High prevalence of Chlamydia pneumoniae antibodies in white-coat hypertensives

Previous studies have linked essential sustained hypertension with Chlamydia pneumoniae (C. pneumoniae) and changes in intima-media thickness (IMT) of carotid arteries. The aim of this study was to examine if similar associations exist in subjects with white-coat hypertension. C. pneumoniae IgA and IgG antibody titers were measured in 125 patients with white-coat hypertension and 54 normotensives. All participants underwent a 24 h ambulatory blood pressure (BP) monitoring, clinic BP readings and common-internal carotid artery IMT measurements. Seventy subjects of the white-coat group (56%) and 15 of the control group (27.8%) had IgG titers >/=80 (crosstabs; P<0.001). IgA titers were elevated in 75 subjects of the white-coat group (60%) and 10 (18.5%) of the control group (crosstabs; P<0.001). The IMT of the carotid arteries in the white-coat group was significantly higher than that of the normotensive group (t-test; P<0.001 and P<0.001, respectively). In contrast, carotid IMT did not differ between C. pneumoniae-seropositive and C. pneumoniae-seronegative groups concerning both IgG and IgA antibody titers. Our findings suggest that both C. pneumoniae antibody titers and carotid IMT were increased in subjects with white-coat hypertension. The preceding associations strengthen prior evidence in favor of the opinion that white-coat hypertension is not an innocent phenomenon.     

Relationship between aortic stiffness and cardiovascular risk factors in a population of normotensives, white-coat normotensives, white-coat hypertensives, sustained hypertensives and diabetic patients.

OBJECTIVE: To evaluate the relationship between carotid-femoral pulse wave velocity (PWV) and office and ambulatory blood pressure (ABP) and other cardiovascular risk factors and to determine the discriminatory value of PWV in a large population including normotensive subjects (NT), white-coat normotensives (masked hypertension) (WCNT), and white-coat hypertensives (WCHT) compared to a group of treated and untreated hypertensive patients. METHODS: The study population included a total of 688 subjects aged from 18 to 80 years, with no previous cardiovascular events, who underwent 24 h ABP monitoring, biochemical evaluation and determination of PWV and left ventricular mass index (LVMI). Subjects were classified as true normotensives (NT, n=132; normal office and ABP values), WCNT (n=39; office BP < 140/90 and daytime BP > or =135 or > or =85 mmHg), WCHT (n=87; office BP > or =140 or > or =90 and daytime BP < 135/85 mmHg). Untreated (UT-HT, n=154) and treated (T-HT, n=171) hypertensive patients and type 2 diabetic patients (DM, n=102) were also studied. RESULTS: Values of PWV (m/s) in all groups were, in ascending order: NT (8.9 +/- 0.2) < WCHT (9.9 +/- 0.2) < T-HT (11.4 +/- 0.2) = WCNT (11.5 +/- 0.4) < UT-HT (11.9 +/- 0.3) < DM (12.6 +/- 0.4) (ANOVA, p = 0.043), and of LVMI (g/m2): NT (59 +/- 2) = WCHT (63 +/- 2) < WCNT (73 +/- 3) = T-HT (75 +/- 3) = UT-HT (77 +/- 3) < DM (84 +/- 4) (ANOVA, p < 0.05). The percentage of subjects with PWV values below the median (10.7 m/s) was higher (p < 0.02) in NT (81.8%) and WCHT (72.6%) than in UT-HT (49.2%), T-HT (43.6%), WCNT (47.6%) and DM (27.7%). In multiple regression analysis, taking PWV as the dependent variable, age (all groups), 24h systolic BP (UT-HT, T-HT, WCNT and DM) and 24h diastolic BP (NT and WCHT) were the variables that independently influenced the PWV value. CONCLUSIONS: Higher values of PWV occur in clinical situations associated with higher cardiovascular risk. This is in agreement with risk stratification based on ABP values but not on office BP values. Lower PWV and LVMI values occur in NT and WCHT subjects, supporting a low cardiovascular risk in these groups. By contrast, higher PWV values were associated with higher ABP values in DM, hypertensive patients and white-coat normotensives, i.e. clinical situations that are associated with higher cardiovascular risk, who in the present study also exhibited higher LVMI than subjects with normal ABP values.     

