QT Dispersion in Acute Myocardial Infarction with Special Reference to Left Ventriculographic Findings

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1 QT Dispersion in Acute Myocardial Infarction with Special Reference to Left Ventriculographic Findings Yoshitaka DOI, M.D., Kazuyuki TAKADA, M.D., Hiroyuki MIHARA, M.D., Tomoki KAWANO, M.D., Osamu NAKAGAKI, M.D., Shigeru OGAWA, M.D., and Kikuo ARAKAWA, M.D.* SUMMARY QT and QT dispersion, which is the time difference between QT maximum and QT minimum, were evaluated in 22 patients with anterior myocardial infarction approximately one month after onset. The purpose of this study was to observe how LV wall motion abnormality is related to these variables. Twenty age-matched patients without overt heart disease were also studied as a control group. QT and QT max in patients with acute myocardial infarction (AMI) were markedly prolonged compared to those in normal controls (472.8 }48.0, }32.1 vs }18.8, and }21.0 msec, respectively). QT dispersion and QTc dispersion in patients with AMI were significantly more prolonged than in normal controls (111.2 }33.9, }32.9 vs 54.3 }15.0, and 60.3 }17.2msec, respectively). QT dispersion has a positive correlation with QT max in AMI patients. Ejection fraction (EF) of the left ventricle was relatively well maintained in cases where only one segment of the left anterior ventricular wall was impaired in its motion. It decreased, however, in accordance with the extent of wall motion abnormality. QT max and QTc max were prolonged as the number of LV wall segments with impairment increased. This, however, was not statistically significant. QT dispersion and QTc dispersion had no relation to the extent of LV wall motion abnormality nor to EF of the left ventricle. In conclusion, no definite relationships between QT dispersion (QTc dispersion) and EF of the left ventricle, or between these variables and the extent of left ventricular wall motion abnormality were found in patients with anterior myocardial infarction in our study. Although both QT max and QT dispersion were prolonged in patients with myocardial infarction, this suggests that electrical heterogeneity or regional variation in electrical ventricular recovery did not always parallel the severity of mechanical abnormality of the left ventricle. (Jpn Heart J 36: , 1995) From the Department of Internal Medicine, Saiseikai Fukuoka General Hospital, Fukuoka, Japan and *Department of Second Internal Medicine, Fukuoka University, Fukuoka, Japan. Address for correspondence: Yoshitaka Doi, M.D., Department of Internal Medicine, Saiseikai Fukuoka General Hospital, , Tenjin, Chuo-ku, Fukuoka 810, Japan. Received for publication March 30, Accepted June 28,

2 574 DOI ET AL Jpn Heart J September 1995 Key words: QT dispersion Acute myocardial infarction Left ventriculography T prolongation and its dispersion, which is defined as the time difference between QT maximum and QT minimum measured from a standard 12-lead ECG, are known to be prolonged in acute myocardial infarction, reflecting regional variation in ventricular recovery.1-4) QT dispersion is thought to represent electrical heterogeneity in the myocardium. A greater QT dispersion is reported in long QT syndrome and in patients with heart failure in relation to sudden death.5-9) In acute myocardial infarction QT dispersion depends on reperfused status and the size of infarction of the myocardium.8) Longer QT and greater QT dispersion are thought to be arrhythmogenic, the longer their duration, the greater the susceptability to ventricular arrhythmias.2,5,8,9) On the other hand, ventricular arrhythmias are often seen in myocardial infarction with ventricular aneurysm10,11) Considering these factors, we tried to evaluate if there was any relationship among electrical instability, ventricular wall motion abnormality and ventricular function in anterior myocardial infarction after one month from the onset of the symptom. METHODS AND SUBJECTS Twenty-two patients with acute anterior myocardial infarction admitted to our hospital between 1988 and 1993 were studied retrospectively. Other patients on antiarrhythmic drugs which might prolong the QT interval, patients with bundle branch block, WPW or intraventricular conduction defect, or patients without any appropriate ECG or left ventriculography (LVG) available were excluded from this study. The ECG was recorded with a multichannel recorder which could record 3 leads or more simultaneously at a speed of 25mm/sec. The ECGs taken nearest to the day of LVG and coronary angiography (CAG) were selected (32 }6.2 days after onset of acute myocardial infarction (AMI) for ECG, and 35.1 }12 days for LVG and CAG). The QT interval was measured for at least 3 consecutive beats in each of 12 leads and averaged. The QT interval was defined as the time interval between the beginning of the QRS and the end of the T wave where the T wave returned to the electrical base line. Leads where the QT interval was not clearly measureable were excluded from analysis. QT was corrected using Bazett's formula. QT dispersion was obtained from the time difference between QT maximum and QT minimum measured in 12 leads, and QTc dispersion was calculated in the same way using QTc interval. LVG, in the right anterior oblique view, was studied according to the AHA definition by two doctors independently. EF was calculated by computer with the center line method.

