Akimitsu Nishiyama

Home blood pressure measurement has a stronger predictive power for mortality than does screening blood pressure measurement: a population-based observation in Ohasama, Japan.

Objective To compare the predictive powers of self-measurement of blood pressure at home (home blood pressure measurement) and casual (screening) blood pressure measurement for mortality. Design A prospective cohort study. Subjects and methods We obtained home and screening blood pressure measurements for 1789 subjects aged ≥ 40 years who were followed up for a mean of 6.6 years. The prognostic significance of blood pressure for mortality was determined by the Cox proportional hazards regression model adjusted for age, sex, smoking status, past history of cardiovascular disease, and the use of antihypertensive medication. Results When the home blood pressure values and the screening blood pressure values were simultaneously incorporated into the Cox model as continuous variables, only the average of multiple (taken more than three times) home systolic blood pressure values was significantly and strongly related to the cardiovascular mortality risk. The average of the two initial home blood pressure values was also better related to the mortality risk than were the screening blood pressure values. Conclusions Home blood pressure measurement had a stronger predictive power for mortality than did screening blood pressure measurement for a general population. This appears to be the first study in which the prognostic significances of home and screening blood pressure measurements have been compared.

Relation Between Nocturnal Decline in Blood Pressure and Mortality ☆: The Ohasama Study

To investigate the relation between nocturnal decline in blood pressure and mortality, we obtained ambulatory blood pressures in 1542 residents aged 40 years or over of a rural Japanese community. Subjects were followed-up for a mean of 5.1 years and were then subdivided into four groups according to the percent decline in nocturnal blood pressure: 1) extreme dippers: percent decline in nocturnal blood pressure > or = 20% of the daytime blood pressure; 2) dippers: decline of > or = 10% but < 20%; 3) nondippers: decline of > or = 0% but < 10%; and 4) inverted dippers: no decline. The relationship between the decline in nocturnal blood pressure and mortality was examined by the Cox proportional hazards regression model adjusted for age, sex, smoking status, previous history of cardiovascular disease, and the use of antihypertensive medication. The mortality risk was highest in inverted dippers, followed by nondippers. There was no difference in mortality between extreme dippers and dippers. This relationship was observed for both treated and untreated subjects, was more pronounced for cardiovascular than for noncardiovascular mortality, and did not change after the data were adjusted for 24-h, daytime, and nighttime blood pressure levels.

Characteristics of blood pressure measured at home in the morning and in the evening : the Ohasama study

OBJECTIVE To determine the qualitative and quantitative differences of blood pressure measured at home (home measurement) in the morning versus the evening. METHODS Of 3744 participants, aged 20 years or older in the Ohasama population, more than 14 home measurements in the morning and in the evening, respectively, were obtained in each of 1207 individuals (881 untreated, 56.1 +/- 11.4 years and 326 treated, 66.0 +/- 9.2 years). A casual/screening measurement was also obtained in these individuals. RESULTS The home measurements in the morning were significantly higher than those in the evening. The bivariate linear regression analysis demonstrated that the difference between diastolic home measurement in the morning and that in the evening increased with an increase in diastolic home measurements. The multiple step-wise linear regression analysis, however, demonstrated that male sex, the use of antihypertensive medication, and SD of home measurements in individuals (blood pressure variability), but not level of home measurements, were positively associated with the difference between home measurement in the morning and that in the evening. The SD of home measurement in the evening in individuals was significantly larger than that in the morning, and the SD in treated individuals was significantly larger than that in untreated individuals. The correlations between casual and home measurements were moderate in untreated individuals (r = 0.509-0.567) but poor in treated subjects (r= 0.223-0.384). The correlations between home systolic measurements in the morning and in the evening were very close in both treated and untreated subjects (r = 0.814-0.902). The correlations between the SD of home measurements in the morning and in the evening were moderate in both treated and untreated individuals (r = 0.585-0.657). CONCLUSIONS Qualitative and quantitative differences in home blood pressure measurement, due to the differential time of measurement, should be taken into consideration in clinical use of home blood pressure measurements.

Factors affecting the nocturnal decrease in blood pressure: a community-based study in Ohasama.

