M Marciniak

Effect of Modest Salt Reduction on Blood Pressure, Urinary Albumin, and Pulse Wave Velocity in White, Black, and Asian Mild Hypertensives

A reduction in salt intake lowers blood pressure. However, most previous trials were in whites with few in blacks and Asians. Salt reduction may also reduce other cardiovascular risk factors (eg, urinary albumin excretion, arterial stiffness). However, few well-controlled trials have studied these effects. We carried out a randomized double-blind crossover trial of salt restriction with slow sodium or placebo, each for 6 weeks, in 71 whites, 69 blacks, and 29 Asians with untreated mildly raised blood pressure. From slow sodium to placebo, urinary sodium was reduced from 165±58 (±SD) to 110±49 mmol/24 hours (9.7 to 6.5 g/d salt). With this reduction in salt intake, there was a significant decrease in blood pressure from 146±13/91±8 to 141±12/88±9 mm Hg (P<0.001), urinary albumin from 10.2 (IQR: 6.8 to 18.9) to 9.1 (6.6 to 14.0) mg/24 hours (P<0.001), albumin/creatinine ratio from 0.81 (0.47 to 1.43) to 0.66 (0.44 to 1.22) mg/mmol (P<0.001), and carotid-femoral pulse wave velocity from 11.5±2.3 to 11.1±1.9 m/s (P<0.01). Subgroup analysis showed that the reductions in blood pressure and urinary albumin/creatinine ratio were significant in all groups, and the decrease in pulse wave velocity was significant in blacks only. These results demonstrate that a modest reduction in salt intake, approximately the amount of the current public health recommendations, causes significant falls in blood pressure in all 3 ethnic groups. Furthermore, it reduces urinary albumin and improves large artery compliance. Although both could be attributable to the falls in blood pressure, they may carry additional benefits on reducing cardiovascular disease above that obtained from the blood pressure falls alone.

Effects of Potassium Chloride and Potassium Bicarbonate on Endothelial Function, Cardiovascular Risk Factors, and Bone Turnover in Mild Hypertensives

To determine the effects of potassium supplementation on endothelial function, cardiovascular risk factors, and bone turnover and to compare potassium chloride with potassium bicarbonate, we carried out a 12-week randomized, double-blind, placebo-controlled crossover trial in 42 individuals with untreated mildly raised blood pressure. Urinary potassium was 77±16, 122±25, and 125±27 mmol/24 hours after 4 weeks on placebo, potassium chloride, and potassium bicarbonate, respectively. There were no significant differences in office blood pressure among the 3 treatment periods, and only 24-hour and daytime systolic blood pressures were slightly lower with potassium chloride. Compared with placebo, both potassium chloride and potassium bicarbonate significantly improved endothelial function as measured by brachial artery flow-mediated dilatation, increased arterial compliance as assessed by carotid-femoral pulse wave velocity, decreased left ventricular mass, and improved left ventricular diastolic function. There was no significant difference between the 2 potassium salts in these measurements. The study also showed that potassium chloride reduced 24-hour urinary albumin and albumin:creatinine ratio, and potassium bicarbonate decreased 24-hour urinary calcium, calcium:creatinine ratio, and plasma C-terminal cross-linking telopeptide of type 1 collagen significantly. These results demonstrated that an increase in potassium intake had beneficial effects on the cardiovascular system, and potassium bicarbonate may improve bone health. Importantly, these effects were found in individuals who already had a relatively low-salt and high-potassium intake.

Effect of Modest Salt Reduction on Skin Capillary Rarefaction in White, Black, and Asian Individuals With Mild Hypertension

Microvascular rarefaction occurs in hypertension. We carried out a 12-week randomized double-blind crossover trial to determine the effect of a modest reduction in salt intake on capillary rarefaction in 71 whites, 69 blacks, and 29 Asians with untreated mildly raised blood pressure. Both basal and maximal (during venous congestion) skin capillary density were measured by capillaroscopy at the dorsum and the side of the fingers. In addition, we used orthogonal polarization spectral imaging to measure skin capillary density at the dorsum of the fingers and the hand web. With a reduction in salt intake from 9.7 to 6.5 g/day, there was an increase in capillary density (capillaries per millimeter squared) from 101±21 to 106±23 (basal) and 108±22 to 115±22 (maximal) at the dorsum, and 101±25 to 107±26 (basal) and 110±26 to 116±26 (maximal) at the side of the fingers (P<0.001 for all). Orthogonal polarization spectral imaging also showed a significant increase in capillary density both at the dorsum of the fingers and the web. Subgroup analysis showed that most of the changes were significant in all of the ethnic groups. Furthermore, there was a significant relationship between the change in 24-hour urinary sodium and the change in capillary density at the side of the fingers. These results demonstrate that a modest reduction in salt intake, as currently recommended, improves both functional and structural capillary rarefactions that occur in hypertension, and a larger reduction in salt intake would have a greater effect. The increase in capillary density may possibly carry additional beneficial effects on target organs.

915 The second regional systolic shortening found in LV lateral wall motion is due to ventricular interaction and should not be used to infer late contraction in this wall when studying LV dysynchrony

Variations in regional systolic velocity profiles (SVP) have been widely used to assess cardiac dyssynchrony. However, regional longitudinal SVP have a non-uniform pattern. SVP in the septum (SEP) and inferior wall are similar being mono-phasic with an early systolic peak. In contrast, SVP in the anterior (ANT) and lateral (LAT) walls differ, being bi-phasic with two systolic peaks. Thus when assessing the timing of delayed contraction in the ANT and LAT walls it is important to know what each peak represents. Ventricular interaction could be responsible for the early deceleration of the first peak in ANT and LAT wall motion and could explain the bi-phasic systolic pattern. We postulated that early cessation of the first systolic motion and appearance of a second shortening motion in the LAT wall may be due either to a combination of cardiac twisting around the long axis of the heart and interaction with right ventricle (RV) contractility rather than local myocardial shortening. As regional strain rates (SR) but not velocities (VEL) reflect myocardial contractile function we investigated the relationship between regional peak systolic SR and SVP in the RV free wall, SEP and LAT wall. Methods: In 23 normals (age 45.5±2) long axis regional SVP and SR were obtained from the basal segments of RV, SEP and LAT. Time to max deceleration of the first peak was measured in the LAT and its relationship to RV peak SVP determined. In addition the time to peak VEL and SR in all walls was calculated. Results: The timing of peak SVP in the RV corresponded to the end of deceleration of the first peak in the LAT SVP (0.199±0.03 vs 0.197±0.03 s. p=NS). There was a consistent and significant difference between the time to peak systolic VEL in LAT vs RV (0.130±0.02 vs 0.199±0.03 s, p<0.001) with the SEP peak systolic VEL in an intermediate position at 0.154±0.03 s (p=NS vs RV and LAT). Systolic SR in all walls had a single peak which occurred in early systole with no significant difference between cardiac walls (0.100±0.02; 0.103±0.02; and 0.105±0.02 s in SEP, LAT and RV respectively). The second systolic peak in the LAT wall was not associated with any measurable deformation on the SR curve. Conclusions: This study showed that the early cessation of the first peak systolic VEL and second VEL peak in the LW wall is due to motion induced by RV contraction and does not represent LV contractile function. Furthermore, first rather second peak in LAT corresponds to peak systolic SR, which reflects true myocardial contraction. Therefore measurement of cardiac synchronization should not be based on SVP but rather on SR profiles.