3 Vol 36 No 5 QT DISPERSION IN ACUTE MYOCARDIAL INFARCTION 575 As a control group, twenty age-matched people were selected from our hospital employees and patients who visited our hospital for annual health examinations who were free of any heart diseases. They were all in sinus rhythm without bundle branch block or intraventricular conduction abnormality. Statistical analysis was done with simple linear regression analysis and with one-way ANOVA followed by Scheffe's test to compare the separate group means when the F ratio was significant. A p value less than 0.05 was defined as significant. RESULTS As seen in the Table, QTmax, QTcmax, QT dispersion and QTc dispersion were significantly more prolonged in patients with acute myocardial infarction than in normal controls (472.8 }48.0, }32.1, }33.9, Table 1. Variables Studied in Normal Subjects (Control) and in Patients with Myocardial Infarction (AMI). msec }SD. QT max = maximal QT interval among all 12 ECG leads; QTc max = maximal QTc interval; QTD = QT dispersion; QTcD = QTc dispersion. Figure 1. The correlation between QTmax and QT dispersion (QTD) and between QTcmax and QTc dispersion (QTcD) among AMI patients. A positive correlation between them suggests that patients with longer QT intervals have larger QT dispersions.

4 576 DOI ET AL Jpn Heart J September 1995 Figure 2. The comparison of EF of the left ventricle among patients with various degrees of LV segmental wall motion abnormalities by left ventriculography. EF was well maintained in cases where only one segment of the left ventricular wall was impaired in its motion. It decreased, however, in accordance with the extent of wall motion abnormality. Figure 3. The comparison of QT max and QTc max among patients with various degrees of LV wall motion abnormalities by left ventriculography. QT max and QTc max were prolonged as the number of LV wall segments with impairment increased. This was, however, not statistically significant }32.9 msec vs }18.8, 418 }21.0, 54.3 }15.0 and 60.3 }17.2msec, respectively). Figure 1 shows that QT dispersion had a positive correlation with QTmax in patients with myocardial infarction. Figure 2 demonstrates how EF of the left ventricle was relatively well maintained in cases where only one segment of the left anterior ventricular wall was

5 Vol 36 No 5 QT DISPERSION IN ACUTE MYOCARDIAL INFARCTION 577 Figure 4. The comparison of QTD and QTcD among patients with various degrees of LV wall motion abnormalities by left ventriculography. QT or QTcD was not influenced by the extent of LV wall motion abnormality. Figure 5. The correlation between EF and QTmax, and between EF and QTc max. There were no correlations, suggesting that EF was not a major determinant in the degree of QT prolongation. impaired in its motion. It decreased, however, in accordance with the extent of wall motion abnormality. QTmax and QTcmax were prolonged as the number of LV wall segments with impairment increased. This was, however, not statistically significant as seen in Figure 3. QTmax and QT dispersion did not have any relation to the extent of LV wall motion abnormality or to left ventricular EF by LVG as shown in Figures 4, 5, and 6.

