Brachial-ankle pulse wave velocity is an independent risk factor for microalbuminuria in patients with essential hypertension--a Japanese trial on the prognostic implication of pulse wave velocity (J-TOPP).

Brachial-ankle pulse wave velocity is a new measure of arterial stiffness. The clinical significance of brachial-ankle pulse wave velocity as a measure of early vascular damage remains unclear. We examined the hypothesis that higher brachial-ankle pulse wave velocity is associated with a much greater risk of albuminuria by employing a cohort of 718 never-treated hypertensive patients registered in a prospective study. The 718 patients consisted of 500 patients with normoalbuminuria (69.6%), 191 patients with microalbuminuria (26.6%) and 27 patients with macroalbuminuria (3.8%). The prevalence of microalbuminuria increased with a graded increase in brachial-ankle pulse wave velocity (17.6, 22.8, 28.2 and 39.6%, p < 0.0001). The prevalence of macroalbuminuria remained constant until the third grade group of the brachial-ankle pulse wave velocity but increased significantly in the highest grade group compared with the lower grade groups (2.3, 3.2, 2.3, 9.9%, p < 0.0001). Age, systolic and diastolic blood pressure, pulse pressure, heart rate, and fasting glucose concentration were also significantly increased with an increase in brachial-ankle pulse wave velocity (p < 0.0001 for all). Multiple logistic regression analysis has shown that systolic blood-pressure, fasting blood glucose, and brachial-ankle pulse wave velocity are significant risk factors for microalbuminuria. After adjusting for other risk factors, the odds ratio for an increase of 200 cm/s in brachial-ankle pulse wave velocity was 1.192 (95% confidence interval: 1.022-1.365; p < 0.05). These data suggest that brachial-ankle pulse wave velocity is an independent risk factor for microalbuminuria and could be used as a marker for early vascular damage in never-treated hypertensive patients.

Higher brachial-ankle pulse wave velocity is associated with more advanced carotid atherosclerosis in end-stage renal disease.

Brachial-ankle pulse wave velocity is a new measure of arterial stiffness. We examined whether higher brachial-ankle pulse wave velocity is associated with more advanced carotid atherosclerosis and left ventricular hypertrophy in patients with end-stage renal disease, and whether this effect would be mediated by the influence of wave reflection on central arterial pressure. In 68 patients with end stage renal disease, we examined blood pressures, brachial-ankle pulse wave velocity and the augmentation index of the left common carotid artery, a measure of the impact of wave reflection on the systolic peak in central arteries. The degree of carotid atherosclerosis was quantified by a plaque score and maximum intimal-medial thickness. Echocardiography was used to determine the left ventricular mass index. In simple regression analysis, brachial-ankle pulse wave velocity was correlated with both plaque score and maximum intimal-medial thickness (r = 0.420, p < 0.001 and r = 0.452, p < 0.0005, respectively) but not with left ventricular mass index. Multiple regression analysis was performed with the plaque score or maximum intimal-medial thickness as the dependent variable and brachial-ankle pulse wave velocity and known clinical risk factors as the independent variables. The brachial-ankle pulse wave velocity was an independent risk factor for both plaque score (beta = 0.006, p = 0.004) and maximum intimal-medial thickness (beta = 0.008, p = 0.04). Independent risk factors for left ventricular mass index were left ventricular diastolic dimension (beta = 3.509, p = 0.000007) and augmentation index (beta = 0.580, p = 0.04). The brachial-ankle pulse wave velocity was unrelated to augmentation index in patients with end stage renal disease. In conclusion, higher brachial-ankle pulse wave velocity was found to be a risk factor for carotid atherosclerosis in patients with end-stage renal disease; this effect was independent of the influence of wave reflection on central arterial pressure. The brachial-ankle pulse wave velocity was unrelated to left ventricular structure.

Effects of valsartan and nifedipine coat-core on systemic arterial stiffness in hypertensive patients.

