Course and prognostic implications of QT interval and QT interval variability after primary coronary angioplasty in acute myocardial infarction.

OBJECTIVES The aim of this study was to determine the influence of early reperfusion on the course of QT interval and QT interval variability in patients undergoing primary percutaneous transluminal coronary angioplasty (PTCA) in acute myocardial infarction (AMI) and its prognostic implications on major arrhythmic events during one-year follow-up. BACKGROUND Although early coronary artery recanalization by primary angioplasty is an established therapy in AMI, a substantial number of patients is still threatened by malignant arrhythmias even after early successful reperfusion, which may be caused by an inhomogeneity of ventricular repolarization despite reperfusion. METHOD Temporal fluctuations of ventricular repolarization were studied prospectively in 97 consecutive patients with a first AMI by measurements of QT interval and QT interval variability during and after successful PTCA (Thrombolysis in Myocardial Infarction flow grades 2 and 3). Continuous beat-to-beat QT interval measurement was performed from 24-h Holter monitoring, which was initiated at admission before PTCA. RESULTS Reperfusion caused a significant continuous increase of mean RR interval (738 +/- 98 to 808.5 +/- 121 ms; p < 0.001) and a significant decrease of parameters of QT interval (QTc: 440 +/- 32 to 416.5 +/- 37ms; p < 0.001) and QT interval variability (QTcSD: 27.5 +/- 3 to 24.9 +/- 6 ms; p < 0.001) in the majority of patients. However, in patients with major arrhythmic events at the one-year follow-up (sudden cardiac death, ventricular fibrillation or sustained ventricular tachycardia, n = 15), parameters of QT interval remained unaltered after successful reperfusion (QTc: 447.3 +/- 41 to 432.9 +/- 45 ms, p = NS; QTcSD: 35.1 +/- 13.4 to 29.0 +/- 9.1 ms, p = NS). CONCLUSIONS Reduction of QT interval and QT interval variability after timely reperfusion of the infarct-related artery may be a previously unreported beneficial mechanism of primary PTCA in AMI, indicating successful reperfusion.

[1]  F. Van de Werf,et al.  Impaired myocardial tissue perfusion early after successful thrombolysis. Impact on myocardial flow, metabolism, and function at late follow-up. , 1995, Circulation.

[2]  J P Huberty,et al.  Microvascular injury in reperfused infarcted myocardium: noninvasive assessment with contrast-enhanced echoplanar magnetic resonance imaging. , 1998, Journal of the American College of Cardiology.

[3]  P. Schwartz,et al.  QT interval prolongation as predictor of sudden death in patients with myocardial infarction. , 1978, Circulation.

[4]  H. S. Mueller,et al.  The Thrombolysis in Myocardial Infarction (TIMI) trial. Phase I findings. , 1985, The New England journal of medicine.

[5]  Felix Zijlstra,et al.  Clinical value of 12-lead electrocardiogram after successful reperfusion therapy for acute myocardial infarction , 1997, The Lancet.

[6]  P. Thorén,et al.  Activation of left ventricular receptors with nonmedullated vagal afferent fibers during occlusion of a coronary artery in the cat. , 1976, The American journal of cardiology.

[7]  A. Jaffe,et al.  Sudden death and its relation to QT-interval prolongation after acute myocardial infarction: two-year follow-up. , 1986, The American journal of cardiology.

[8]  G. Dagenais,et al.  Revascularization after myocardial infarction. , 1999, Circulation.

[9]  E. Prystowsky,et al.  Influence of the autonomic nervous system on the Q-T interval in man. , 1982, The American journal of cardiology.

[10]  C. Vrints,et al.  Determinants and prognostic implications of persistent ST-segment elevation after primary angioplasty for acute myocardial infarction: importance of microvascular reperfusion injury on clinical outcome. , 1999, Circulation.

[11]  H. Bazett,et al.  AN ANALYSIS OF THE TIME‐RELATIONS OF ELECTROCARDIOGRAMS. , 1997 .

[12]  E. Gilpin,et al.  Prognostic importance of QTc interval at discharge after acute myocardial infarction: a multicenter study of 865 patients. , 1984, American heart journal.