Determinants of the white-coat effect in normotensives and never-treated mild hypertensives

The prognostic significance of the white-coat effect (WCE) is unclear. Knowledge of the predictors of the WCE may help illuminate the clinical significance of this phenomenon. The purpose of this study was to (i) compare characteristics of subjects demonstrating a WCE, those not demonstrating a WCE, and those demonstrating a reverse WCE and (ii) determine clinical features that may influence the size of the WCE. Forty-one subjects with normotension or mild hypertension who had never been treated with antihypertensive medications were recruited for the study. All subjects underwent a battery of anthropometrical measurements and clinic blood pressure (BP) measurements. To calculate arterial compliance, impedance cardiography was used to measure resting stroke volume in each subject. All subjects performed a laboratory mental stress protocol to determine the size of the BP reactivity. Ambulatory blood pressure (ABP) profiles were studied in each subject with the use of an oscillometric ABP recorder. White-coat effect was determined by subtracting the awake period of the ambulatory systolic blood pressure (SBP) from the clinical SBP. Subjects were grouped according to the size of their WCE. Those who showed a WCE of 5 mmHg and above were assigned to the WCE group; those who showed a WCE of between -5 and 5 mmHg were assigned to the no white coat effect (NWCE) group; those who exhibited a WCE of -5 mmHg and lower were assigned to the reverse white-coat effect (RWCE) group. Subjects with a positive WCE had significantly higher body mass index (BMI) than those without a WCE and those with a RWCE. The WCE group had significantly higher clinic SBP and heart rate (HR) than the RWCE group. Arterial compliance was significantly lower in the WCE group as compared to the NWCE group and the RWCE group. The three groups had comparable ABP profiles. In terms of BP variability, the increase in SBP in response to mental stress did not differ among the three study groups nor did the 24-hour and awake BP variability. For the sample as a whole, clinic HR and clinic-ambulatory SBP difference were higher and arterial compliance were lower in women than in men. Furthermore, clinic SBP significantly correlated with the systolic WCE (r = 0.40, P = 0.009). When men and women were analyzed separately, the correlation between clinic SBP and the systolic WCE was significant in women (r = 0.63, P = 0.001) but not in men (P = 0.95). Multiple linear regression showed that sex (P = 0.013) and clinical SBP (P = 0.003) were the only two variables that significantly influenced the systolic WCE. These two variables together accounted for 29% of the variation in the systolic WCE. In conclusion sex and clinic BP are two major determinants of the WCE. The results of this study indicate that WCE is not related to higher stress reactivity or higher BP variability.     

Different frequencies of inducible nitric oxide synthase genotypes in older hypertensives

A locus for essential hypertension has been found recently on chromosome 17 in the general vicinity of the inducible nitric oxide synthase (iNOS) gene (NOS2A at 17cen-q11.2). We therefore tested NOS2A markers for association and linkage with hypertension in affected Australian Anglo-Caucasians. Patients for the association study (n=112) were from our cohort of hypertensives (systolic/diastolic=175+/-25 SD/112+/-19 mm Hg) who were the offspring of 2 hypertensive parents; control subjects (n=164) were normotensives whose parents were both normotensive. The linkage study involved 156 hypertensive sib-pairs. Genotypes for an 8-allele pentameric repeat located 2.6 kb upstream of NOS2A and of a biallelic tetranucleotide repeat 0.7 kb upstream were determined by polymerase chain reaction and automated gene scan analysis. In the association study, the frequency of the minor allele of the biallelic marker was 0.18 in the hypertensives and 0.14 in the normotensives (chi21 df=1.1, P=0.3). Allele frequencies for the multiallelic marker were also similar in each group (chi2 7 df=9.8, P=0.2). Furthermore, no genotypic differences in blood pressure were apparent. In the sib-pair study, SPLINK APM, and MAPMAKERS/SIBS did not indicate excess allele sharing. We also examined genotype as a function of age. In the younger (< 60 years) hypertensives as well as younger or older normotensives, genotype and allele frequency of the biallelic marker was similar (0.12 to 0.14). However, in hypertensives >/=60 years of age, frequency of the minor allele was 0.28 (chi2=7.4, P=0.006). Homozygotes for this allele were rare. Frequency of heterozygotes was 0.19 for normotensives but 0.39 for the older hypertensives (chi2=8.0, P=0.018) and was 0.40 for hypertensive sibs >/=60 years of age with a diastolic pressure >/=100 mm Hg. Furthermore, homozygotes for the major allele were 7 years younger than heterozygotes (P=0.05 by ANOVA). In conclusion, the present study shows (1) no evidence for a role of NOS2A in hypertension and (2) a genotypic difference in frequency of a NOS2A promoter variant in older hypertensives, seen in 2 different cohorts. A possible interpretation of the latter observation is that NOS2A genotype could affect longevity, at least in patients at high risk by having moderate to severe hypertension.     