6 578 DOI ET AL Jpn Heart J September 1995 Figure 6. The correlation between EF and QTD, and between EF and QTcD. There were no correlations, indicating that EF was not related to QTD or QTcD. DISCUSSION Several problems were encountered while measuring the QT interval. These included difficulty in determining the end of the T wave, in differentiation from U wave, in avoidance of the influence of HR, and in selection of leads.1,11, The QT interval measurement was done according to Campbell's method.1) The QT interval was defined as the time interval from the beginning of the QRS and the end of the T wave where the T wave returned to the TP baseline. When the T wave was biphasic, the time of the final return to baseline was measured. In the case of difficulty in determining the end of the T wave due to isoelectric or low amplitude T wave in some leads, measurements of the QT interval in those leads were not done. Moreno et al calculated the QT dispersion when the T wave was measured in more than 5 leads which they thought was the lower limit of number of leads per ECG.3) Day et al used adjusted QT dispersion calculated as QT dispersion / square root of the number of measurable leads to correct for the influence of the number of measurable leads on QT dispersion.6) Fortunately, there were no ECG records which had more than two leads with unmeasureable QT in 12 leads in our series, probably because we measured the QT interval manually. Although QT dispersion, interlead variation of QT interval on the 12-lead ECG, was thought to represent electrical myocardial heterogeneity, there is an argument against estimating QT dispersion from standard a 12-lead ECG implying that it must simply be the difference in the direction of the electrical vector.1) Cowan et al and Higham et al reported that the QT dispersion obtained from a

7 Vol 36 No 5 QT DISPERSION IN ACUTE MYOCARDIAL INFARCTION lead ECG was not due to the difference in the electrical vector, and that QT dispersion was more prolonged in AMI with ventricular arrhythmia than in AMI without arrhythmia.1) They suggested that prolonged QT dispersion obtained from a conventional ECG stood for electrical heterogeneity. Today it is well accepted to measure QT dispersion from a standard 12-lead ECG.9) The controls in our study revealed the QT dispersion to be slightly longer than that found by Higham et al4) and Linker et al7) (54.3 }15 v.s }14 and 43 }12msec). It was, however, almost comparable with those reported by others (54 }20 by Moreno et al3)), 54 }27 by Sylven et al,13) 59 }12.3 by Mirvis et al,14) 48 }18 by Cowan et al1)). It is apparent that a faster recording speed such as 50mm/sec and more was preferable for this kind of study,1,3,4,7,13,14) so that more minute changes would be appreciated. However, since the value of QT dispersion in our controls driven from an ECG recorded at 25mm/sec coincided with other studies, and as the difference between controls and patients with AMI was significant with this paper speed, there seems to be no problem using a 25mm/ sec speed in determining QT dispersion in clinical practice. Ventricular arrhythmias are one of the ominous signs of myocardial infarction. It is very important to recognize the appearance and the character of ventricular arrhythmias as early as possible. QT prolongation is seen in many diseases such as long QT syndrome, mitral valve prolapse, asymmetric septal hypertrophy and torsade de pointes due to various causes, and is reported to be a risk factor for ventricular arrhythmias and sudden death.15) Saikawa et al reported that in acute myocardial infarction QT remained prolonged for days or several months depending on the state of coronary arterial reperfusion. With successful reperfusion QTc became shorter and EF of LV was relatively well preserved compared with that in patients with unsuccessful reperfusion.16) QT dispersion has also been reported recently in several conditions such as AMI, long QT syndrome, congestive heart failure and hypertrophic cardiomyopathy related to arrhythmias or sudden death.1,3) Day et al found that the QT dispersion was a slightly different variable from the QT interval in terms of variability in ventricular repolarization. They reported that although sotatol prolonged the QT interval as much as the long QT syndrome, the QT dispersion was smaller in patients receiving sotatol than in patients with long QT syndrome. This indicated that the state of regional variation of electrical recovery was not the same in the case of sotatol treatment as it was in the case of patients with long QT syndrome.5) Therefore it is clinically important to study QT dispersion as well as QT interval in order to evaluate the repolarization in more detail. Cowan et al did not find any significant difference in the QT dispersion between patients with anterior myocardial infarction and in patients with inferior myocardial infarction.1) Moreno et al, however, did recognize significant prolon-

