Usefulness of frequent arrhythmias after epicardial recanalization in anterior wall acute myocardial infarction as a marker of cellular injury leading to poor recovery of left ventricular function.
Ventricular arrhythmias are associated with epicardial reperfusion but may also be a sign of cellular injury, which affects recovery of left ventricular (LV) function. To assess the correlation between reperfusion arrhythmias and the change in LV function after the acute phase in reperfused acute myocardial infarction (AMI), 62 patients with reperfused anterior wall AMI were studied. All patients underwent 24-hour Holter recording, echocardiography, and coronary angiography during the acute phase of AMI. Echocardiography was repeated at 1 to 2 months after AMI. Correlations between ventricular arrhythmias in the reperfusion phase and the change in LV wall motion score (WMS) during follow-up were studied. The number of reperfusion arrhythmias was significantly higher in patients with further deterioration of LV function; there were 5-, 14-, 131-, and 11-fold increases in isolated premature ventricular complexes (PVCs), PVCs in couplets, PVCs in bigeminy, and total PVCs, respectively, in patients with further increases in WMS after the acute phase. The incidence of repetitive, frequent, and early accelerated idioventricular rhythms (AIVRs) was correlated significantly with the change in LV function, with 129- and 105-fold increases in numbers of early AIVRs and total AIVRs, respectively, in patients with further worsening of LV function during follow-up. The incidence and the number of long-lasting nonsustained ventricular tachycardias as well as the number of rapid ventricular tachycardias and total ventricular tachycardia episodes were also correlated significantly with further deterioration. Thus, frequent arrhythmias associated with epicardial reperfusion strongly correlate with further worsening of LV function after the acute phase of AMI. This supports the hypothesis that these reperfusion arrhythmias are probably a noninvasive marker of cellular injury.
Engelen
Domien J
DJ
Department of Cardiology, University Hospital Maastricht, Cardiovascular Research Institute Maastricht, Maastricht, The Netherlands. dengelen@diakhuis.nl
Gressin
Virginie
V
Krucoff
Mitchell W
MW
Theuns
Dominic A
DA
Green
Cindy
C
Cheriex
Emile C
EC
Maison-Blanche
Pierre
P
Dassen
Willem R
WR
Wellens
Hein J
HJ
Gorgels
Anton P
AP
D000328:Adult; D000368:Aged; D015906:Angioplasty, Balloon, Coronary / Q000009:adverse effects*; D001145:Arrhythmias, Cardiac / Q000209:etiology* / Q000503:physiopathology; D005260:Female; D005500:Follow-Up Studies; D006801:Humans; D008297:Male; D008875:Middle Aged; D009203:Myocardial Infarction / Q000503:physiopathology / Q000628:therapy*; D015428:Myocardial Reperfusion Injury / Q000209:etiology* / Q000503:physiopathology; D032383:Myocytes, Cardiac / Q000502:physiology; D020127:Recovery of Function / Q000502:physiology; D015912:Thrombolytic Therapy / Q000009:adverse effects*; D016896:Treatment Outcome; D018487:Ventricular Dysfunction, Left / Q000209:etiology* / Q000503:physiopathology