Silent and clinically overt stroke in older Japanese subjects with white-coat and sustained hypertension

BACKGROUND: Whether white-coat hypertension in older subjects is a benign condition or is associated with an increased risk for stroke remains uncertain. White-coat hypertension as a risk factor for stroke was investigated in relation to silent cerebral infarct in the older Japanese population. METHODS: The prognosis for stroke was studied in 958 older Japanese subjects [147 normotensives (NT), 236 white-coat hypertensives (WCHT), and 575 sustained hypertensives (SHT)] in whom ambulatory blood pressure monitoring was performed in the absence of antihypertensive treatment. Silent cerebral infarct was also assessed using brain magnetic resonance imaging in 585 subjects (61%). RESULTS: Silent cerebral infarcts were found in 36% of NT (n = 70), 42% of WCHT (n = 154), and 53% of SHT (n = 361), and multiple silent cerebral infarcts(presence of > or = 2 silent cerebral infarcts) were found in 24% of NT, 25% of WCHT, and 39% of SHT. During a mean 42-month-follow-up period, clinically overt strokes occurred in 62 subjects [NT 3(2.0%), WCHT 5(2.1%), SHT 54(9.4%)], with 14 fatal cases [NT 1(0.7%), WCHT 0(0%), SHT 13 (2.3%)]. Cox regression analysis showed that age (p = 0.0001) and SHT [RR(95% confidence interval): 4.3 (1.3-14.2), p = 0.018] were independent stroke predictors, whereas WCHT was not significant. Adding presence/absence of silent cerebral infarct at baseline into this model, the RR (95% confidence interval) for silent cerebral infarct was 4.6 (2.0-10.5) (p = 0.003), and that of SHT was 5.5 (1.8-18.9) vs WCHT (p = 0.004) and 3.8 (0.88-16.7) vs NT (p = 0.07). CONCLUSIONS: The incidence of stroke in WCHT is similar to that of NT, and one fourth the risk in SHT in older subjects. Although silent cerebral infarct is a strong predictor of stroke, the difference in stroke prognosis between SHT and WCHT was independent of silent cerebral infarct. It is clinically important to distinguish WCHT from SHT even after assessment of target organ damage in the elderly.     

Silent and clinically overt stroke in older Japanese subjects with white-coat and sustained hypertension.

OBJECTIVES: We investigated whether white-coat hypertension is a risk factor for stroke in relation to silent cerebral infarct (SCI) in an older Japanese population. BACKGROUND: It remains uncertain whether white-coat hypertension in older subjects is a benign condition or is associated with an increased risk of stroke. METHODS: We studied the prognosis for stroke in 958 older Japanese subjects (147 normotensives [NT], 236 white-coat hypertensives [WCHT] and 575 sustained hypertensives [SHT]) in whom ambulatory blood pressure monitoring was performed in the absence of antihypertensive treatment. In 585 subjects (61%), we also assessed SCI using brain magnetic resonance imaging. RESULTS: Silent cerebral infarcts were found in 36% of NT (n = 70), 42% of WCHT (n = 154), and 53% of SHT (n = 361); multiple SCIs (the presence of > or =2 SCIs) were found in 24% of NT, 25% of WCHT and 39% of SHT. During a mean 42-month follow-up period, clinically overt strokes occurred in 62 subjects (NT: three [2.0%]; WCHT: five [2.1%]; SHT: 54 [9.4%]), with 14 fatal cases (NT: one [0.7%]; WCHT: 0 [0%]; SHT: 13 [2.3%]). A Cox regression analysis showed that age (p = 0.0001) and SHT (relative risk, [RR] [95% confidence interval, CI]: 4.3 [1.3-14.2], p = 0.018) were independent stroke predictors, whereas WCHT was not significant. When we added presence/absence of SCI at baseline into this model, the RR (95% CI) for SCI was 4.6 (2.0-10.5) (p = 0.003) and that of SHT was 5.5 (1.8-18.9) versus WCHT (p = 0.004) and 3.8 (0.88-16.7) versus NT (p = 0.07). CONCLUSIONS: In older subjects the incidence of stroke in WCHT is similar to that of NT and one-fourth the risk in SHT. Although SCI is a strong predictor of stroke, the difference in stroke prognosis between SHT and WCHT was independent of SCI. It is clinically important to distinguish WCHT from SHT even after assessment of target organ damage in the elderly.     