BACKGROUND: The aim of this study was to compare the effects of long-term antihypertensive treatment on brachial-ankle pulse wave velocity (PWV), a marker of systemic arterial stiffness, between angiotensin II receptor blocker valsartan and long-acting calcium channel blocker nifedipine coat-core. METHODS: Forty-one patients (54 +/- 3 years of age, 20 men and 21 women) with essential hypertension (155 +/- 3/95 +/- 3 mm Hg) were randomly allocated to the treatment with valsartan (80 mg once daily) or nifedipine coat-core (20 mg once daily). Brachial-ankle PWV and 24-h ambulatory blood pressures (BP) were measured before and 3 months after treatment. RESULTS: Baseline data did not differ between the valsartan and nifedipine groups. The PWV also was similar between the groups (1669 +/- 65 v 1622 +/- 64 cm/sec). Three months of treatment similarly reduced resting systolic and diastolic BP (nifedipine, -18.4 +/- 4.2/-11.9 +/- 2.7 mm Hg; valsartan, - 17.4 +/- 3.3/-9.8 +/- 2.1 mm Hg, all P < .001). The PWV was significantly reduced compared with baseline values in the valsartan group (-195 +/- 42 cm/sec, P < 0.001) but not in the nifedipine group (-69 +/- 40 cm/sec, NS). The 24-h mean heart rate increased in the nifedipine group but remained unchanged in the valsartan group, although BP were similarly lowered for 24 h. A tachycardic response was associated with an increase or lesser reduction in PWV in a group treated with nifedipine (r = 0.584, P < .01). CONCLUSIONS: These data suggest that long-term treatment with valsartan could reduce arterial stiffness better than nifedipine-coat core. The favorable vascular effect of valsartan was due in part to its nonhypotensive effect. The expected decrease in arterial stiffness may be offset by reflex sympathetic activation in some patients treated with nifedipine.

Utility of automated brachial ankle pulse wave velocity measurements in hypertensive patients.

BACKGROUND: We examined whether pulse wave velocity (PWV), determined by brachial ankle arterial pressure wave measurements, using a newly developed, fully automated device could be a surrogate measure for carotid femoral PWV. METHODS & RESULTS: This device (AT-form PWV/ABI, Nippon Colin, Komaki, Japan) can simultaneously monitor bilateral brachial and ankle pressure wave forms using the volume plethysmographic method, with two optional tonometry sensors for carotid and femoral arterial wave measurements. We examined the right brachial-right ankle PWV and left carotid-left femoral PWV in 89 normotensive and untreated hypertensive patients. The brachial ankle PWV correlated well with carotid femoral PWV (r = 0.755, P <.00001). The Bland-Altman plots of the two variables, however, showed a significant difference exists between the two techniques over the range of measurement. The within-observer and between-observer coefficients of variation of the brachial ankle PWV were 6.5% +/- 4.1% and 3.6% +/- 3.9%, respectively. To determine the factors affecting brachial ankle PWV, we studied treated and untreated hypertensive patients with World Health Organization stage I (n = 146), stage II (n = 74), or stage III (n = 54). In multiple regression analysis, age, brachial ankle PWV, and the presence of diabetes were significant predictors of the severity of hypertensive organ damage. Age, systolic blood pressure, and the stage of hypertensive organ damage were major determinants of brachial ankle PWV. CONCLUSIONS: Although the brachial ankle PWV does not agree with the carotid femoral PWV, this parameter may yet become a new, useful measure for arterial stiffness. Further longitudinal studies are necessary to confirm the clinical significance of the brachial ankle PWV.

The influence of one-year treatment by angiotensin converting enzyme inhibitor on baroreflex sensitivity and flow-mediated vasodilation of the brachial artery in essential hypertension--comparison with calcium channel blockers.

