Beat-to-beat QT interval variability is primarily affected by the autonomic nervous system.

BACKGROUND: Beat-to-beat QT interval variability is associated with life-threatening arrhythmias and sudden death, however, its precious mechanism and the autonomic modulation on it remains unclear. The purpose of this study was to determine the effect of drugs that modulate the autonomic nervous system on beat-to-beat QT interval. METHOD: RR and QT intervals were determined for 512 consecutive beats during fixed atrial pacing with and without propranolol and automatic blockade (propranolol plus atropine) in 11 patients without structural heart disease. Studied parameters included: RR, QTpeak (QRS onset to the peak of T wave), QTend (QRS onset to the end of T wave) interval, standard deviation (SD) of the RR, QTpeak, and QTend (RR-SD, QTpeak-SD, and QTend-SD), coefficients of variation (RR- CV, QTpeak-CV, and QTend-CV) from time domain analysis, total power (TP; RR-TP, QTpeak-TP, and QTend-TP), and power spectral density of the low-frequency band (LF; RR-LF, QTpeak-LF, and QTend-LF) and the high-frequency band (HF; RR-HF, QTpeak-HF and QTend-HF). RESULTS: Administration of propranolol and infusion of atropine resulted in the reduction of SD, CV, TP, and HF of the QTend interval when compared to controlled atrial pacing (3.7 +/- 0.6 and 3.5 +/- 0.5 vs 4.8 +/- 1.4 ms, 0.9 +/- 0.1 and 0.9 +/- 0.1 vs 1.2 +/- 0.3%, 7.0 +/- 2.2 and 7.0 +/- 2.2 vs 13.4 +/- 8.1 ms(2), 4.2 +/- 1.4 and 4.2 +/- 1.2 vs 8.4 +/- 4.9 ms(2), respectively). Administration of propranolol and atropine did not affect RR interval or QTpeak interval indices during controlled atrial pacing. CONCLUSIONS: Beat-to-beat QT interval variability is affected by drugs that modulate the autonomic nervous system.

Sodium channel blockers enhance the temporal QT interval variability in the right precordial leads in Brugada syndrome.

BACKGROUND: Temporal QT interval variability is associated with sudden cardiac death. The purpose of this study was to evaluate temporal QT interval variability in Brugada syndrome (BS). METHODS: We measured QT and RR intervals in precordial leads (V(1)-V(6)) based on 12-beat resting ECG recordings from 16 BS patients (B group) with spontaneous ST elevation in right precordial leads (V(1)-V(2)) and from 10 patients with normal hearts (C group). We measured the response in B group before and after administration of pilsicainide (1 mg/kg). The standard deviation (QT-SD, RR-SD) of the time domain and total frequency power (QT-TP, RR-TP) were calculated for all precordial leads, and the latter was to analyze the frequency domain. RESULTS: The right precordial leads in BS exhibited an additional and prominent ST elevation (coved-type) after pilsicainide administration. Both QT-SD and QT-TP values were significantly more increased in B, than in C (5.1 +/- 1.2 vs 3.6 +/- 0.2 and 23.4 +/- 2.9 vs 12.3 +/- 1.7 msec(2), P < 0.01, respectively) and after pilsicainide administration in B. (5.1 +/- 0.4 vs 3.9 +/- 0.3, 25.8 +/- 3.4 vs 16.3 +/- 2.6 msec(2), P < 0.01, respectively) However, QT-SD and QT-TP did not significantly change in any of other leads (V(3)-V(6)) and RR-SD and RR-TP were similar for both groups, as well as after intravenous pilsicainide administration in B. CONCLUSIONS: The temporal QT interval variability was identified in BS. Moreover, sodium channel blocker induced temporal fluctuation in QT interval and it may possibly provide a substrate for ventricular arrhythmia in BS patients.

Correlation between beat-to-beat QT interval variability and impaired left ventricular function in patients with previous myocardial infarction.

BACKGROUND: Beat-to-beat QT interval variability (QTV) is associated with sudden cardiac death and New York Heat Association functional class severity. We sought to evaluate the relationship between QTV and left ventricular (LV) function in patients with previous myocardial infarction (MI). METHODS: Fifty-nine patients with previous anterior MI were enrolled. LV ejection fraction (EF), LV end-systolic volume index (LVESVI), and LV end-diastolic volume index (LVEDVI) were measured by LV contrast angiography. QT interval was measured by automated analysis of 512-beat records of 12-lead electrocardiogram. The mean interval, standard deviation and variance in RR and QT intervals, and the QT variability index (QTVI) were calculated for each patient using two leads that corresponded with and without the infarction site. High-frequency power, low-frequency power, total-frequency power, and the ratio of low-frequency to high-frequency power in RR and QT intervals were calculated. RESULTS: While measured indices of RR intervals and indices of QT intervals, which did not correspond with the infarction site, did not correlate with differences in LV function, measured indices of QT intervals, which corresponded with the infarction site, did correlate with differences in LV function. However, there were no correlations between the ratio of low-frequency to high-frequency power in QT intervals and EF or LVEDVI. Correlations between QTVI and LV function were observed, particularly between QTVI and LVESVI (r = 0.712, P < 0.0001). CONCLUSION: In patients with previous anterior MI, there was variability in temporal dispersion of QT interval and a strong correlation between QTV corresponded with the infarcted site and LV function.

