A Comparison of Electrocardiographic Changes During Reperfusion of Acute Myocardial Infarction by Thrombolysis or Percutaneous Transluminal Coronary Angioplasty

Xander H.T. Wehrens, MSc, Pieter A. Doevendans, MD, PhD, Ton J. Oude Ophuis, MD, PhD, Hein J.J. Wellens, MD, PhD, FACC, Department of Cardiology, University Hospital Maastricht, Cardiovascular Research Institute, Maastricht, The Netherlands.

Am Heart J. 2000;139(3) 

In This Article


Clinical Data

In total, 108 patients with a mean age of 59 years admitted for an acute myocardial infarction were included in this study. All patients are characterized by documented successful reperfusion therapy of the infarct-related coronary artery, achieved by thrombolytic therapy (A), primary PTCA (B), or a combination of both (rescue PTCA; C). All 3 groups were comparable with respect to mean age, sex, and cardiac history and did not differ significantly in infarct localization and enzyme release, the severity of coronary artery disease, and TIMI flow after reperfusion. However, the mean duration of pain from onset of symptoms until reperfusion was significantly shorter in patients receiving only thrombolytic therapy (group A) compared with patients undergoing primary (B) and rescue PTCA (C) (P < .001). Excluding the 20 patients referred to our institute for primary PTCA, the difference in time interval was still statistically significant (3.5 ± 1.4 vs 2.0 ± 1.0 hours; P < .01). The time interval from onset of symptoms until peak of the serum glutamic oxaloacetic transaminase levels was significantly longer in group B compared with group A. No differences were noted in the use of anticoagulant therapy (aspirin and heparin; data not shown). The baseline clinical characteristics of the patients are listed in Table I.

ST-Segment Analysis

Illustrative electrocardiographic tracings at the moment of reperfusion are shown in Figure 1, A through C. Typically, ST-segment deviation was the first electrocardiographic change after coronary artery reperfusion. ST-segment normalization was documented in 84% (A), 61% (B), and 64% (C) of patients after reperfusion (Table II). In patients undergoing a PTCA, it was observed that normalization of the ST segment typically took <5 minutes after the moment of reperfusion. Interestingly, an increase (temporary) in ST-segment deviation was seen significantly more often in patients receiving thrombolytic therapy (59%) compared with patients undergoing a primary or rescue PTCA (12% and 5%, respectively; P < .05). Terminal T-wave inversion was seen in 57% vs 64% of the tracings. Only 12 (11%) of 108 patients showed no ST-segment changes upon reperfusion of the infarct-related artery. Comparing patients in whom reperfusion was achieved within or after 3 hours of ischemia, ST-segment normalization occurred significantly more often in patients with fast reperfusion (75% vs 45%; P < .05). In Table III, electrocardiographic changes after reperfusion are compared for TIMI grades 2 and 3 flow in the infarct-related coronary artery. ST-segment changes occurred significantly more often in conjunction with TIMI grade 3 flow after reperfusion (94% vs 71%; P < .05; Table III).

A, Typical electrocardiographic changes indicating reperfusion during thrombolytic therapy. Alteration intervals (time from start therapy) show acute anterior myocardial infarction, increase of ST-segment deviation, terminal negative T waves, AIVR, and electrocardiogram during coronary angiography. B, Reperfusion in inferior wall myocardial infarction induced by contrast injection. Note development of AIVR ST-segment normalization and terminal negative T waves. C, Reperfusion during rescue PTCA. Note ST-segment normalization, terminal T-wave inversion, and appearance of ventricular premature complexes.

Reperfusion Arrhythmias

In most patients with reperfusion arrhythmias, an increase in the number of ventricular premature complexes was the first arrhythmic event to occur. A 2-fold increase in the number of ventricular premature complexes after reperfusion of the infarct-related artery was observed in 55% (A), 52% (B), and 41% (C) of patients (Table II). In addition, AIVR developed in 45 (42%) patients and nonsustained ventricular tachycardia developed in 8 (7%). Atrial (6%) and ventricular (3%) fibrillation occurred less frequently. Transient slow heart rate was observed in 19 (18%) patients; sinus bradycardia was seen most often (n = 15). In 14 patients, no arrhythmias occurred after reperfusion. In a comparison of patients with TIMI grades 2 and 3 flow through the infarct-related artery after reperfusion, no differences were observed in the occurrence of arrhythmias (Table III). In patients in whom reperfusion arrhythmias developed, serum creatine kinase (CK) levels were significantly higher compared with patients without arrhythmias (3145 ± 2032 vs 2090 ± 1138 U/L; P < .05). This difference in serum CK levels could not be explained by preexisting differences in ST-segment deviations before reperfusion.

Influence of Infarct Location

The ST-segment changes and arrhythmias were not dependent on the location of myocardial infarction, with bradycardia being the only exception. Transient slow heart rates occurred significantly more often in the setting of an inferoposterior (31%) than in anterior (4%) myocardial infarction (P < .01).


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