8 580 DOI ET AL Jpn Heart J September 1995 gation of QT dispersion in patients with anterior myocardial infarction compared with those with inferior myocardial infarction.3) A reasonable expanation for this remains uncertain. The effect of antiarrhythmic drugs on the QT dispersion must be considered in patients with AML We excluded patients with antiarrhythmic drugs which might prolong the QT interval from our study. Ĉ adrenergic antagonists have been reported to shorten the QT interval15), and to have no influence on the QT dispersion.7) To the best of our knowledge, the effect of calcium antagonists on QT dispersion has not clearly been demonstrated. Histologically there is said to be varying degrees of scar tissue mixed with normal tissue in the infarct region. This histological heterogeneity brings about the electrical inhomogeneity forming re-entrant pathways which make it possible to induce ventricular arrhythmias. In addition, it is well known that patients with ventricular aneurysms are prone to ventricular arrhythmias.9) The QT dispersion after a myocardial infarction depends on the coronary arterial reperfusion state as reported by Moreno et al.3) We hypothesized that there must be some relationship between the QT dispersion and the LV wall motion abnormality in AMI. However, we could not find any correlation between either the QT dispersion (QTc dispersion) and the EF of LV, or between the QT dispersion (QTc dispersion) and the extent of LV wall motion abnormality. There appear to be several explanations for this: 1) Some discrepancy must exist between the infarct size determined by the biochemical method and the extent of left ventricular wall motion abnormality by the LVG, even though Moreno et al mentioned that QT dispersion depended on biochemically estimated infarct size. 2) Electrical heterogeneity was not always parallel to ventricular wall motion abnormality. 3) The study group was too small to reveal statistical significance. 4) The period of examination of ECG and CAG in this study differed from that in previous studies. 5) Furthermore, the lack of correlation may depend on the reperfused state of the myocardium after AMI. In our study, we evaluated the relationship between QT dispersion and LV function irrespective of the reperfused state of the coronary artery. REFERENCES 1. Cowan JC, Yusoff K, Moore M, Amos PA, Gold AE, Bourke JP, Tansuphaswadikul S, Campbell RWF: Importance of lead selection in QT interval measurement. Am J Cardiol 61: 83, Schwartz PF, Wolf S: QT prolongation as predictor of sudden death in patients with myocardial infarction. Circulation 57: 1074, Moreno FL, Villanueva MT, Karagounis LA, Anderson JL, for the TEAM-2 study investigators: Reduction in QF interval dispersion by successful thrombolytic therapy in acute myocardial infarction. Circulation 90: 94, Higham PD, Furniss SS, Campbell WRF: QT dispersion in ischemia and infarction; a marker of

9 Vol 36 No 5 QT DISPERSION IN ACUTE MYOCARDIAL INFARCTION 581 primary ventricular fibrillation? Eur Heart J 12 (Suppl): 87, 1991 (abstract) 5. Day CP, McComb JM, Campbell RW: QT dispersion; an indication of arrhythmia risk in patients with long QT intervals. Br Heart J 63: 432, Day CP, McComb JM, Campbell RW: QT dispersion in sinus beats and ventricular extrasystoles in normal hearts. Br Heart J 67: 39, Linker NJ, Colona P, Kekwick CA, Till J, Camm AJ, Ward DE: Assessment of QT dispersion in symptomatic patients with congenital long QT syndromes. Am J Cardiol 69: 634, Barr CS, Naas A, Freeman M, Lang CC, Struthers AD: QT dispersion and sudden unexpected death in chronic heart failure. Lancet 343: 327, Moller M: QT interval in relation to ventricular arrhythmias and sudden cardiac death in post myocardial infaction patients. Acta Med Scand 210: 73, Krilder DM, Perelman M, Rowland ER: Ventricular tachycardia and ventricular fibrillation. In Cardiac Arrhythmias; Their Mechanisms, Diagnosis and Management, ed by Mondal WJ, Second ed, J.B. Lippincott Co., Philadelphia, p 517, Schweitzer P: The values and limitations of the QT interval in clinical practice. Am Heart J 124: 1121, Todt H, Krumpel G, Krejcy K, Raberger G: Mode of QT correction for heart rate; implications for the detection of inhomogenous repolarization after myocardial infarction. Am Heart J 124: 602, Sylven JC, Horacek BM, Spencer A, Klassen GA, Montague TJ: QT interval variability on the body surface. J Electrocardiol 17: 179, Mirvis DM: Spacial variation of QT intervals in normal persons and patients with acute myocardial infarction. J Am Coll Cardiol 5: 625, Ahnve S, Gilpin E, Madsan EB, Froelicher V, Henning H, Ross J Jr: Prognostic importance of QTc interval at discharge after acute myocardial infarction; a multicenter study of 865 patients. Am Heart J 108: 395, Saikawa T, Niwa H, Maeda T, Shimoyama N, Kohmatsu K, Tonda K, Yonemochi H, Hara M: Serial changes in QT interval during the course of acute ischemic episode; with special reference to intracoronary electrograms. Jpn J Clin Pathol 39: 801, 1991