Sinus Mapping in Patients with Cardiac Arrest and Coronary Disease—Results and Correlation with Outcome

Authors

  • ALAN H. KADISH,

    1. Clinical Electrophysiology Laboratory, Hospital of the University of Pennsylvania, Cardiovascular Section, Department of Medicine, University of Pennsylvania School of Medicine.
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    • *

      Division of Cardiology, University Hospital, 1500 E. Medical Center Drive, UH-BI-F-2450022, Ann Arbor, MI 48109–0020.

  • MARK E. ROSENTHAL,

    1. Clinical Electrophysiology Laboratory, Hospital of the University of Pennsylvania, Cardiovascular Section, Department of Medicine, University of Pennsylvania School of Medicine.
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  • JOSEPH A. VASSALLO,

    1. Clinical Electrophysiology Laboratory, Hospital of the University of Pennsylvania, Cardiovascular Section, Department of Medicine, University of Pennsylvania School of Medicine.
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      5530 Wisconsin Avenue, Suite 505, Chevy Chase, MD 20815.

  • DENNIS M. CASSIDY,

    1. Clinical Electrophysiology Laboratory, Hospital of the University of Pennsylvania, Cardiovascular Section, Department of Medicine, University of Pennsylvania School of Medicine.
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    • ***

      Barnes Hospital, Box 8086, 660 South Euclid Avenue, St. Louis, Missouri 63110.

  • ALFRED E. BUXTON,

    1. Clinical Electrophysiology Laboratory, Hospital of the University of Pennsylvania, Cardiovascular Section, Department of Medicine, University of Pennsylvania School of Medicine.
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  • FRANCIS E. MARCHLINSKI,

    1. Clinical Electrophysiology Laboratory, Hospital of the University of Pennsylvania, Cardiovascular Section, Department of Medicine, University of Pennsylvania School of Medicine.
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  • JOHN M. MILLER,

    1. Clinical Electrophysiology Laboratory, Hospital of the University of Pennsylvania, Cardiovascular Section, Department of Medicine, University of Pennsylvania School of Medicine.
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  • MARK E. JOSEPHSON

    Corresponding author
    1. Clinical Electrophysiology Laboratory, Hospital of the University of Pennsylvania, Cardiovascular Section, Department of Medicine, University of Pennsylvania School of Medicine.
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    • Dr. Josephson is the Robinette Foundation Professor of Medicine in Cardiology.


  • Supported in part by grants from the American Heart Association. Southeastern Pennsylvania Chapter, Philadelphia, PA, and National Heart, Lung, and Blood Institute, Bethesda, MD (HL28O93, HL24278, HL07346).

Address for reprints: Mark E. Josephson, M.D., Chief, Cardiovascular Section, Room 994 Founders Building, Hospital of the University of Pennsylvania, 3400 Spruce Street, Philadelphia, PA 19104.

Abstract

Electrophysiological testing and left ventricular endocardial mapping in sinus rhythm were performed in 61 patients with coronary artery disease who presented with cardiac arrest in an attempt to relate the results of these studies to clinical outcome. Forty-one patients (67%) had inducible sustained arrhythmias (18 uniform ventricular tachycardia, 23 polymorphic ventricular tachycardia/ventricular fibrillation) and 20 had no inducible arrhythmia. Patients with inducible arrhythmia had 45% abnormal and 6% fractionated electrograms versus 33% and 0% for those without inducible arrhythmia (P > 0.05 for both comparisons). Sixteen of 59 patients (27%) with adequate follow-up had arrhythmia recurrence (11/39 [31%] with inducible arrhythmia and 5/20 [25%] without inducible arrhythmia) over a mean follow-up period of 27 months. Of five patients without inducible arrhythmia who experienced recurrence, two did so despite the anti-ischemic therapy. In the 20 patients without inducible arrhythmia, the 15 who remained arrhythmia-free had a mean of 78 ± 22% normal sites versus 46 ± 24% normal sites in those with recurrence (P > 0.05). We conclude that in patients with coronary artery disease and cardiac arrest: 1) patients without inducible arrhythmia have less marked endocardial electrical abnormality than those with inducible arrhythmia, 2) those patients who have marked endocardial abnormality despite the lack of inducible arrhythmia are at risk for clinical recurrence which suggests that these abnormalities may represent an anatomic substrate for arrhythmia which cannot be identified by programmed stimulation, These patients are candidates for AICD implantation and 3) patients with relatively normal endocardial electrograms do well with anti-ischemic therapy alone. (PACE, Vol. 12 February 1989)

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