N Parchure1, V Batchvarov, M Malik, A J Camm, J C Kaski. 1. Coronary Artery Disease Research Unit, Department of Cardiological Sciences, St George's Hospital Medical School, Cranmer Terrace, London SW17 0RE, UK.
Abstract
OBJECTIVES: We sought to compare QT dispersion in patients presenting with Prinzmetal's variant angina complicated by cardiac arrest or syncope and patients with uncomplicated variant angina. BACKGROUND: Despite the usually benign course of treated Prinzmetal's variant angina, a proportion of vasospastic angina patients develop ventricular arrhythmias and sudden death in association with coronary spasm. Increased QT dispersion has been suggested to increase susceptibility to ventricular arrhythmias in patients with coronary artery spasm. METHODS: We studied 25 consecutive patients (mean age 58 years; 14 men) with classical Prinzmetal's variant angina and documented coronary artery spasm. None of the patients had coronary artery stenoses < or =40%. Five patients had suffered a documented cardiac arrest, two had recurrent syncope and 18 had no arrhythmic events or syncopal episodes. In all patients QT dispersion (QT maximum-QT minimum in every ECG lead) was measured on the baseline 12-lead electrocardiogram at study entry using a digitising board. RESULTS: Mean (+/-S.D.) QT dispersion of study patients was 62.3+/-19.5 ms. QT dispersion in patients with cardiac arrest and syncope (79.4+/-17.3 ms) was significantly higher compared to patients with no such events (56.3+/-16.9 ms), (95% CI 7.5-38.8, P=0.005). No significant clinical, biochemical or angiographic differences were found between patients with and those without cardiac arrest or syncope. CONCLUSION: QT dispersion is increased in patients with Prinzmetal's variant angina complicated by cardiac arrest and syncope compared to patients without such events. Increased QT dispersion may be both a substrate for sudden cardiac death and a marker of risk in patients with Prinzmetal's variant angina.
OBJECTIVES: We sought to compare QT dispersion in patients presenting with Prinzmetal's variant angina complicated by cardiac arrest or syncope and patients with uncomplicated variant angina. BACKGROUND: Despite the usually benign course of treated Prinzmetal's variant angina, a proportion of vasospastic anginapatients develop ventricular arrhythmias and sudden death in association with coronary spasm. Increased QT dispersion has been suggested to increase susceptibility to ventricular arrhythmias in patients with coronary artery spasm. METHODS: We studied 25 consecutive patients (mean age 58 years; 14 men) with classical Prinzmetal's variant angina and documented coronary artery spasm. None of the patients had coronary artery stenoses < or =40%. Five patients had suffered a documented cardiac arrest, two had recurrent syncope and 18 had no arrhythmic events or syncopal episodes. In all patients QT dispersion (QT maximum-QT minimum in every ECG lead) was measured on the baseline 12-lead electrocardiogram at study entry using a digitising board. RESULTS: Mean (+/-S.D.) QT dispersion of study patients was 62.3+/-19.5 ms. QT dispersion in patients with cardiac arrest and syncope (79.4+/-17.3 ms) was significantly higher compared to patients with no such events (56.3+/-16.9 ms), (95% CI 7.5-38.8, P=0.005). No significant clinical, biochemical or angiographic differences were found between patients with and those without cardiac arrest or syncope. CONCLUSION: QT dispersion is increased in patients with Prinzmetal's variant angina complicated by cardiac arrest and syncope compared to patients without such events. Increased QT dispersion may be both a substrate for sudden cardiac death and a marker of risk in patients with Prinzmetal's variant angina.
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