In this study, our data indicated that only 48.1% of the patients had normal SBP both at the clinic and in the morning at home, and 43.6% of the patients had MHT. In the Ohasama study, diastolic home hypertension was associated with no significant increase in risk (16), so in this study, we analyzed MHT according to systolic home BP. The Japan Home versus Office Blood Pressure Measurement Evaluation (J-HOME) study was conducted to assess BP control as evaluated by home BP measurement (17). It reported that BP levels were not adequately controlled among approximately 60% of patients, according to the reference values described in the national guidelines (office BP:
MS is characterized as abdominal obesity with the clustering of moderate glucose, lipid metabolism and hypertension issues. In our study population, MS patients had a higher prevalence of MHT. Unfortunately, the mechanism of MS in MHT has not been clarified. Although the mechanism of MS in MHT has not been clarified, several possible mechanisms have been proposed. First, Sironi et al. reported that visceral adiposity is quantitatively related to both the rate of BP and the severity of insulin resistance (18). Essential hypertension has been reported to be associated with insulin resistance. Visceral obesity has been reported to have a significant effect on glucose metabolism; moreover, Alvarez et al. reported that muscle sympathetic nerve activity was elevated in obese humans (19). MHT is therefore understood in the context of sympathetic nerve activities (20). Thus, it is thought that subjects with MS had MHT through sympathetic nerve activities. With respect to a second possible mechanism, Nakazato et al. reported that sympathetic baroreflex sensitivity was significantly lower during sleep than while subjects were awake in the evening and it remained low after the subjects woke up in the morning (21). Sympathetic nerve traffic was found to be significantly greater in subjects with MS than in without MS (22), so subjects with MS might have had MHT through baroreflex sensitivity. With respect to a third possible mechanism, Panza et al. reported a circadian rhythm of basal vascular tone, due either partly or entirely to increased α-sympathetic vasoconstrictor activity during the morning; this variation may contribute to higher BP (23). Wofford et al. suggested that overweight was indirectly correlated with vascular α-tone via a relationship with arterial plasma norepinephrine concentration, a marker of sympathetic drive (24). It seems likely that one or more of these three mechanisms are responsible for the connection between MS and MHT.
In our hypertensive patients, the prevalence of MS was 44.0% in men and 23.3% in women. In another Japanese analysis, the Tanno and Sobetsu study reported that the prevalence of MS in a rural Japanese sample was 25.3% in men (25), and in Okinawa, the prevalence of MS was 30.2% in men and 10.3% in women (26); compared with these results, our study data were much higher. Naturally, this may be because our study subjects were all being treated for hypertension and thus both the prevalence of MS and the average age were much higher than in other previous cohorts. For example, in the Tanno and Sobetsu study, the prevalence of MS was higher in treated patients than in untreated patients (men: 23% in untreated vs. 32% in treated patients; women: 7% in untreated vs. 11% in treated patients) (25). This is possibly because the criteria for MS in their study were based on the criteria of NCEP-ATP III, whereas we used the new MS criteria for Japanese (14, 15). In addition, since Ford et al. reported that the prevalence of MS is associated with age (27), our cohort, which included relatively older subjects than the study of Tanno and Sobetsu, would be expected to show a higher prevalence of MS.
There are some limitations in our study. First, because home BP records were simply written down by the subjects themselves, and were written only once, there may have been inaccurate data. Second, not all patients in our outpatient clinic were enrolled in this study. We studied 181 subjects (43.7%) who used the equipment for home-use BP measurements and came back to the hospital; their compliance was very good. However, we could not study the remaining patients, whose compliance may not have been as good as the studied patients. Third, Imai et al. reported that seasonal variation in BP should be considered (28); however, in this study, the seasonal variation of BP was not taken into consideration. In conclusion, 43.6% of treated hypertensive patients showed MHT, and there was a significantly higher prevalence of MHT among patients with MS. Our results suggest the need for a more vigorous intervention for controlling BP.
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