Arterial distensibility in subjects with white-coat hypertension with and without diabetes or dyslipidaemia: comparison with normotensives and sustained hypertensives

BACKGROUND: Arterial distensibility can be assessed by measuring pulse-wave velocity (PWV). OBJECTIVE: To determine whether diabetes, smoking and dyslipidaemia were associated with greater than normal stiffness of aortic walls in subjects with white-coat hypertension. METHODS: Arterial distensibility was assessed by automatic measurement of carotid-femoral PWV in 35 healthy normotensives, 46 white-coat hypertensives (WCH, clinic blood pressures >140/90 mm Hg, daytime blood pressures <130/85 mm Hg) and 81 ambulatory hypertensives (clinic blood pressures >140/90 mmHg, daytime blood pressures > or =130 mm Hg systolic or > or =85 mm Hg diastolic, or both) all matched for age, sex and body mass index. Nineteen normotensives (subgroup A), 28 WCH (subgroup A) and 37 ambulatory hypertensives (subgroup A) had only one or no other major cardiovascular risk factor whereas 16 normotensives (subgroup B), 18 WCH (subgroup B) and 44 ambulatory hypertensives (subgroup B) had also some combination of non-insulin-dependent diabetes, a smoking habit and dyslipidaemia. RESULTS: Both for the WCH and for ambulatory hypertensives diabetes and dyslipidaemia (subgroups B) were associated with higher (P<0.04) PWV (11.6+/-0.3 and 12.8+/-0.3m/s, respectively) than for subgroups A (9.3+/-0.5 and 10.9+/-0.6 m/s, respectively). In contrast, PWV for WCH in subgroup A (9.3+/-0.5m/s) did not differ (P>0.35) from those for the normotensive subgroups A (9.2+/-0.3m/s) and B (9.6+/-0.4m/s). PWV was not correlated to levels of glycaemia, glycosylated haemoglobin and cholesterolaemia. CONCLUSIONS: These results suggest that, both for ambulatory hypertensives and for WCH, diabetes and dyslipidaemia are associated with an impairment of arterial distensibility that can entail a greater than normal cardiovascular risk, which might dictate a more than usually stringent treatment of concomitant risk factors and possibly of high blood pressure. In contrast, PWV in WCH of the subgroup A did not differ from those in normotensives, reinforcing the hypothesis that WCH is associated with a benign cardiovascular outcome in the absence of other cardiovascular risk factors.     

Stroke prognosis and abnormal nocturnal blood pressure falls in older hypertensives

It remains uncertain whether abnormal dipping patterns of nocturnal blood pressure influence the prognosis for stroke. We studied stroke events in 575 older Japanese patients with sustained hypertension determined by ambulatory blood pressure monitoring (without medication). They were subclassified by their nocturnal systolic blood pressure fall (97 extreme-dippers, with >/=20% nocturnal systolic blood pressure fall; 230 dippers, with >/=10% but <20% fall; 185 nondippers, with >/=0% but <10% fall; and 63 reverse-dippers, with <0% fall) and were followed prospectively for an average duration of 41 months. Baseline brain magnetic resonance imaging (MRI) disclosed that the percentages with multiple silent cerebral infarct were 53% in extreme-dippers, 29% in dippers, 41% in nondippers, and 49% in reverse-dippers. There was a J-shaped relationship between dipping status and stroke incidence (extreme-dippers, 12%; dippers, 6.1%; nondippers, 7.6%; and reverse-dippers, 22%), and this remained significant in a Cox regression analysis after controlling for age, gender, body mass index, 24-hour systolic blood pressure, and antihypertensive medication. Intracranial hemorrhage was more common in reverse-dippers (29% of strokes) than in other subgroups (7.7% of strokes, P=0.04). In the extreme-dipper group, 27% of strokes were ischemic strokes that occurred during sleep (versus 8.6% of strokes in the other 3 subgroups, P=0.11). In conclusion, in older Japanese hypertensive patients, extreme dipping of nocturnal blood pressure may be related to silent and clinical cerebral ischemia through hypoperfusion during sleep or an exaggerated morning rise of blood pressure, whereas reverse dipping may pose a risk for intracranial hemorrhage.     