Circadian variation of beat-to-beat QT interval variability in patients with prior myocardial infarction and the effect of beta-blocker therapy.

BACKGROUND: Recent studies have demonstrated that increased QT interval variability (QTV) is associated with a greater susceptibility to ventricular arrhythmias and that patients with prior myocardial infarction (MI) were prone to ventricular arrhythmias during the daytime. The goal of the present study was to investigate the circadian variation of the QTV and to determine whether beta-blocker therapy improves the temporal fluctuation of the ventricular repolarization in patients with MI. METHODS: The study population consisted of 15 MI patients who had not received beta-blocker therapy, 11 MI patients who had received beta-blocker therapy, and 12 healthy subjects. Twenty-four hour Holter monitoring was obtained, and the RR and QT intervals were calculated automatically from 512 consecutive sinus beats for every 2 hours. RESULTS: In the daytime, the QT-SD was significantly greater in the MI group than in the healthy subjects (P<0.01), but there was no difference in the QT-SD when comparing the beta-blocker group to the control group. Moreover, the QT variability index and the QT variance normalized for the mean QT were similar pattern with QT-SD. The heart rate variability did not significantly differ when compared between the three study groups. CONCLUSION: These data indicate that the QTV increases during the daytime in patients with MI and that this circadian effect is prevented by beta-blocker therapy. Thus, beta-blocker therapy may reverse the maladaptation of the ventricular repolarization to the change in the heart rate and may thereby reduce the ventricular arrhythmias and decrease the mortality in patients with MI.

Discordant repolarization alternans-induced atrial fibrillation is suppressed by verapamil.

BACKGROUND: Ventricular alternans of repolarization produces serious ventricular arrhythmias in experimental models. The present study investigated the role of alternans of atrial repolarization in patients with atrial fibrillation (AF). METHODS AND RESULTS: Electrophysiological studies were performed in 19 patients without structural heart disease. Monophasic action potentials (MAP) were recorded with 2 Franz catheters during steady state pacing, starting at a cycle length (CL) of 400 ms with subsequent decrements of 10 ms. Duration from the onset of upstroke to 90% repolarization of the MAP were measured. If discordant alternans (DA) was present during pacing, verapamil was administrated, and MAP measurements were repeated. Rapid pacing resulted in concordant alternans to DA in 13 of 19 (68%) patients. AF was initiated after the induction of DA in 8 of 13 patients (p=0.012). Verapamil treatment resulted in a significant decrease in the longest pacing CL at which DA was induced (207+/-19 vs 178+/-17 ms, p<0.0001). CONCLUSIONS: Rapid atrial pacing induced DA and was associated with initiation of AF. Furthermore, induction of DA was suppressed by verapamil. Reducing the spatiotemporal repolarization heterogeneity may be how the calcium-channel blockade prevents initiation of AF.

Depiction of residual emboli following pulmonary embolism with thrombotic scintigraphy.

BACKGROUND: In the treatment of pulmonary embolism (PE), the presence of residual emboli is known to seriously affect the recurrence and prognosis. We attempted to depict the residual emboli in the subacute stage of PE using indium-111-oxine labeled platelet scintigraphy (In-plt). METHODS: In-plt was performed on 22 patients with PE who showed an improvement according to lung perfusion scintigraphy. Their accumulation was assessed along with the blood coagulation ability measured on the same day. In addition, radioisotope venography (RI-veno) was performed simultaneously with In-plt to measure the circulatory findings in the lower limb for comparison. All patients received systemic heparin during the acute stage and received warfarin at the time of testing. RESULTS: Accumulation of In-pit was observed in 7 patients (32%), and positive signals were found in the lower limbs or pelvic cavity in all cases. Two patients were suspected of having poor lower limb circulation from their RI-veno findings, and these findings were largely consistent with the areas of In-plt accumulation. DISCUSSION: Some emboli persist after extensive anti-coagulation therapy. The use of In-pit is effective in determining the therapeutic measures and assessing the prognosis as this method allows us to clearly depict the existence of such emboli.

Wavelet transform analysis of heart rate variability to assess the autonomic changes associated with spontaneous coronary spasm of variant angina.

We used Wavelet transform (WT) to investigate whether variation in autonomic tone was associated with spontaneous coronary spasm in patients with variant angina by analysis of heart rate variability (HRV). Twenty-one episodes preceding ST-segment elevation were selected under Holter monitoring in 12 men and 3 women with variant angina. HRV indices were calculated at 10 second intervals with the continuous WT, and analyzed within 30 minutes preceding ST-segment elevation. High frequency (HF; 0.15 approximately 2.00 Hz) increased significantly during the 4 minutes prior to ST-segment elevation, low frequency (LF; 0.04 approximately 0.15 Hz) decreased significantly during the period from 10 to 5 minutes and increased significantly during the 2 minutes prior to ST-segment elevation, the LF/HF ratio decreased significantly during the period from 10 to 3 minutes and increased significantly during the 2 minutes prior to ST-segment elevation. The RR interval decreased significantly during the 2 minutes prior to ST-segment elevation. These results suggest that the acute variation in autonomic tone was associated with spontaneous coronary spasm in patients with variant angina. A reduction in sympathetic activity, then enhancement of vagal activity may play a key role in triggering the spontaneous coronary spasm, and the secondary activation of sympathetic activity may worsen the coronary spasm resulting in the attack.