Left ventricular function and calcium phosphate plasma levels in uraemic patients.

UNLABELLED: BACKGROUND. Recent investigations have focused on the pathogenetic role of disturbances of calcium phosphate metabolism in causing cardiovascular morbidity and mortality in haemodialysis patients. The aim of the present study was to assess left ventricular function and its relationship to phosphate and calcium plasma levels in stable uraemic patients on haemodialysis treatment. METHODS: Twenty uraemic patients (mean age 51+/-13 years) on maintenance haemodialysis and free from overt cardiac dysfunction, and 20 healthy volunteers underwent standard echocardiography, tissue Doppler-derived early (E(m)) and late (A(m)) diastolic velocities, tissue characterization with cyclic variations of integrated backscatter (CV-IBS), and serum biochemistry. RESULTS: With respect to tissue Doppler imaging (TDI), uraemic patients showed a lower E(m) peak, a higher A(m) peak, and a reduced E(m)/A(m) ratio of both interventricular septum and lateral wall (0.01>P<0.001) than controls. CV-IBS of both septum and posterior wall was significantly smaller in uraemic patients than in the control subjects (P<0.001). Moreover, the E(m)/A(m) ratio of septum and lateral wall were negatively related to serum phosphorus and to calcium phosphate product (P<0.001 for all). Accordingly, an inverse relationship was also found between CV-IBS of septum and lateral wall and calcium phosphate product and phosphorus (P<0.05 for all). CONCLUSIONS: These results showed early cardiac impairment of diastolic myocardial function evaluated by TDI and IBS analysis, and a close relationship between these changes and the calcium-phosphate plasma levels. These findings are well in keeping with the important role of hyperphosphataemia as a risk factor for cardiovascular damage, and justify the effort for optimal control of calcium phosphate metabolism in uraemic patients.

Antihypertensive effect of oral potassium aspartate supplementation in mild to moderate arterial hypertension.

BACKGROUND: Previous studies showed that potassium chloride (48-120 mmol/day) supplementation reduced arterial blood pressure (BP) in hypertensive patients. OBJECTIVES: Our aim was to evaluate the effect of a lower dose of potassium aspartate salt on BP in individuals with essential arterial hypertension. METHODS: One hundred and four patients (65 males, age 53 +/- 12 years) with mild to moderate essential hypertension (systolic/diastolic BP 154.2/96.2 +/- 10.8/5.4 mmHg) were allocated in two comparable groups of 52 to receive or not 30 mmol/day per os of potassium aspartate supplementation for four weeks. Office and 24-h BP, as well as serum and urinary electrolytes, were measured at baseline and at the follow-up visit after four weeks. RESULTS: Office and 24-h BP did not change in the control group, while these values were significantly reduced in the potassium supplementation group. Changes in office (systolic BP: 154.4 +/- 8.2 vs. 142.2 +/- 7.6 mmHg; diastolic BP: 95.0 +/- 5.6 vs. 87.2 +/- 4.3 mmHg, P < 0.001 for both) and 24-h BP (systolic BP: 142.7 +/- 8.2 vs. 134.8 +/- 6.3 mmHg; diastolic BP: 90.8 +/- 4.4 vs. 84.6 +/- 3.8 mmHg, P < 0.001 for both) following potassium supplementation were highly significant. The changes in day time and night time BP were similar. The treated group showed significantly increased potassium serum level and 24-h urinary excretion of potassium (P < 0.01 in both cases) after four weeks, while the untreated group showed no significant changes of the same parameters. Urinary Na/K ratio decreased significantly with potassium supplementation (P < 0.001). In the treated group changes in office (r = 0.58, P < 0.001) and 24-h SBP (r = 0.51, P < 0.001), but not in DBP (r = 0.29 and r = 0.25, n.s.), correlated positively with the urinary Na/K ratio at baseline. CONCLUSIONS: A relatively low supplementation of 30 mmol/day of potassium as aspartate lowered office and 24-h ambulatory BP in subjects with mild to moderate essential hypertension. The antihypertensive effect was sustained throughout the day, and was greater in the patients with high basal urinary Na/K ratio.

