40 research outputs found

    Correlation of pulse wave velocity with left ventricular mass in patients with hypertension once blood pressure has been normalized

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    Vascular stiffness has been proposed as a simple method to assess arterial loading conditions of the heart which induce left ventricular hypertrophy (LVH). There is some controversy as to whether the relationship of vascular stiffness to LVH is independent of blood pressure, and which measurement of arterial stiffness, augmentation index (AI) or pulse wave velocity (PWV) is best. Carotid pulse wave contor and pulse wave velocity of patients (n=20) with hypertension whose blood pressure (BP) was under control (<140/90 mmHg) with antihypertensive drug treatment medications, and without valvular heart disease, were measured. Left ventricular mass, calculated from 2D echocardiogram, was adjusted for body size using two different methods: body surface area and height. There was a significant (P<0.05) linear correlation between LV mass index and pulse wave velocity. This was not explained by BP level or lower LV mass in women, as there was no significant difference in PWV according to gender (1140.1+67.8 vs 1110.6+57.7 cm/s). In contrast to PWV, there was no significant correlation between LV mass and AI. In summary, these data suggest that aortic vascular stiffness is an indicator of LV mass even when blood pressure is controlled to less than 140/90 mmHg in hypertensive patients. The data further suggest that PWV is a better proxy or surrogate marker for LV mass than AI and the measurement of PWV may be useful as a rapid and less expensive assessment of the presence of LVH in this patient population

    Drug Treatment of Hypertension: Focus on Vascular Health

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    Changes in arterial pressure hemodynamics in response to renal nerve stimulation both before and after renal denervation

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    BackgroundRenal nerve denervation (RDN) is developed as a potential treatment for hypertension. Recently, we reported the use of renal nerve stimulation (RNS) to localize sympathetic nerve tissue for subsequent selective RDN. The effects of RNS on arterial pressure dynamics remain unknown. The current study aimed to describe the acute changes in arterial pressure dynamics response to RNS before and after RDN.Methods and resultsTwenty six patients with drug-resistant hypertension referred for RDN were included. RNS was performed under general anesthesia before and after RDN. We continuously monitored heart rate (HR) and invasive femoral blood pressure (BP). Augmentation pressure (AP) and index (Aix), pulse pressure (PP), time to reflected wave, maximum systolic BP and dicrotic notch were calculated. Systolic and diastolic BP at site of maximum response significantly increased in response to RNS (12016/62 +/- 9 to 150 +/- 22/75 +/- 15mmHg) (p0.10). RNS increased Aix (29 +/- 11 to 32 +/- 13%, p=0.005), PP (59 +/- 14 to 75 +/- 17mmHg, p0.18). All changes were BP dependent. RNS had no influence on HR or the time to dicrotic notch (p>0.12). ConclusionRNS induces temporary rises in Aix, PP, time to maximum systolic pressure and time to reflected wave. These changes are BP dependent and were completely blunted after RDN
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