[QT dispersion in insulin-dependent diabetics]. / QT dispersione nei diabetici insulino-dipendenti.

BACKGROUND: The measurement of the dispersion of the QT interval reflects regional repolarization differences in the heart which in turn can elicit the onset of arrhythmias by means of re-entry mechanism. Therefore, inter-lead QT dispersion has been proposed as novel indicator of arrhythmogenic risk that can predict severe ventricular arrhythmias or sudden death. The present study was conducted to evaluate QT dispersion in diabetic insulin-dependent patients with autonomic neuropathy. METHODS: We recruited three groups of 10 patients with the same age, sex, body weight distribution: 1) group DAN+ (diabetics with neuropathy); 2) group DAN- (diabetics without neuropathy); and 3) group CTRL (healthy control group). The patients underwent two-dimensional color-Doppler echocardiography and 12-lead electrocardiogram, 25 and 50 mm/s paper speed (gain 10 mm/mU). The QTc dispersion was determined as the difference between the maximum and the minimum value of the QTc interval in different leads of the ECG recording. QT interval was corrected (QTc) by heart rate according to the Bazett's formula. Cardiovascular autonomic function was evaluated by Ewing's tests (heart rate and blood pressure measurement during lying to standing, deep breathing, hand-grip isometric stress test and Valsalva's maneuver). RESULTS: QT dispersion was significantly greater (p < 0.01) in the patients with autonomic neuropathy (51 +/- 10 ms) than in the patients without autonomic neuropathy (29 +/- 6 ms) or in healthy control subjects (26 +/- 5 ms). CONCLUSIONS: Our data suggest that diabetic neuropathy, associated with an increased QT dispersion, shows a higher risk for serious ventricular arrhythmias and sudden cardiac death.

Potassium removal increases the QTc interval dispersion during hemodialysis.

This study was planned to clarify the mechanism(s) by which hemodialysis increases the QTc dispersion, a marker of risk of ventricular arrhythmias. To this aim, 10 uremic patients, without any relevant heart diseases, underwent two different types of hemodialysis schedules. In the first, 1 h of isolated high rate ultrafiltration preceded the standard diffusive procedure. In the second, during the first hour of standard bicarbonate hemodialysis, the decrease of plasma potassium concentration was prevented by increasing K+ concentration in the dialysate, according to its pre dialysis plasma levels. During the high rate ultrafiltration period, together with ECG signs of increased sympathetic nervous system activity and catecholamines secretion, the QTc dispersion did not change significantly. Instead, an evident increment was observed 1 h after the start of the diffusive hemodialysis, then slowly progressing until the end of the dialysis and finally returning to the pre dialysis values within 2 h after the end of the session. To the contrary, the increase of the QTc dispersion was totally blunted during a standard hemodialysis procedure in absence of plasma K+ decrease, but appeared again when the K+ dialysate fluid concentration was restored to 2 mmol/l. This study provides evidence that the increase of QTc dispersion occurring on hemodialysis is mainly related to the diffusive process, more precisely to the K+ removal. This is one more reason to focus attention on K+ removal rate especially when hemodialysis treatment is given in uremics affected by cardiac diseases with high risk of arrhythmias.

Effect of hemodialysis on the dispersion of the QTc interval.

The QTc dispersion reflects the underlying regional heterogeneity of the recovery of the ventricular excitability, thereby it is considered as a novel marker of risk of ventricular arrhythmias. Because a higher incidence of ventricular arrhythmias is described during and after hemodialysis, the aim of this study has been to evaluate the QTc dispersion before and after uncomplicated hemodialysis session. Twenty chronic uremics without heart failure, ischemic heart disease or dialysis hypotension were selected. The QTc dispersion was determined as the difference between the longer and the shorter QTc interval measured on a 12-lead electrocardiogram. Following the hemodialysis session, the QTc dispersion increased from 30 +/- 9 to 54 +/- 17 ms (p < 0.001) associated with the expected reduction of potassium and magnesium and with the increase of extracellular calcium concentration. However, no correlation has been observed between the QTc dispersion increase and the degree of the intradialytic changes of plasma electrolytes, blood pressure or body weight. In summary, the hemodialysis treatment per se does induce an increase of the QTc dispersion, likely due to the rapid changes of electrolyte plasma concentrations. This can potentially contribute to the arrhythmogenic effect of the hemodialysis procedure, reflecting an enhanced regional heterogeneity of ventricular repolarization. The clinical importance of the increase of QTc dispersion as risk factor of ventricular arrhythmias, particularly in hemodialyzed patients suffering from ischemic or hypertrophic heart diseases, should be the matter of further investigations.

Cutaneous vasodilation to acetylcholine in patients with essential hypertension.

Endothelium-dependent vasodilation is reduced in the forearm of patients with essential hypertension. To evaluate whether endothelium-dependent vasodilation is also reduced in the skin microcirculation of patients with essential hypertension, we evaluated the effect of acetylcholine, an endothelium-dependent vasodilator, and sodium nitroprusside, an endothelium-independent vasodilator, on cutaneous and total forearm blood flow in normotensive subjects (n = 8) and matched patients with essential hypertension (n = 9). We infused acetylcholine (0.15, 0.45, 1.5, 4.5, and 15 microg/100 ml forearm tissue/min) and sodium nitroprusside (1, 2, and 4 microg/100 ml forearm tissue/min) into the brachial artery, and we measured cutaneous blood flow (laser Doppler flowmeter) and muscle blood flow (strain-gauge venous plethysmography) modifications. Both the cutaneous and muscle blood flow increases induced by acetylcholine were reduced in patients with essential hypertension as compared with normotensive controls, whereas the skin and muscle vasodilation induced by sodium nitroprusside was similar in the two groups of patients. These data confirm the impairment of endothelium-dependent vasodilation in the muscle vascular bed of patients with essential hypertension and demonstrate the presence of endothelial dysfunction in skin microcirculation.

Laser Doppler flowmeter assessment of skin microcirculation in uremic patients on hemodialysis treatment.

Vascular disease is frequent in uremics and may contribute to tissue malnutrition and damage. The aim of this study was to detect whether uremic patients show also changes of microcirculation and to evaluate the effects induced by hemodialysis (HD) session. Eleven uremics on HD (7 males, 4 females, aged 25-65 years) were studied; 11 healthy subjects, age- and sex-matched, served as controls. Skin microcirculatory basal flow (BF), maximal postischemic flow (PIF-max) and flow motion index (FMI) were determined at the upper limb contralateral to arteriovenous fistula, by means of a laser Doppler flowmeter. The measurements were taken before, at 1 and 2 h after starting HD and 30 min after the end of HD. In uremics, FMI was lower than in controls (mean +/- SD: 15.2 +/- 13.6 vs. 29.1 +/- 7.4%; p < 0.005); just 1 h after the start of HD, a significant improvement (28.4 +/- 17.7%; p < 0.01) versus basal values was observed and it persisted throughout the HD session. No statistical correlation was observed between the changes of FMI and those of plasma levels of Na+, K+, HCO-3, urea, iPTH or rate of ultrafiltration. BF and PIF-max were similar in uremics and controls, and no changes were observed during HD. Our study shows that the physiological flow motion is reduced in the skin microcirculation of uremics on HD. This abnormality is rapidly corrected by HD.