BACKGROUND: Both baroreflex sensitivity and flow-mediated vasodilator function have been recognized to have prognostic significance in cardiovascular diseases. Long-term antihypertensive treatment effects on these parameters, however, remain unclear. SUBJECTS AND METHODS: We examined the effects of long-term treatment by angiotensin converting enzyme inhibitors (ACEI) orcalcium channel blockers (CCB) on baroreflex and flow-mediated vasodilator function in patients with essential hypertension (EH). We recruited 36 patients aged 56 +/- 11 years, with systolic blood pressure > or = 160 mmHg and/or diastolic blood pressure > or = 95 mmHg. Patients were assigned either to treatment by long-acting ACEI (n = 12) or CCB (n = 24). All patients were followed for 12 months. Optimal BP was achieved by two optional increases in treatment: dose-doubling of the primary drug during the first three months and the addition of diuretics or beta-blockers thereafter. Target blood pressure was 140/90 mmHg or a fall > or = 20/10 mmHg. Baroreflex sensitivity was examined by spectral analysis of blood pressure and RR interval variabilities before treatment and after 3 and 12 months of treatment. The flow-mediated vasodilator function was determined before and 12 months after treatment by measuring the change in brachial artery diameter during increases in flow induced by reactive hyperemia. RESULTS: Baseline blood pressures were similar between the ACEI and CCB groups (172 +/- 5/103 +/- 2 vs. 172 +/- 4/101 +/- 3 mmHg). Blood pressures after 3 and 12 months of treatment also did not differ between the ACEI and CCB groups (149 +/- 4/91 +/- 2 vs. 145 +/- 2/85 +/- 2 mmHg, and 133 +/- 5/84 +/- 2 vs. 133 +/- 2/81 +/- 2 mmHg, respectively). Baseline baroreflex sensitivity was similar between the groups (6.7 +/- 0.8 vs. 5.9 +/- 0.6 msec/mmHg). This parameter remained unchanged at three months but increased after 12 months of treatment in both the ACEI (9.5 +/- 1.6 msec/mmHg, p = 0.05) and CCB (9.1 +/- 1.2 msec/mmHg, p = 0.006) groups. Percent increases in brachial arterial diameter and flow during reactive hyperemia increased in the group treated with ACEI (12.4 +/- 3.5 vs. 25.8 +/- 6.3% and 618 +/- 72 vs. 953 +/- 166, p < 0.05 for both) but both parameters remained unchanged in the group treated with CCB. CONCLUSION: These data suggest that long-term blood pressure control with modem antihypertensive drugs improves baroreflex function. Treatment with ACEI may be more favorable for flow-mediated vasodilator function than treatment with CCB.

Clinical significance of blood pressure response triggered by a doctor's visit in patients with essential hypertension.

The clinical significance of the pressor response triggered by blood pressure measurement, the so-called "white-coat effect," was studied in relation to left ventricular structure and function in patients with essential hypertension. We studied 75 consecutive, never-before treated patients with essential hypertension (54 +/- 2 (SE) years; 31 men). Beat-to-beat blood pressure (Finapres) was monitored at rest, during conventional blood pressure measurement by a doctor, and during a mental stress test. The left ventricular mass index and diastolic function (EIA ratio) were determined by echocardiography. The systolic blood pressure response triggered by the doctor's visit (deltaSBP) correlated positively with the left ventricular mass index (r= 0.326, p<0.03) and negatively with the EIA ratio (r=-0.325, p<0.02). A positive relationship between the deltaSBP and left ventricular mass index was observed in men (r=0.556, p<0.01) but not in women. The greater ASBP also was associated with lower EIA ratio in women (r=-0.434, p<0.02). The deltaSBP correlated with the mental stress-induced increase in systolic blood pressure in men (r=0.586, p<0.005) but not in women (r=0.148, n.s.). Blood pressures outside the clinic were higher in men than in women (p<0.05 for systolic and p<0.005 for diastolic) despite the similar level of clinic blood pressures between the sexes. Stepwise multiple linear regression analysis showed that the deltaSBP was an independent predictor of the left ventricular mass index in men (beta=0.783, p=0.0009) and of the EIA ratio in women (beta=-0.003, p=0.05). These data suggest that the pressor response triggered by a doctor's visit has clinical significance in never-before treated hypertensive patients, possibly because it mirrors real-life stress reactivity in men.