Effect of oral potassium supplementation on QT dispersion in anorexia nervosa.

UNLABELLED: The aim of this study was to evaluate the degree of QT dispersion in a group of young women with anorexia nervosa and its changes after oral potassium supplementation. Twenty-eight patients with self-induced starvation were matched with 20 thin and 20 normal-weight women (body mass index > or = 20). All participants underwent a complete clinical examination, including electrocardiogram (ECG) for QT interval measurements. QT dispersion was defined as the difference between the longest and the shortest QT interval occurring in the 12-lead ECG. QT dispersion was corrected (QTc) with Bazett's formula. Anorexic patients were later allocated two subgroups of 14 to receive or not to receive potassium aspartate (2 vials K-Flebo d(-1) = 60 mEq d(-1), per os). ECG was repeated in both the subgroups of anorexic patients after 4 wk. QT dispersion was significantly greater in starving patients than in thin or normal-weight women (QT dispersion = 62.2 +/- 12.4 vs 33.4 +/- 7.1 or 31.7 +/- 6.3ms; QTc dispersion = 56.5 +/- 12 vs 34 +/- 9.1 or 33.2 +/- 11 ms, p < 0.001). After 4 wk, anorexic women treated with oral potassium aspartate supplementation, compared with untreated patients. showed an increased kalaemia (4.21 +/- 0.16 vs 3.91 +/- 0.32 mmol 1(-1), p < 0.05) and a significant reduction in the QT interval dispersion (QT dispersion = 44.2 +/- 8.1 vs 63.2 +/- 9.1 ms, QTc dispersion = 41.3 +/- 9.7 vs 57.4 +/- 9 ms, p < 0.001). CONCLUSION: Patients with anorexia nervosa have greater QT dispersion than constitutionally thin and normal-weight women, and oral potassium supplementation tends to reduce it. This suggests that the reduction in the pool of potassium may be the critical factor inducing the enhancement of the QT dispersion in anorexia nervosa.

Effective blood pressure treatment improves LDL-cholesterol susceptibility to oxidation in patients with essential hypertension.

OBJECTIVES: LDL-cholesterol particles from hypertensive patients exhibit enhanced susceptibility to in vitro oxidation, an abnormality thought to increase cardiovascular risk. We tested whether blood pressure (BP) normalization can reverse this abnormality. DESIGN: Double-blind, randomized pharmacological intervention trial. SETTING: Clinical research centre. Subjects. A total of 29 nondiabetic, normolipidaemic patients with essential hypertension (BP= 151 +/- 3/99 +/- 1 mmHg) and 11 normotensive controls (BP=125 +/- 3/85 +/- 1 mmHg) matched for gender, age, obesity, glucose tolerance and lipid profile. Intervention. Anti-hypertensive treatment for 3 months with a calcium-antagonist in randomized combination with either an ACE inhibitor or a beta-blocker. MAIN OUTCOME MEASURES: Lag phase of copper-induced LDL oxidation, cell-mediated (human umbilical vein endothelium) generation of malondialdehyde (MDA) by LDL and vitamin E content in LDL. RESULTS: At baseline in hypertensives versus controls, lag phase was shorter (89 +/- 3 vs. 107 +/- 6 min, P < 0.04), MDA generation was higher (5.8 +/- 0.1 vs. 5.1 +/- 0.2 nmol L(-1), P=0.002), and vitamin E was reduced (6.40 +/- 0.05 vs. 6.67 +/- 0.11 microg mg(-1), P=0.03). At 3 months, BP was normalized (124 +/- 3/81 +/- 1, P < 0.0001 vs. baseline, P=ns versus controls), lag phase was prolonged (to 98 +/- 3 min, P=0.0005), MDA generation was reduced (5.6 +/- 0.1 nmol L-1, P = 0.001), and vitamin E was increased (6.53 +/- 0.05 microg mg(-1), P=0.003), with no significant differences between the randomized groups. CONCLUSIONS: In nondiabetic, nonobese, normolipidaemic patients with essential hypertension, LDL susceptibility to copper- and cell-mediated oxidation is increased. BP normalization is associated with a significant improvement, but not a full reversal, of this abnormality.