low-salt (20 mmol sodium/d) and high-salt (300 mmol sodium/d) intake were investigated in a single-blind randomized study in 163 white, nonobese normotensive subjects (65 women and 98 men; mean age, 38±1.2 years). The individuals were classified as salt sensitive when mean arterial blood pressure rose by at least 5 mm Hg during high-salt intake, as salt resistant when mean arterial blood pressure changed by less than 5 mm Hg, and as "counterregulator" when mean arterial blood pressure fell by at least 5 mm Hg during the high-salt diet. Reexamination of 31 subjects showed that this approach to the testing of salt sensitivity was reliable and reproducible. Thirty subjects (18.4%) were classified as salt sensitive, 108 (66.3%) as salt resistant, and 25 (15.3%) as counterregulators. Multiple regression analysis revealed that age, body weight, and family history of hypertension contributed significantly to the change in blood pressure after the diets. Salt sensitivity was more frequent in older subjects and in those with a positive family history of hypertension. An increase in blood pressure after salt restriction was more likely in younger individuals and in those with a negative family history of hypertension. Plasma renin activity and plasma aldosterone concentrations were lower in salt-sensitive compared with salt-resistant and counterregulating subjects. The rise in plasma renin activity during salt restriction was most pronounced in counterregulating subjects. Plasma norepinephrine concentrations were not different among the groups. Plasma levels of atrial natriuretic peptide increased during high-salt intake in all groups, the rise being most pronounced in salt-sensitive subjects. The increase in blood pressure during salt restriction in counterregulating subjects may be partially due to an overstimulation of the renin-angiotensin system. The exaggerated response of the secretion of atrial natriuretic peptide to high-salt intake in salt-sensitive subjects may point to an impaired capability of the kidney to excrete a salt load. 7 It has been assumed recently that the effect of a concerted health care program directed toward lowering salt intake of the general population would be extremely small. 6 The blood pressure response to sodium chloride is heterogeneous, at least during relatively short-term changes in salt intake. Salt sensitivity, defined as a significant rise in blood pressure when individuals switch from a low to a high sodium chloride intake, is seen in a considerable number of patients with essential hypertension and, although less frequent, in normotensive subjects.8 On the other hand, some individuals increase their blood pressure with sodium depletion 910 and therefore could be at higher risk when ingesting a salt-restricted diet.Little attention has focused so far on this issue. This may partially be due to the design of most of the previous studies dealing with salt sensitivity in which subjects reacting to low-salt intake with no change or a rise in pre...

No abstract