The effects of ischemia and reperfusion on QT interval dispersion (QTD: QTmax-QTmin in the 12-lead ECG) were analyzed in 15 patients (12 males, 57 +/- 13 years) undergoing coronary angioplasty (PTCA). All patients had single-vessel coronary artery disease (only one > or = 85% stenosis in a major coronary artery) and normal left ventricular function. All were in sinus rhythm with normal atrioventricular and intraventricular conduction on the surface ECG. No patient was on therapy that could affect the QT interval. The ECG was recorded (all 12 leads simultaneously) at 50 mm/s speed before the first balloon inflation, at the end of the first inflation during PTCA, and at 30" and 60" during reperfusion following the first inflation. In order to avoid ischemic preconditioning, only recordings of the first inflation were used. In each tracing QTmax and QTmin were evaluated. All values were rate corrected using a simple linear equation (QT linear corrected = QT + 0.154 [1-RR]). QTD increased significantly during both ischemia and reperfusion. QTmax was not changed by ischemia and was increased by reperfusion. QTmin was reduced by ischemia and increased by reperfusion. These results indicate that both ischemia and reperfusion alter ventricular repolarization, inducing a less homogeneous ventricular recovery pattern.
Abstract.In this paper we prove that a unipotent automorphism group
This study evaluated: (1) if three orthogonal leads can provide the same information about QT dispersion (QT-D) as 12-lead ECG; (2) the circadian pattern of QT-D adopting 3-OL during 24hour Holter monitoring; (3) if the QT-D circadian pattern is influenced by therapy. In the first part of the study, we evidenced a significant direct correlation (r = 0.91; P < 0.0005) between QT-D values of 12 ECG leads and of 3-OL simultaneously recorded in 15 normal subjects and 11 patients with myocardial infarction. The second part of the study evaluated the circadian pattern of QT-D adopting 3-OL during Holter (ELA Medical, Mod. Synesis) monitoring in 15 patients with congestive heart failure (CHF: aged 73 t 8 yrs, Ill NYHA) in pharmacological washout and after 10 days of therapy (furosemide, digoxin, captopril) and in 15 age-matched normal subjects (N: aged 70 ? 3 yrs). Mean QT-D values of CHF before therapy were significantly higher at each hour than those of N (always P < 0.001). Mean hourly QT-D values after therapy were significantly lower than those before therapy (P < 0.03 up to P < O.OOl), except for the value at 9:00 A.M. Our results suggest that: (1) 3-OL can evaluate QT-D as much as the usual 12-lead ECG; (2) the use of 3-OL during Holter monitoring allows the evaluation of the QT dispersion circadian pattern both in N and in CHF; and (3) therapy is able to modify the circadian pattern of QT-D. A.N.E. 1998;3(1):32-37 QT dispersion; heart fa i I u re Address for reprints: Antonio Michelucci, M.D.al. Circadian Pattern of the QT Dispersion 33Holter monitoring; and (3) how the circadian pattern of QT-D could be useful in controlling the effects of therapy.
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