Noriyoshi Yamawake

Increased QT dispersion in patients with vasospastic angina.

BACKGROUND The risk factors for ventricular arrhythmias in patients with coronary vasospasm have not been identified. We evaluated QT dispersion in patients with vasospastic angina and its relation to susceptibility to ventricular arrhythmias during myocardial ischemia and reperfusion. METHODS AND RESULTS We assessed the corrected QT (QTc) dispersion before induction of coronary artery spasm by intracoronary injection of acetylcholine (baseline) and 30 minutes after administration of isosorbide dinitrate in 50 patients with vasospastic angina and 50 patients with atypical chest pain. The baseline QTc dispersion was significantly greater in patients with vasospastic angina than in patients with atypical chest pain (mean+/-SD: 69+/-24 versus 44+/-19 ms, 95% confidence interval of mean difference [CI]: 16 to 33 ms; P<0.001). QTc dispersion decreased significantly, to 48+/-15 ms (CI: 15 to 26 ms; P<0.001 versus baseline), after administration of isosorbide dinitrate in patients with vasospastic angina but did not change significantly in patients with atypical chest pain (mean+/-SD: 41+/-17 ms, CI: -3 to 9 ms). During the provocation test, 24 of 50 patients with vasospastic angina experienced ventricular arrhythmias. The baseline QTc dispersion was significantly greater in patients with than without ventricular arrhythmias (mean+/-SD: 77+/-23 versus 61+/-19 ms, CI: 4 to 26 ms; P<0.05). CONCLUSIONS Patients with vasospastic angina exhibited an increased baseline QTc dispersion compared with patients with atypical chest pain, which suggests that inhomogeneity of repolarization and susceptibility to ventricular arrhythmias are increased in patients with vasospastic angina, even when asymptomatic. The association between increased QTc dispersion and ventricular arrhythmias during the provocation test suggests that measurement of QT dispersion may help predict which patients with vasospastic angina are at high risk for ventricular arrhythmias during ischemia.

Effects of glucose-induced insulin secretion on ST segment elevation in the Brugada syndrome.

Introduction: ST segment elevation in patients with Brugada syndrome is known to fluctuate occasionally, influenced by multiple factors. Insulin has been shown to affect QT dispersion in healthy volunteers, as well as result in abnormality of ventricular repolarization in patients with congenital long QT syndrome.

Association of insulin with QTc dispersion

1 Ravindran R, Priddy S. Uvular edema, a rare complication of endotracheal intubation. Anesthesiology 1978; 48: 374. 2 Stubbing JF. Anaesthetic morbidity from trauma to the uvula. Anaesthesia 1990; 45: 886–87. 3 Commings DJ, Whittet H, Okoli UC, Ewart M. Postintubation uvular necrosis. Anaesthesia 1994; 49: 457–58. 4 Seigne TD, Felske A. Uvular oedema. Anesthesiology 1978; 49: 375–76. 5 Kranz MA, Solomon DL, Poulos JG. Uvular necrosis following endotracheal intubation. J Clin Anaesthesiol 1994; 6: 139–41.

Induction of polymorphic ventricular tachycardia by programmed ventricular stimulation in vasospastic angina pectoris.

This study was designed to examine the ventricular vulnerability of patients with vasospastic angina. Fourteen patients (mean age 57 +/- 9 years) with vasospastic angina underwent electrophysiologic testing during the asymptomatic phase (baseline) and after the relief of acetylcholine-induced spasm with isosorbide dinitrates. Twenty patients without structural heart disease served as a control group. By programmed ventricular stimulation, polymorphic ventricular tachycardia (VT) was induced at baseline in 6 of 14 patients, with 1 patient developing ventricular fibrillation and 7 of 14 patients developing repetitive ventricular responses. After isosorbide dinitrate, polymorphic VT was induced in only 1 patient who had ventricular fibrillation at baseline. Repetitive ventricular responses were induced in 3 of 5 patients who had VT at baseline and in 4 of the 7 patients with repetitive ventricular responses at baseline. There was a significant difference in the incidences and severity of induced ventricular arrhythmias between the 2 phases (p <0.01). Among 20 control subjects, repetitive ventricular responses were induced only in 6 patients, but no VT was induced. There was a significant difference in the incidence of induced ventricular arrhythmias and VT at baseline between the vasospastic angina and control groups (p <0.001 and <0.01, respectively). Thus, patients with vasospastic angina had increased ventricular vulnerability, even during the symptom-free period without ischemic events, which could predispose to the development of life-threatening arrhythmias aggravated by vasospastic attacks.

