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Alterations in the initial portion of the signal-averaged QRS complex in acute myocardial infarction with ventricular tachycardia

  • Michael G. Kienzle
    Correspondence
    Address for reprints: Michael G. Kienzle, MD, Department of Internal Medicine, University of Iowa, Iowa City, Iowa 52242.
    Footnotes
    Affiliations
    From the Medical Intensive Care Unit, Hospital of the University of Pennsylvania, Philadelphia, Pennsylvania, USA

    From the Cardiovascular Section, Department of Medicine, University of Pennsylvania, School of Medicine, Philadelphia, Pennsylvania, USA
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  • Rita A. Falcone
    Affiliations
    From the Medical Intensive Care Unit, Hospital of the University of Pennsylvania, Philadelphia, Pennsylvania, USA

    From the Cardiovascular Section, Department of Medicine, University of Pennsylvania, School of Medicine, Philadelphia, Pennsylvania, USA
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  • Michael B. Simson
    Affiliations
    From the Medical Intensive Care Unit, Hospital of the University of Pennsylvania, Philadelphia, Pennsylvania, USA

    From the Cardiovascular Section, Department of Medicine, University of Pennsylvania, School of Medicine, Philadelphia, Pennsylvania, USA
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  • Author Footnotes
    1 Dr. Kienzle was an American Heart Association Research Fellow, Southwestern Pennsylvania Affiliate, at the time of the study.
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      Abstract

      This study was designed to examine 2 hypotheses: that acute myocardial infarction (AMI) alters early cardiac activation measured by signal-averaging; and that the magnitude of abnormality of early activation may be greater in patients with post-AMI ventricular tachycardia (VT). We examined the root-mean square voltage amplitude in 10-ms intervals over the first 80-ms of the signal-averaged QRS complex. Data from 42 healthy volunteers were compared with those from 52 patients with previous AMI (24 anterior) but no VT and 46 post-AMI patients (33 anterior AMI) with recurrent sustained VT. Patients with VT differed from other post-AMI patients because of lower left ventricular ejection fraction, more frequent aneurysm formation and higher levels of ventricular ectopic activity. A significant decrease in initial voltage amplitude occurred at 30 to 40 ms after the beginning of the QRS in both anterior and inferior AMI patients compared with the normal group. A further significant decrease in initial amplitude occurred in VT patients both after anterior and inferior AMI. These differences persisted for the remainder of the 80-ms interval. These changes were weakly related to QRS duration (r = 0.45), ejection fraction (r = 0.50) and poorly correlated with the presence of Q waves On 12-lead electrocardiogram (r = 0.21). Direct endocardial catheter recordings performed in VT patients confirmed abnormalities of local septal activation after anterior and inferior AMI. An amplitude at 40 ms of <50 μV was significantly related to the presence of VT in anterior AMI patiente (28 of 33 with VT vs 10 of 24 without VT, p < 0.001, chisquare analysis). A similar trend existed for inferior AMI patiente but was not statistically significant (p = 0.07). We conclude that MI alters early activation measured by signal-averaging. The presence and extent of septal abnormalities may be important in the development of VT.
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