Objective To investigate factors affecting the nocturnal decrease in blood pressure. Design A cross-sectional study of 823 community-based untreated subjects aged > 20 years. Screening and ambulatory blood pressures were measured and the effects of age and the ambulatory blood pressure on the nocturnal decrease were examined. Results The magnitude of the decrease and the percentage decrease in the nocturnal blood pressure increased with increasing daytime ambulatory blood pressure and decreased with increasing night-time ambulatory blood pressure. Although the magnitude of the nocturnal decrease in blood pressure increased with increasing daytime blood pressure, the nocturnal blood pressure levels in hypertensives were still higher than those in normotensive subjects. The magnitude decreased with increasing age for men but not for women, whereas the percentage decrease decreased with increasing age both for men and for women. The SD of the 24 h blood pressure correlated strongly to the magnitude of the nocturnal decrease (systolic blood pressure r = 0.62, P < 0.0001; diastolic blood pressure r = 0.52, P < 0.0001), suggesting that the SD of the 24 h blood pressure is representative of the nocturnal decrease. A minimal nocturnal decrease was observed frequently in elderly normotensive men but infrequently in hypertensive individuals from the general population. A marked nocturnal decrease was observed frequently in hypertensive women aged > 70 years. Conclusion Although the magnitude of the nocturnal decrease in blood pressure increased with increasing daytime blood pressure, the nocturnal blood pressure levels increased with increasing daytime ambulatory blood pressure. Therefore, the blood pressure in hypertensive subjects should essentially be lowered throughout the 24 h period. A marked nocturnal decrease in blood pressure in some elderly hypertensive women was observed without treatment. The nocturnal blood pressure levels of such subjects should be considered during treatment.

Muscle cramps and elevated serum creatine phosphokinase levels induced by β-adrenoceptor blockers

We have assessed the propensity of β-adrenoceptor blockers to cause muscle cramps and to raise the serum creatine phosphokinase (CPK) level in 78 patients with essential hypertension. After a control period, a β-adrenoceptor blocker without intrinsic sympathomimetic activity (ISA; propranolol, metoprolol or arotinolol) was administered for three months. Thereafter, the patients were randomised to receive a β-adrenoceptor blocker with ISA (pindolol or carteolol) for three months or a β-adrenoceptor blocker without ISA for a further three months. This pattern was continued until all β-adrenoceptor blockers had been given. At the end of each period, CPK and CPK-MB levels were measured.Of the 78 subjects, muscle cramps occurred in 27 during treatment with pindolol and 32 during treatment with carteolol. No complaints were made by subjects treated with propranolol and arotinolol, but muscle cramps were reported in 2 treated with metoprolol. While muscle cramps were caused both by pindolol and carteolol in 16 subjects, they were caused by either of these drugs in the remainder of the subjects. Muscle cramp occurred mainly in the calves when the patients were in bed at night. Serum CPK and CPK-MB levels increased significantly during treatment with pindolol (control period vs pindolol, CPK=96 vs 133 IU · ml−1, CPK-MB=14 vs 18 IU · ml−1) or carteolol (CPK=117 IU · ml−1, CPK-MB=18 IU · ml−1) while the levels during treatment with propranolol, arotinolol and metoprolol did not change from those in the control period. The change in serum CPK during treatment with carteolol or pindolol was significantly correlated with the control serum CPK level. No correlation was observed between muscle cramps and serum CPK level. There were individual differences in the severity of muscle cramps, with some subjects complaining frequently of severe muscle cramps.Because muscle cramps are frequently experienced at night, they disturb sleep and lower the quality of life in patients. This problem should be considered during treatment with β-adrenoceptor blockers with ISA.

Pressor Effect of Recombinant Human Erythropoietin: Results of Ambulatory Blood Pressure Monitoring and Home Blood Pressure Measurements

We investigated whether treatment of anemic hemodialysis patients with a low dose of recombinant human erythropoietin (erythropoietin) for a short period would increase their blood pressure. Ambulatory blood pressure monitoring and home blood pressure measurements were used to detect minute increase in blood pressure. Thirty-two patients with a hematocrit of 25% or less received erythropoietin at the dose of 4500 IU/week, by the intravenous route for 8 weeks. Erythropoietin increased the hematocrit from 20.9 +/- 2.1 to 26.2 +/- 2.1%. Erythropoietin elevated mean ambulatory blood pressure by 5 mmHg or more in two-thirds of patients (n = 20; pressor group), while it elevated home mean blood pressure by 5 mmHg or more in one-third of patients (n = 11). An increase in clinic mean blood pressure by more than 5 mmHg was observed only in one-fourth of patients (n = 7). Circadian variation of blood pressure (nocturnal fall and diurnal rise) had been attenuated in the patients of the pressor group before erythropoietin treatment and erythropoietin decreased the nocturnal fall of blood pressure further more. Erythropoietin elevated nocturnal blood pressure more than diurnal blood pressure. Therefore, the increase in blood pressure induced by erythropoietin was detected more reliably by ambulatory blood pressure monitoring. There was no relation between the change in hemoglobin concentration and the increase in ambulatory blood pressure induced by erythropoietin. Erythropoietin tended to decrease cardiac output and plasma volume while it increased total peripheral resistance. It also decreased plasma norepinephrine and vasopressin levels but did not affect other humoral factors. Although the pressor effect of erythropoietin treatment for 8 weeks at the dose of 4500 IU/week was not evident on clinic blood pressure measurements, any increase in blood pressure determined by ambulatory blood pressure should be treated carefully to reduce the risk of a cardiovascular complication in patients receiving hemodialysis.