Arterial Stiffness In Hypertensive Patients Research Articles

Efficacy of Irbesartan on Left Ventricular Mass and Arterial Stiffness in Hypertensive Patients

BackgroundIncreased aortic stiffness measured by pulse wave velocity (PWV) and left ventricular hypertrophy (LVH) are independent risk factors of cardiovascular events in hypertensive patients. We have conducted a prospective study to examine the effects of the angiotensin II receptor antagonist (irbesartan) on PWV and LVH in hypertensive patients.MethodsA total of 52 untreated hypertensive patients (age:53.3±8.0 yrs) were enrolled; they had no evidence of associated cardiovascular complications. Blood pressure, heart rate, aortic PWV and left ventricular mass index (LVMI) by 2-D echocardiography were measured at baseline and after irbesartan treatment (150 mg or 300 mg/day) at 12 weeks and 24 weeks.ResultsBlood pressure was significantly decreased after 12 weeks and 24 weeks of treatment compared to baseline (SBP: 134.6±13.3 mmHg, 134.0±11.0 mmHg vs 163.7±13.8 mmHg p<0.001, DBP: 86.0±10 mmHg, 83.07 mmHg vs 102.4±9.6 mmHg p<0.001, respectively) without significant change in heart rate. LVMI decreased at 12 weeks and at 24 weeks after treatment compared to baseline (from 145.5±35.1 g/m2 at baseline to 137.5±35.4 g/m2 at 12 weeks, p=0.017 and 135.3±35.4 g/m2 at 24 weeks, p=0.008). Aortic PWV was decreased after irbesartan treatment at 12 weeks (from 9.6±2.8 m/sec to 8.7±3.1 m/sec at 12 weeks, p=0.064) and at 24 weeks (from 9.6±2.9 m/sec to 7.7±2.1 m/sec at 24 weeks, p=0.007).ConclusionsLong-term treatment with irbesartan may reduce arterial stiffness and regression of LVH in hypertensive patients. The pleiotropic effects of irbesartan, further decreasing PWV without change of BP between 12 and 24 weeks of treatment, may have favorable vascular effects on arterial stiffness and LVH.

Clinical Usefulness and Limitations of Brachial-Ankle Pulse Wave Velocity in the Evaluation of Cardiovascular Complications in Hypertensive Patients

The goal of this study was to clarify the clinical usefulness and limitations of brachial-ankle pulse wave velocity (PWV) to evaluate hypertensive complications, in comparison with carotid-femoral PWV. Patients with essential hypertension (n=296, male/female=161/135; age=61.1+/-0.7 years) were enrolled. We measured brachial-ankle PWV, femoral-ankle PWV and carotid-femoral PWV simultaneously, and evaluated target organ damage and associated clinical conditions (cerebrovascular and cardiovascular disease) using the World Health Organization classification modified in 1999. Carotid-femoral PWV (p<0.0001; r=0.521) and brachial-ankle PWV (p<0.0001; r=0.478) but not femoral-ankle PWV were significantly correlated with age. Carotid-femoral PWV was significantly higher in patients with associated clinical conditions compared with that in patients with target organ damage (p<0.05) and those with no complications (p<0.0001). Brachial-ankle PWV was significantly higher in patients with associated clinical conditions (p<0.05) and target organ damage (p<0.05) compared to those with no complications, but there was no significant difference in brachial-ankle PWV between these two groups. Moreover, femoral-ankle PWV was significantly lower in patients with associated clinical conditions compared with that in patients with target organ damage (p<0.05). These data suggest that brachial-ankle PWV could underestimate arterial stiffness in hypertensive patients with a history of cardiovascular events.

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

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. 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. 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). 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.

Arterial stiffness index: A new evaluation for arterial stiffness in elderly patients with essential hypertension

Background: Arterial stiffness is one of the predictors of cardiovascular event. Arterial stiffness is commonly measured by pulse wave velocity between the carotid and femoral arteries. Recently the arterial stiffness index which is measured by computerized oscillometry at the upper arm was developed. As this procedure is a convenient means of measuring pulse wave velocity, we considered it suitable to evaluate arterial stiffness in elderly patients. We evaluated this arterial stiffness index and compared it with other methods of evaluating arterial stiffness in hypertensive patients, including the elderly.Methods: Forty‐two patients with essential hypertension, including 26 subjects over 60 years old were enrolled. We evaluated the arterial stiffness index by computerized oscillometry, and also evaluated arterial stiffness between the carotid‐femoral artery and the brachial‐tibial artery, the second derivative of photoplethysmogram, the forearm vasodilator response to reactive hyperemia by strain‐gauge plethysmography.Results: Arterial stiffness index was positively correlated with pulse wave velocity between the carotid‐femoral artery (P &lt; 0.0001; r = 0.579), the heart‐carotid artery (r = 0.454) and right brachial‐tibial artery (r = 0.549). It was also correlated with b/a (r = 0.474) and d/a (r = 0.568) by a second derivative of photoplethysmogram, but not correlated with a reactive vasodilator response. In elderly patients, arterial stiffness index was also correlated with carotid‐femoral pulse wave velocity (P &lt; 0.05; r = 0.456) but not correlated with a vasodilator response to reactive hyperemia.Conclusion: These data suggest that arterial stiffness index is correlated to common pulse wave velocity between the carotid and femoral arteries, so this index might be useful to evaluate arterial stiffness in hypertensive patients including the elderly.

Association of the auscultatory gap with vascular disease in hypertensive patients.