[13]  J. Bourke,et al.  Reduction in incidence of inducible ventricular tachycardia after myocardial infarction by treatment with streptokinase during infarct evolution. , 1990, Journal of the American College of Cardiology.

[14]  J. Willerson,et al.  Reduced Myocardial Reflow and Increased Coronary Vascular Resistance following Prolonged Myocardial Ischemia in the Dog , 1975, Circulation research.

[15]  G Baumann,et al.  Autonomic Effects of Dipyridamole Stress Testing on Frequency Distribution of RR and QT Interval Variability , 1998, Pacing and clinical electrophysiology : PACE.

[16]  Q Xue,et al.  Algorithms for computerized QT analysis. , 1998, Journal of electrocardiology.

[17]  MasatsuguHori,et al.  Clinical Implications of the ‘No Reflow’ Phenomenon , 1996 .

[18]  H. Calkins,et al.  Beat-to-beat QT interval variability: novel evidence for repolarization lability in ischemic and nonischemic dilated cardiomyopathy. , 1997, Circulation.

[19]  Hc. Bazett An analysis of the time relationships of the heart , 1920 .

[20]  A. Michelucci,et al.  Effects of Ischemia and Reperfusion on QT Dispersion During Coronary Angioplasty , 1996, Pacing and clinical electrophysiology : PACE.

[21]  A Malliani,et al.  A sympathetic reflex elicited by experimental coronary occlusion. , 1969, The American journal of physiology.

[22]  R. Campbell,et al.  QT dispersion and components of the QT interval in ischaemia and infarction. , 1995, British heart journal.

[23]  Jan Pool,et al.  QTc Prolongation Measured by Standard 12‐Lead Electrocardiography Is an Independent Risk Factor for Sudden Death Due to Cardiac Arrest , 1991, Circulation.

[24]  D. Wyse,et al.  Effect of coronary angioplasty on precordial QT dispersion. , 1997, The American journal of cardiology.

[25]  M Malik,et al.  Agreement and reproducibility of automatic versus manual measurement of QT interval and QT dispersion. , 1998, The American journal of cardiology.

[26]  R. M. Conant,et al.  Autonomic Disturbance at Onset of Acute Myocardial Infarction , 1972, British medical journal.

[27]  W. Ganz,et al.  The thrombolysis in myocardial infarction (TIMI) trial. , 1985, The New England journal of medicine.

[28]  C. Sylvén,et al.  Cardiac repolarization properties during standardized exercise test as studied by QT, QT peak and terminated T-wave intervals. , 1989, Clinical physiology.

[29]  E. Braunwald,et al.  Cardiovascular Reflexes Stimulated by Reperfusion of Ischemic Myocardium in Acute Myocardial Infarction , 1983, Circulation.

[30]  M. Hori,et al.  Clinical implications of the 'no reflow' phenomenon. A predictor of complications and left ventricular remodeling in reperfused anterior wall myocardial infarction. , 1996, Circulation.

[31]  P. Coumel,et al.  Changes in Repolarization Dynamicity and the Assessment of the Arrhythmic Risk , 1997, Pacing and clinical electrophysiology : PACE.

[32]  S. Juul-Möller,et al.  Corrected QT-interval during one year follow-up after an acute myocardial infarction. , 1986, European heart journal.

[33]  Y. Hirota,et al.  Prominent negative T waves with QT prolongation indicate reperfusion injury and myocardial stunning. , 1992, Journal of cardiology.

[34]  A Murray,et al.  Accuracy of four automatic QT measurement techniques in cardiac patients and healthy subjects. , 1996, Heart.

[35]  E. Braunwald,et al.  Myocardial reperfusion, limitation of infarct size, reduction of left ventricular dysfunction, and improved survival. Should the paradigm be expanded? , 1989, Circulation.

[36]  E. Braunwald,et al.  Ultrastructural Evidence of Microvascular Damage and Myocardial Cell Injury After Coronary Artery Occlusion: Which Comes First? , 1980, Circulation.

[37]  D. Kromhout,et al.  The incidence of suspected myocardial infarction in Dutch general practice in the period 1978-1994. , 1998, European heart journal.