The renin-angiotensin system. Normal physiology and changes in older hypertensives

The long-term effects of angiotensin (ANGII) on arterial pressure regulation appear to be closely linked to volume homeostasis, via the renal-pressure natriuresis mechanism, both in normal humans and in older hypertensives. In response to disturbances such as increased sodium intake, suppression of ANGII and aldosterone formation greatly amplifies the effectiveness of the pressure natriuresis mechanism, thereby preventing large increases in body fluid volumes and minimizing the rise in blood pressure needed to maintain sodium balance. When ANGII levels are inappropriately elevated, the antinatriuretic effects of ANGII cause increased arterial pressure, which then serves to maintain sodium and water balance via the pressure natriuresis mechanism. The primary intrarenal and extrarenal mechanisms by which ANGII controls renal excretion and arterial pressure include: (1) a direct effect of ANGII on tubular sodium transport; (2) a preferential constrictor action of ANGII on efferent arterioles, which increases sodium reabsorption by altering peritubular capillary physical forces (efferent arteriolar constriction also prevents excessive decreases in glomerular filtration rate when renal perfusion is compromised, such as in renal artery stenosis); and (3) extrarenal effects of ANGII, including stimulation of aldosterone secretion. Current evidence suggests that the direct effects of ANGII on the kidney are quantitatively more important than indirect effects mediated by aldosterone. In older hypertensives, plasma renin activity and aldosterone concentration are often suppressed, perhaps due to loss of functional nephrons and increased sodium chloride delivery to the macula densa of the remaining nephrons.(ABSTRACT TRUNCATED AT 250 WORDS)     

Role of angiotensin converting enzyme genotype in sodium sensitivity in older hypertensives

BACKGROUND: Individuals differ in their blood pressure (BP) response to changes in dietary sodium (Na+) intake. It is possible that differences in BP responses to dietary Na+ are influenced by genes. METHODS: A total of 35 older (62.9 +/- 1.2 years) hypertensive subjects had their mean arterial blood pressure (MABP) determined after 8 days of low (20 mmol/day) and high (200 mmol/day) Na+ intake. The insertion/ deletion polymorphism of the angiotensin converting enzyme (ACE) gene was genotyped with standard polymerase chain reaction methods. RESULTS: Of the 35 subjects, 24 were classified as sodium-sensitive (> or = 5 mm Hg increase in MABP in response to the increase in dietary Na+) and 11 were classified as sodium-resistant (<5 mm Hg increase in MABP). Those homozygous for the insertion allele of the ACE gene (insertion/insertion [II]; n = 8) had lower (P = .04) MABP responses to the increase in dietary Na+ (0 +/- 3 mm Hg) compared to heterozygotes (insertion/deletion [ID]; n = 20) (9 +/- 2 mm Hg; P = .0001) and those homozygous for the deletion allele (deletion/deletion [DD]; n = 7) (9 +/- 3 mm Hg; P = .05). The prevalence of sodium sensitivity was higher (P = .0083) in DD (71%) and ID (83%) compared to II (25%) genotype groups. CONCLUSIONS: Based on these data in older hypertensive individuals, we conclude that the ACE gene ID and DD genotypes are associated with an increase in BP during a high Na+ diet, which is consistent with the phenotypic characteristic of sodium sensitivity.     

