P wave dispersion increases during hemodialysis sessions.

BACKGROUND/AIMS: Atrial fibrillation (AF) is common among hemodialysis (HD) patients and is associated with high mortality. P wave dispersion (PWD) is a noninvasive electrocardiographic marker of paroxysmal AF. Our aim was to evaluate the effect of HD session on PWD. METHODS: Twenty-five patients (mean age 63 years, 10 males) with sinus rhythm and undergoing chronic HD treatment were included. Blood samples were drawn and 12-lead electrocardiograms were recorded immediately before HD session, at the 2nd hour during HD and at the end of the HD session. The difference between maximum and minimum P wave durations was calculated as PWD. RESULTS: PWD significantly increased during HD sessions compared with predialysis values (41 +/- 12 vs. 21 +/- 10 ms, respectively, p < 0.001), then decreased to a value of 24 +/- 7 ms at the completion of HD, which was not significantly different from the predialysis values. PWD during HD was significantly correlated with predialysis systolic and diastolic blood pressure (r = 0.42, p = 0.037, and r = 0.59, p = 0.002, respectively) and predialysis serum potassium level (r = 0.44, p = 0.031). Linear regression model revealed that predialysis diastolic blood pressure (p = 0.002), predialysis serum potassium level (p = 0.037) and the amount of ultrafiltration (p = 0.048) were the significant predictors of prolonged PWD during HD. CONCLUSION: PWD increases significantly during HD sessions. This may increase the risk of AF episodes during HD. High diastolic blood pressure and serum potassium level before HD and ultrafiltration amount may predict prolonged PWD during HD.

QT dispersion increases during intubation in patients with coronary artery disease.

Anesthetic drugs have been shown to increase QT interval, however data regarding their effects on QT dispersion (QTd) are scarce, especially in patients with coronary artery disease (CAD). We tested whether induction of Anesthesia with thiopental and etomidate would increase QTd in patients with CAD. Thirty American Society of Anesthesiologists (ASA) physical status I-II patients without CAD were randomly allocated to groups I (n = 15) and II (n = 15) and 30 ASA physical status III patients with CAD were randomly allocated to groups III (n = 15) and IV (n=15). Anesthesia was induced with thiopental 5-7 mg/kg IV in groups I and III and with etomidate 0.2-0.3 mg/kg IV in groups II and IV. Endotracheal intubation was facilitated with vecuronium bromide 0.1 mg/kg IV. Twelve-lead electrocardiogram (ECG) was recorded in all patients at baseline (ECG(1)), 1 min after the induction agent (ECG(2)), 1 min (ECG(3)) and 5 min (ECG(4)) after intubation. Anesthesia was maintained with isoflurane and nitrous oxide in 34 % oxygen after ECG(2) recording. QTd and corrected QT dispersion (QTcd) were calculated. In patients with CAD induced with thiopental, QT dispersion increased significantly during the intubation period compared with baseline (from 43.0 +/- 25.6 ms to 69.2 +/- 25.3 ms; P <.01). Likewise, QT dispersion also increased during intubation in patients with CAD induced with etomidate (from 41.5 +/- 17.2 ms to 80.0 +/- 33.6 ms; P <.001). There was no increase in QT dispersion in patients without known CAD. QT dispersion seems to be increased during the intubation period in patients with CAD regardless of the induction agents used.

Acute stroke increases QT dispersion in patients without known cardiac diseases.

BACKGROUND: Electrocardiographic changes are well known to appear with acute cerebrovascular events. OBJECTIVE: To investigate if QT dispersion (QTd) is increased in patients who have an acute stroke and if this increase could be related to lesion extent and/or localization. DESIGN: The study group consisted of 36 patients who had an acute stroke and no history or signs of cardiovascular disease. An age-matched control group (n = 19) free of cardiovascular disease was also included. Simultaneous 12-lead electrocardiograms (ECGs) were recorded within the first 24 hours (24h-ECG) and after 72 hours (72h-ECG) from stroke onset. QT dispersion was assessed both manually and automatically with assessors blinded to the clinical data. RESULTS: QT dispersion, corrected QTd, and automated QTd were significantly increased in the 24h-ECG compared with the 72h-ECG (60 [range, 20-80] milliseconds vs 40 [range, 0-80] milliseconds, P<.005; mean [SD], 56 [19] vs 36 [21] milliseconds, P<.001; and 50 [range, 14-94] vs 34 [range, 0-84] milliseconds, P<.005, respectively). However, QTd in the 72h-ECG was similar to QTd in the control group. While in the 24h-ECG corrected QTd was significantly greater in patients with large infarcts and large hemorrhages (mean [SD], 70 [20] vs 51 [20] milliseconds, P<.05), in the 72h-ECG corrected QTd was greater in patients with right vs left-sided lesions (mean [SD], 39 [18] vs 24 [18] milliseconds, P<.05). CONCLUSIONS: QT dispersion is increased in the first 24 hours in patients with acute stroke and no cardiovascular disease compared with the control group. Although this finding seems to be related to the size of the lesion rather than to the localization or type of stroke, after 72 hours specific lesion localization could also influence the QTd.