Increased QTc dispersion predicts lethal ventricular arrhythmias complicating coronary angioplasty

This study found that increased QT dispersion just before angioplasty is an useful marker to predict the risk for lethal ventricular arrhythmias during angioplasty. The fact that successful coronary revascularization decreased QT dispersion suggested that a part of increased QT dispersion is related to myocardial ischemia.

Influence of Meals on Variations of ST Segment Elevation in Patients with Brugada Syndrome

Background: Glucose‐induced insulin secretion is one of the contributing factors to fluctuation of ST segment elevation in Brugada syndrome.

Effect of Dipyridamole on QT Dispersion in Vasospastic Angina Pectoris

Life-threatening ventricular arrhythmias have frequently been documented in patients with vasospastic angina. Moreover, the incidence of ventricular arrhythmias has been closely associated with increased QT dispersion. However, the underlying mechanism responsible for this arrhythmogenesis has not been clarified. The effects of dipyridamole and subsequent aminophylline administration on QT dispersion were examined in 35 patients with vasospastic angina and 30 patients with atypical chest pain. None of the patients enrolled in this study revealed any significant stenosis in coronary angiography. QT dispersion during dipyridamole followed by aminophylline administration was compared between the 2 groups. The baseline QT dispersion was similar in both groups (vasospastic angina: 27 +/- 8 ms; atypical chest pain: 28 +/- 7 ms). No significant changes in QT dispersion were observed in patients with atypical chest pain by dipyridamole (23 +/- 9 ms) and subsequent aminophylline administration (23 +/- 5 ms). However, the QT dispersion in patients with vasospastic angina increased significantly by dipyridamole administration (53 +/- 14 ms, p <0.0001) and returned to baseline by subsequent aminophylline administration (26 +/- 10 ms). Our data suggest that the disparity of ventricular repolarization in vasospastic angina may be mediated by increased endogenous adenosine.

Autonomic and pharmacological responses of idiopathic ventricular tachycardia arising from the left ventricular outflow tract.

Background: It is well recognized that the mechanism of idiopathic ventricular tachycardia (VT) arising from the right ventricular outflow tract (RVOT) is mostly due to cyclic AMP‐mediated triggered activity. The mechanism of VT arising from the left ventricular outflow tract (LVOT) has not been well clarified whether it is the same as VT of RVOT.

Ambulatory Electrocardiogram-Based T-Wave Alternans in Patients With Vasospastic Angina During Asymptomatic Periods

T-wave alternans (TWA) is a useful method for evaluating repolarization abnormalities and as a predictor of life-threatening ventricular arrhythmias. Although life-threatening ventricular arrhythmias are occasionally observed during ischemic attacks in patients with vasospastic angina (VSA), there have been no studies to detect repolarization abnormalities using TWA analysis in these patients during the asymptomatic phase. The aim of this study was to analyze modified moving average (MMA) TWA using Holter recordings in 40 patients with VSA and in 40 control subjects. The incidence of positive TWA was higher in the VSA group than in the control group (24 of 40 [60%] vs 0 of 40 [0%], p <0.01). The value of the maximum MMA TWA was also greater in the VSA group than in the control group (68.6 ± 21 vs 34.0 ± 11 μV, p <0.01). In the VSA group, although there was no significant difference in maximum MMA TWA values between patients with multiple- and single-vessel spasm, patients with ventricular tachycardias had higher values than those without (83.0 ± 15 vs 65.9 ± 20 μV, p <0.05). Patients taking calcium channel blockers exhibited decreased values of maximum MMA TWA compared with subjects not taking these drugs (73.8 ± 18 vs 59.5 ± 21 μV, p <0.05). In conclusion, high values and incidences of TWA events were observed in patients with VSA. In the VSA group, maximum values of MMA TWA were high in patients with ventricular tachycardias but decreased in those taking calcium channel blockers. The results suggest that the patients with VSA during asymptomatic phases exhibit repolarization abnormalities leading to a potential risk for life-threatening arrhythmias.

ST-T wave changes in a patient complicated with vasospastic angina and Brugada syndrome: differential responses to acetylcholine in right and left coronary artery

A 49-year-old man with chest pain and syncope presented saddleback or occasionally coved type ST elevation in V1–V3. Coronary spasm in the left anterior descending artery was induced by acetylcholine injection and ST elevation changed from saddleback to coved type in V2–V3 together with ST depression in V4–V5, whereas acetylcholine injection into the right coronary artery did not provoke spasm, but induced augmented and coved type ST elevation in V2 without ST-T changes in V4–V5. These electrocardiographic changes in response to acetylcholine administration into each coronary artery are compatible with pathogenesis of vasospastic angina and Brugada syndrome, respectively.