Uncontrolled hypertension in older patients: markers and associated factors to masked and white-coat effect

Background Hypertension is the main risk factor for cardiovascular diseases, affecting more than half the elderly population. It is essential to know if they have proper control of hypertension. The aim of this study was to identify the associated factors to masked uncontrolled hypertension and false uncontrolled hypertension in older patients. Methods Two-hundred seventy-three individuals (70.1 ± 6.7 years-old) had blood pressure (BP) measured at the office and by ambulatory BP monitoring (ABPM), with the definition of controlled group (C), individuals with high office BP and adequate ABPM, called white-coat effect group (WCE), uncontrolled (UC), and subjects with appropriate office BP and elevated ABPM denominated masked effect group (ME). Age, body mass index, diabetes, pulse pressure (PP) and BP dipping during sleep were evaluated (Kruskal-Wallis test and logistic regression models). Results Age was higher in UC than in C and ME (P < 0.01), and 24-h ABPM PP was lower in C (48 ± 7 mmHg) and WCE (51 ± 6 mmHg) than in UC (67 ± 12 mmHg) and ME (59 ± 8 mmHg) (P < 0.01). Sleep systolic BP dipping was lower in ME than in C (P = 0.03). Female gender was associated with a greater chance of being of ME group, which showed a higher PP and lower BP dipping during sleep. Conclusions In older individuals, office BP measurements did not allow the detection of associated factors that would permit to differentiate WCE from UC group and C from ME group. ABPM favored the identification of a higher PP and a lower BP dipping during sleep in the masked effect and uncontrolled groups.     

Circadian blood pressure pattern and cognitive function in newly diagnosed older hypertensives

Hypertensive subjects can be subdivided in two groups, dippers and non-dippers, according to the presence or the lack of a nocturnal fall of blood pressure (BP) of over 10%. Several studies have investigated cardiovascular and cerebrovascular organ damage in the two groups with discordant results, but fewer of them analysed the relationship between circadian BP pattern and cognitive function, and none in the early phases of hypertension. To this purpose, we selected 40 older hypertensives, 23 dippers and 17 non-dippers, with newly diagnosed hypertension, never treated, who underwent to 24-h ambulatory BP monitoring (ABPM), Mini-Mental State Examination (MMSE) and recording of event-related potentials (ERPs). No significant differences between dippers and non-dippers were found in the MMSE scores and P300 latency values, as we expected, and not even in N2 wave latency values, showing that the non-dipping pattern is not associated with lower cognitive function in the early phases of hypertension.     

Amlodipine 2.5 mg once daily in older hypertensives: a Brazilian multi-centre study

OBJECTIVES: The use of low-dose amlodipine has not yet been well established in the elderly. This study therefore aimed to evaluate the efficacy and tolerability of low-dose amlodipine in elderly patients with Joint National Committee VI stage I or II hypertension. PATIENTS AND METHODS: Sixty-five hypertensive individuals (aged 66.3 +/- 5.3 years) received amlodipine 2.5 mg per day for 12 weeks before and after two periods of 4 weeks of placebo. At weeks 0, 12 and 16, patients were submitted to office, 24 h ambulatory blood pressure monitoring and home blood pressure measurement. RESULTS: Office systolic and diastolic blood pressure showed decreases at weeks 8 (153 +/- 17, 90 +/- 9 mmHg) and 12 (152 +/- 16, 90 +/- 9 mmHg) compared with weeks 0 (164 +/- 16, 99 +/- 6 mmHg) and 16 (162 +/- 19, 95 +/- 9 mmHg). During ambulatory monitoring, a decrease was observed in the average 24 h systolic and diastolic pressure at week 12 (143 +/- 13, 86 +/- 7 mmHg) compared with weeks 0 (155 +/- 15, 93 +/- 6 mmHg) and 16 (152 +/- 16, 92 +/- 8 mmHg). A daytime and night-time reduction in systolic and diastolic pressure was observed on home blood pressure monitoring at week 12 (146 +/- 16/88 +/- 8, 144 +/- 16/93 +/- 8 mmHg) compared with weeks 0 (159 +/- 17/94 +/- 8, 161 +/- 19/93 +/- 8 mmHg) and 16 (153 +/- 16/93 +/- 8, 154 +/- 17/92 +/- 8 mmHg). Adverse reactions were infrequent. CONCLUSIONS: Amlodipine at a dose of 2.5 mg per day showed efficacy and good tolerability in elderly hypertensives.     