To assess the relation of the auscultatory gap during blood pressure measurement to cardiovascular structure and function. Cross-sectional study. A hypertension center in a university hospital. 168 persons with hypertension who were otherwise healthy and were not receiving medication. Wideband external pulse recordings and ultrasonographic examination of the left ventricle and extracranial carotid arteries. Vascular stiffness was evaluated using simultaneous carotid pressure waveforms obtained by applanation tonometry of the contralateral carotid artery. Classic auscultatory gaps were present in 21% of patients and were associated with older age (mean age SD, 64 11 years for patients with gaps and 55 13 years for patients without gaps; P < 0.001), female sex (67% of patients with gaps and 44% of patients without gaps were female; P < 0.05), and increased arterial stiffness (arterial stiffness index, 8.5 4.6 in patients with gaps and 5.8 3.2 in patients without gaps; P < 0.005). The prevalence of atherosclerotic plaques was increased more than twofold among patients with gaps compared with patients without gaps (50% compared with 22%; p < 0.002). Patients with and without auscultatory gaps had similar blood pressures, left ventricular structure and function, serum cholesterol levels, and smoking history. Logistic regression analysis indicated that only female sex (P < 0.02), arterial stiffness (P < 0.002), and atherosclerotic plaque (P < 0.02) were independently associated with the presence of an auscultatory gap. This study provides strong evidence that auscultatory gaps are related to carotid atherosclerosis and to increased arterial stiffness in hypertensive patients, independent of age. Although these observations need to be confirmed prospectively, they suggest that auscultatory gaps may have prognostic relevance.

901-80 Auscultatory Gaps and Target Organ Damage in Hypertensive Patients

Auscultatory gaps are a common finding in clinical practice but their clinical and prognostic importance has never been assessed. To examine the relation of auscultatory gaps to left ventricular and arterial structure and function, wideband external pulse recordings during cuff deflation to detect auscultatory gaps and ultrasonographic examination of left ventricle and extracranial carotid artery were performed in 168 unmedicated, asymptomatic hypertensive subjects. Vascular stiffness was also evaluated by simultaneous carotid pressure waveforms obtained by applanation tonometry of the contralateral carotid artery. Auscultatory gaps were present in 21% of the population and were associated with older age (64 ± 11 vs 55 ± 13 years, p &lt; 0.0005). female gender (66 vs 44%, p &lt; 0.05) and increased arterial stiffness (beta = 8.5 ± 4.6 vs 5.8 ± 3.2, P &lt; 0.005). Differences in arterial stiffness persisted after controlling for the confounding effects of age and gender. The prevalence of atherosclerotic plaques was more than two-fold increased among subjects with gaps (50 vs 22%, p &lt; 0.005). No significant differences were found in left ventricular structure and function between the subjects with and without gaps. The two populations had similar systolic and diastolic blood pressures, serum lipid levels and smoking history. Logistic regression analysis including age in the model indicated that only female gender, beta (an index of arterial stiffness) and the presence of plaque were independently related to the presence of auscultatory gaps. This study provides the first evidence that auscultatory gaps are related to the presence of carotid atherosclerosis and to increased arterial stiffness in hypertensive patients, independently of age. Although these observations need to be confirmed by prospective studies they suggest a prognostic relevance of the auscultatory gaps.

781-4 Relation of Pulse Pressure to Target Organ Damage in Hypertensive Patients

Wide arterial pulse pressure has been previously reported to reflect changes in arterial structure and stiffness and predicts myocardial infarction in hypertensive patients. Ultrasonic detection of carotid atherosclerosis also predicts subsequent myocardial infarction. To determine the relation of pulse pressure to the presence of target organ damage, as “preclinical” anatomic and functional cardiovascular disease, 198 asymptomatic, unmedicated hypertensive subjects underwent ultrasonographic evaluation of left ventricular (LV) and extracranial carotid artery structure and function. Vascular stiffness was also evaluated by simultaneous applanation tonometry of the contralateral carotid artery pressure waveform. Based on the 97 th percentile of pulse pressure in 324 normotensive adults (70 mmHg), patients were divided into groups with higher (≥ 70 mmHg, group 1, n = 55) or lower (&lt; 70 mmHg, group 2, n = 143) pulse pressures. Higher pulse pressure was associated with older age (67 ± 10 vs 52 ± 10 years, p &lt; 0.0001), female gender (53 vs 30%, p &lt; 0.005) and higher LV mass indexed by body surface area (96 ± 21 vs 89 ± 19 g/m2, p &lt; 0.05) or height 2.7 (44 ± 9 vs 40 ± 9 g/m 2.7 , p &lt; 0.01) as well as with increased end-systolic stress (80 ± 24 vs 72 ± 19 dynes/cm2 x 103, P &lt; 0.05) and arterial stiffness (Peterson's elastic modulus = 667 ± 323 vs 452 ± 192 dynes/cm 2 x to-6, p &lt; 0.0001). The differences in LV mass and arterial stiffness persisted after adjusting for the effect of age and gender but became insignificant in analysis of covariance after adjusting for mean arterial pressure. The prevalence of isolated systolic hypertension was higher in the group with pulse pressure ≥ 70 mmHg (29 vs 2%, p &lt; 0.0001). The prevalence of discrete or diffuse carotid atherosclerosis was two-fold increased in group 1 (49 vs 25%, p &lt; 0.005) as was the prevalence of LV hypertrophy (LV masslbody surface area, 27 vs 13%, p &lt; 0.05). The two groups had similar serum lipid levels and smoking history. Logistic regression analysis indicated that age, mean arterial pressure and the presence of atherosclerosis — but not gender or LV mass — were independently associated with higher pulse pressure. The present findings suggest that higher mean BP mediates the relation of high pulse pressure to changes in cardiac structure and arterial stiffness in hypertensive patients. However, the independent relation of carotid atherosclerosis with higher arterial pulse pressure confirms the prognostic relevance of higher levels of pulse pressure.