Isolated systolic hypertension of young-to-middle-age individuals implies a relatively low risk of developing hypertension needing treatment when central blood pressure is low.

OBJECTIVES: The clinical significance of isolated systolic hypertension (ISH) in the young is still controversial. Aim of the present study was to investigate whether prognosis of ISH in young-to-middle-age individuals differs according to central blood pressure (BP). DESIGN: We studied 354 participants screened for stage 1 hypertension and 34 normotensive controls to determine which individuals developed hypertension needing drug therapy. Among the hypertensive patients, 67 had ISH and were divided according to whether their central SBP, measured with applanation tonometry, was above (ISH-high) or below (ISH-low) the median (120.5 mmHg). Large artery (C1) and small artery (C2) compliance were also measured. RESULTS: Compared to normotensive individuals, ISH-high had decreased C1 (P = 0.02) and C2 (P = 0.01), and higher peripheral resistance (P = 0.01). In contrast, in ISH-low, all these variables were similar to those in normotensive individuals. During 9.5 years of follow-up, incident hypertension was more common among participants with systolic-diastolic hypertension (SDH) and ISH-high than the other two groups [odds ratio (OR) = 6.2, 95% confidence interval (CI) = 1.8-21.1, P = 0.003 for SDH; OR = 6.0, 95% CI = 1.5-24.0, P = 0.01 for ISH-high, versus normotensive individuals]. Among ISH-low, incidence of hypertension was only slightly higher than that in normotensive individuals (OR = 1.1, 95% CI 0.2-5.3, P = 0.90) and lower than that in ISH-high (P = 0.03). These associations remained significant when ambulatory BP was included in the models or when the 125 mmHg cut-off for central BP was used to identify ISH subgroups. CONCLUSION: These data show that young-to-middle-age ISH individuals with low central BP have a lower risk of hypertension needing treatment than those with high central BP. These results are applicable mainly to male individuals.

Regular physical activity attenuates the blood pressure response to public speaking and delays the development of hypertension.

OBJECTIVES: The objective of this study was to investigate the effect of regular physical activity on the haemodynamic response to public speaking and to evaluate the long-term effect of exercise on development of hypertension. PARTICIPANTS: We assessed 75 sedentary and 44 active participants screened for stage 1 hypertension with consistent activity habits and 63 normotensive individuals as control. METHODS: The blood pressure (BP) response to public speaking was assessed with beat-to-beat noninvasive recording. Definition of incident hypertension was based either on clinic or 24-h BP measurement. RESULTS: The BP response to public speaking was greater in the hypertensive than the normotensive participants (P=0.018/0.009). Among the former, sedentary participants showed increased BP reactivity to the speech test (45.2+/-22.6/22.2+/-11.5mmHg, P<0.01/<0.001 versus controls), whereas physically active participants had a response similar to that of controls (35.4+/-18.5/18.5+/-11.5mmHg, P=not significant). During a median follow-up of 71 months, ambulatory BP did not virtually change in the active participants (-0.9+/-7.8/-0.0+/-4.7mmHg) and increased in their sedentary peers (2.8+/-9.8/3.2+/-7.4mmHg, P=0.08/0.003 versus active). Active participants were less likely to develop incident hypertension than sedentary ones. After controlling for several confounders including baseline heart rate, the hazard ratio was 0.53 [95% confidence interval (CI) 0.31-0.94] for clinic hypertension and 0.60 (95% CI 0.37-0.99) for ambulatory hypertension. Inclusion of BP response to public speaking into the Cox model influenced the strength of the association only marginally [hazard ratio=0.55 (95% CI 0.30-0.97) and hazard ratio=0.59 (95% CI 0.36-0.99), respectively]. CONCLUSION: Regular physical activity attenuates the BP reaction to psychosocial stressors. However, this mechanism seems to be only partially responsible for the long-term effect of exercise on BP.