The Study Of Relations Between QT Dispersion Of AMI Patients And Emergency Percutaneous Coronary Intervention And The Infarct Size

QT dispersion is defined as the difference between the maximum andminimum QT interval duration on standard 12-lead electrocardiograms(ECGs), and has a correlation with the regional variation of ventricularrepolarization. QT intervals reflect the times of ventricular depolarizationand repolarization. The QT intervals vary signifantly among individualleads of the surface ECG, which reflect the difference of repolarization atdifferent cardiac muscle regions. The QTd increase when the blood supplyof cardiac muscle is absence.The QT dispersion increase in many diseasesincluding: coronary heart disease especial acute myocardialinfarction(AMI),maligant arrhythmia,chronic congestive heart failure,hypertension,mitral valve prolapse,congenital long QT syndrome,diabetes and so on. AMI can arose electrical instability because of partialischemic,scathe and ncerosis pathological changes, lead to QT dispersionincreasing, and result in severe arrhythmia. It has been known that earlyperfusion can decrease QT dispersion of AMI. Percutaneous coronaryintervention (PCI) is a conservative means of dilatating coronary artery,solving the narrow and improving blood supply of cardiac muscle.Emercency PCI (EPCI) is an intervention treament within 12 hours ofAMI, which is the most effective means of reaching early perfusion now.But the study of internal and external literature is absence about the effectof EPCI on QT dispersion, and the reports of relationship between QTdispersion of AMI patients'ECGs and infarct size are seldom, and at thesame time the reports are not in accordance. 180 patients of AMI werestudied retrospectively. The study group included 60 patients with AMIwho were treated with EPCI and 60 patients didn't accepted EPCI. 30healthy cases were employed as controls. In order to evaluate thedifference of QT dispersion (QTcd) between acute myocardial infarction(AMI) patients and the healthy cases. AMI patients who accepted theEPCI were observed changes of the QT dispersion (QTd) and correctedQT dispersion (QTcd) prior to and after interventional therapy.Forecasting the relation between QTd (QTcd) of 120 AMI patients whodidn't accept EPCI and the infarct size estimated by the peak creatinephosphokinase. Result: The QTcmax of AMI patients was more increased thanhealthy controls (466.5±29.7ms vs 417.8±27.3ms) (P<0.01), and theQTd,QTcd ofAMI patients was also more increased than healthy controls(71.6±30.1ms,79.3±34.7ms vs 36.0±12.4ms,40.9±13.3ms respectively)(P<0.01). But QTcmin hadn't obvious difference between AMI andhealthy controls (388.6±34.7ms vs 376.9±30.4ms) (P>0.05). QTd inpatients with AMI who acceped EPTCA (for every period of QTd afterMI) was significantly more shortened than the controls who unacceptedEPTCA (63.3±24.3ms, 59.6±22.5ms 44.9±13.3ms, 40.0±9.26 ms vs74.7±34.5ms, 75.8±27.9ms, 78.2±33.4ms, 75.4±29.3ms at 1D, 2D, 3D,1W respectively) (p<0.05), and the QTcd also educed the same conclusion(70.9±28.3ms, 66.5±24.8ms, 50.8±16.1ms, 44.0±11.2ms vs 83.8±39.6ms,84.3±31. 4ms, 87.9±36.6ms, 84.8±33.3ms at1D, 2D, 3D, 1W respectively)(P<0.05). The group who acceped EPTCA concluded that QTd(63.3±24.3ms vs 70.5±25.6ms) and QTcd (70.9±28.3 ms vs 77.8±29.8ms)hadn't obvious difference between before and after the 1st day of EPTCA(P>0.05). But the QTd of the 2nd day,3rd day and 1st week after EPTCAwas obvious shortened than that prior to EPTCA (59.6±22.5ms,44.9±13.3ms, 40.0±9.26ms vs 70.5±25.6ms) (P<0.05) and the QTcdeduced the same conclusion (66.5±24.8ms, 50.8±16.1ms, 44.0±11.2ms,2D, 3D, 1W respectively) (P<0.05). There were significant positivecorrelations between QTd (r=0.454, p<0.01) or QTcd (r=0.437, p<0.01)and the infarct size evaluated by peak creatine phosphokinase levels. The QTcmax,QTd and QTcd of AMI patients were more increasedthan the healthy controls,but the QTcmin had no significant differencewith the healthy controls. So I think that the QTmax is a leading station inthe mechanism of QTd. Succeeding melting and PCI can renew occlusivecoronary artery, which can increase blood,oxygen for cardiac muscle,renew the metabolizing function and electric activity of hibernatingcardiac muscle cells, improve the inhomogeneity of ventricular recoverytimes and decrease QT dispersion. EPCI can resume repusion early. Butthe failure reperfusion may lead to QT dispersion increasing. I study thechanges of QTd within 3 days and one week of PCI of AMI patients. Myopinion about this study is that QT dispersion is a simple and noneintruding method to evaluate the effect of early repusion of AMI. Creatinephosphokinase begin to increase within 6 hours of AMI, and get to thepeak at 24 hours, the number is 2~10 times of the normal upper limit, and...