Silent ST depression and cardiovascular end-organ damage in newly found, older hypertensives

In hypertension, both reduced vascular supply and increased cardiac demand contribute to the development of (silent) myocardial ischemia. Our aim was to determine the prevalence of ST-segment depression and to analyze contributing factors in asymptomatic, previously untreated, older hypertensives. From a population survey, in 184 patients with mild hypertension (4 times systolic blood pressure >/=160 mm Hg and/or diastolic blood pressure >/=95 mm Hg), 60 to 75 years of age, cardiovascular end-organ damage was measured. Episodes of ST-segment depression were measured by 48-hour ambulatory Holter monitoring and were observed in 21 hypertensives (12%). They showed a significantly higher combined far-wall intima-media thickness of carotid and femoral arteries and more arterial plaques as measured by B-mode ultrasound compared with hypertensives without ST depression (0.00098+/-0.00021 versus 0.00088+/-0.00016 mm and 5.2+/-3.7 versus 3.7+/-2.8 plaques, P<0.05, respectively), whereas left ventricular mass index was not different (111+/-18 versus 104+/-24 g/m(2); P=0.18, respectively). In hypertensives with transient ST-segment depression, a significant relation was found between left ventricular mass and ischemic burden (r=0.51, P=0.02). Approximately 1 of 8 unselected and previously untreated older hypertensives show asymptomatic ST-segment depression, suggestive of silent myocardial ischemia. These data suggest that vascular factors mainly determine the occurrence of ischemic ST-segment depression and cardiac factors determine the ischemic burden in older hypertensives.     

Serum cortisol in the white-coat phenomenon

BACKGROUND: The rise in blood pressure associated with a clinic visit (the white-coat phenomenon) may result from anxiety or an alerting reaction. There is evidence to suggest that glucocorticoids may be involved in the mechanism of stress-related blood pressure elevation, but the relationship between the white-coat phenomenon and glucocorticoids has not been assessed. DESIGN: Forty-eight young subjects with essential hypertension were compared with 12 control normotensive subjects. METHODS: Home blood pressure monitoring for 7 days and serum cortisol at 0900 h and 2 h rest at 1100 h were measured. The white-coat phenomenon was calculated for systolic and diastolic blood pressure and average home blood pressure. RESULTS: The serum cortisol level was significantly greater at 0900 h than that at 1100 h in the hypertensive subjects and was higher in the hypertensive subjects than in the normotensive subjects (21.5 +/- 0.5 versus 14.3 +/- 0.9 μg/dl), but there was no difference between serum cortisol levels at 1100 h in the two groups. The magnitude of the white-coat phenomenon, which was greater in the hypertensive subjects than in the normotensive group (22 +/- 2/12 +/- 1 versus 4 +/- 3/1 +/- 3 mmHg), correlated with serum cortisol at 0900 h, but not at 1100 h. The higher level of serum cortisol at 0900 h was confirmed by another measurement conducted 4 months later in a subsample of the hypertensive subjects ( n = 18). CONCLUSIONS: These results suggest that the white-coat phenomenon is related to the transient increase in serum cortisol or psychological stress, or both, which can trigger arousal of the hypothalamic pituitary adrenocortical axis.     

Heart rate variability in white-coat hypertension

OBJECTIVES: The objective of this study was to compare heart rate variability (HRV) in patients with essential hypertension, in patients with white-coat hypertension and in normotensive control individuals, and to investigate a possible relation between HRV and vasoactive hormones. METHODS: Patients with essential hypertension (n=19, 61 years, median and interquartile range: 40-66 years), patients with white-coat hypertension (n=8, 52 years, median and interquartile range: 41-64 years) and normotensive participants (n=13, 50 years, median and interquartile range: 39-57 years) participated in the study. HRV was measured at rest in the supine position, during standing and during controlled forced breathing (respiration frequency >20/min). Power spectral density was calculated using Fourier transformation. RESULTS: Controlled breathing caused a decrease in low frequency (LF) variation and LF/high frequency variation (LF/HF) in all blood pressure groups. The decrease in LF was smaller in the hypertensive group (-60 ms2) than in the normotensive group (-139 ms2) (P=0.03; hypertensive group vs. normotensive group). The decrease in LF/HF induced by controlled breathing was -0.9 ms in the hypertensive group, -2.0 ms2 in the white-coat hypertensive group and -2.8 ms2 in the normotensive group, (P=0.037; hypertensive group vs. normotensive group). We found a positive correlation between baseline plasma renin concentration and LF (r=0.330, P=0.037) and LF/HF (r=0.378, P=0.016) at rest. CONCLUSION: The observed differences in HRV might reflect the impaired responsiveness to autonomic challenge in hypertensive patients. We did not find the HRV spectrum in white-coat hypertension different from the HRV spectrum in hypertension or normotension.     

The white-coat hypertension response

This study was designed to determine the clinical characteristics of hypertensive patients whose blood pressures are substantially higher in the medical office than in their natural environments. Thirty-nine percent of patients enrolled in a nonpharmacologic hypertension treatment program had systolic or diastolic office blood pressures (OBPs) that were at least 10 mm Hg higher than their ambulatory blood pressures (ABPs). Although these white-coat responders (WCRs) had higher systolic OBPs than did non-white-coat responders (NRs), both their systolic (p<0.02) and their diastolic (p<0.0001) ABPs were significantly lower than those of NRs. Furthermore, patients with white-coat hypertension did not have greater blood pressure reactivity in their natural environments, suggesting that their blood pressure elevations may be specific to the medical setting. White-coat hypertensives were older (p<0.005), had less angry dispositions (p<0.01), and reported less overt anger expression (p<0.005). They were also taking more antihypertensive medications than were the other patients in the study (p<0.001).     

Effect of aerobic exercise training on blood pressure sensitivity to dietary sodium in older hypertensives

Although aerobic exercise training has been shown to lower blood pressure (BP) in older adults, its effect on BP sensitivity to dietary sodium (Na(+)) is unknown. Therefore, the present study was undertaken to examine the effect of aerobic exercise training on BP sensitivity to dietary Na(+) in older hypertensive individuals. Blood pressure was measured after 8 days of low (20 mEq) and high (200 mEq) Na(+) diets in 31 older (63+/-7 years, mean+/-standard deviation), hypertensive (152+/-11/88+/-5 mm Hg) individuals at baseline and following 6 months of aerobic exercise training (at 75% VO(2)max, 3 times/week, 40 min/session). Subjects were grouped on the basis of the difference in mean arterial BP (MAP) between diets (Na(+) sensitive: >or=5 mm Hg increase in MAP on high Na(+), n=20; Na(+) resistant: <5 mm Hg increase in MAP on the high Na(+) diet, n=11). Following 6 months of aerobic exercise training, there was a significant increase in maximal aerobic capacity (VO(2)max: 18.3+/-3.8 vs 20.7+/-4.2 ml/kg/min, P<0.017). Aerobic exercise training had a significant (P=0.02) effect on Na(+) sensitivity status, with the proportion of Na(+)-resistant individuals increasing from 35% at baseline to 61% following the 6-month aerobic exercise training programme. This study demonstrates the importance of physical activity on BP sensitivity to dietary Na(+).     

Haemoconcentration, shear-stress increase and carotid artery diameter regulation after furosemide administration in older hypertensives

The aim of the present study was to determine whether changes of carotid wall shear stress induced by changes in blood viscosity after diuretic administration cause carotid arterial dilatation in elderly hypertensives, as reported in the cat. Arterial wall shear rate (ultrasound technique, profilmeter FRP III), the systo-diastolic diameter (echotracking technique) and the mean blood flow velocity and volume of the common carotid artery, the blood viscosity (rotational viscometer) and the finger arterial blood pressure (Finapress Ohmeda) were measured in 12 young volunteers (aged 25+/-2 years) and in 12 elderly hypertensives (aged 80+/-4 years) treated with short-acting calcium antagonists up to 24h before the study, both at baseline and after intravenous furosemide infusion (0.5mg/min), when the haematocrit had increased by at least two percentage points.After furosemide administration the mean arterial blood pressure decreased and blood viscosity and carotid systolic shear stress increased in both groups. However, common carotid artery diameter increased only in the young controls but not in the elderly hypertensives. These data show that an increase in carotid shear stress caused by haemoconcentration induces carotid vasodilatation only in young healthy subjects, and not in elderly hypertensives. This effect may be related to impaired endothelium function and/or arterial wall mechanics.