Postinfarction sudden death: Significance of inducible ventricular tachycardia and infarct size in a conscious canine model

https://doi.org/10.1016/0002-8703(85)90409-0Get rights and content

Abstract

The relationship between inducible ventricular tachycardia in the convalescent phase of myocardial infarction and subsequent spontaneous ventricular fibrillation is uncertain. Thirty conscious instrumented dogs underwent programmed ventricular stimulation 5 days after anterior infarction; 15 had inducible ventricular tachycardia and 15 were noninducible. Following programmed ventricular stimulation, the application of a 150 uA current to the intima of the proximal circumflex artery initiated intimal damage, thrombosis, and acute ischemia of the posterolateral wall. After 20 minutes of ischemia, 73% inducible and 15% noninducible anlmals developed ventricular fibrillation (p < 0.005) without previous hypotension. At 24 hours, 7% inducible and 85% noninducible animals survived (p < 0.001). Anterior infarct size (percentage of left ventricular mass) was much larger in inducible (24.7 ± 1.7%) than in noninducible (5.3 ± 1.1%) (p < 0.001) animals. Inducible ventricular tachycardia following infarction was highly predictive of spontaneous ventricular fibrillation during a later ischemic episode in this model. The mass of previously injured myocardium was a critical determinant of both.

References (59)

  • E Patterson et al.

    Ventricular fibrillation resulting from ischemia at a site remote from previous infarction

    Am J Cardiol

    (1982)
  • MC Fishbein et al.

    Acute phase early myocardial infarct size quantitation: Validation of the triphenyltetrazolium chloride tissue enzyme staining technique

    Am Heart J

    (1981)
  • HS Cabin et al.

    Relation of healed transmural infarct size to length of survival after acute myocardial infarction, age at death, and amount and extent of coronary arterial narrowing by atherosclerotic plaques

    Am Heart J

    (1982)
  • BA Jones-Collins et al.

    Quantitative measurement of electrical instability as a function of myocardial infarct size in the dog

    Am J Cardiol

    (1981)
  • EL Michelson et al.

    Electrophysiologic and anatomic correlates of sustained ventricular tachyarrhythmias in a model of chronic myocardial infarction

    Am J Cardiol

    (1980)
  • DP Rardon et al.

    Parasympathetic effects on electrophysiologic properties of cardiac ventricular tissue

    J Am Coll Cardiol

    (1983)
  • IP Panidis et al.

    Sudden death in hospitalized patients: Rhythm disturbances detected by ambulatory electrocardiographic monitoring

    J Am Coll Cardiol

    (1983)
  • JB Allen et al.

    The effect of the level of the ligature on the mortality following ligation of the circumflex coronary artery in the dog

    Am Heart J

    (1950)
  • T Fujimoto et al.

    Electrophysiologic observations during the spontaneous initiation of ischemia-induced ventricular fibrillation

    Am Heart J

    (1983)
  • T Endo et al.

    Relationship between the extent of the hypoperfused zone of the myocardium and the occurrence of ventricular fibrillation

    Am Heart J

    (1983)
  • RR Hope et al.

    Ventricular arrhythmias in healing myocardial infarction

    J Thorac Cardiovasc Surg

    (1978)
  • AG Freifeld et al.

    Nontrasmural versus transmural myocardial infarction: A morphologic study

    Am J Med

    (1983)
  • G Baroldi et al.

    Morphology of acute myocardial infarction in relation to coronary thrombosis

    Am Heart J

    (1974)
  • RJ Myerburg et al.

    Electrophysiologic consequences of experimental acute ischemia superimposed upon healed myocardial infarction in cats

    Am J Cardiol

    (1982)
  • W Merx et al.

    The role of local disparity in conduction and recovery time on ventricular vulnerability to fibrillation

    Am Heart J

    (1977)
  • J Mukharji et al.

    Ventricular arrhythmia and left ventricular dysfunction six months after myocardial infarction as risk factors for sudden death

    Circulation

    (1983)
  • AJ Moss et al.

    Ventricular ectopic beats and their relation to sudden and nonsudden cardiac death after myocardial infarction

    Circulation

    (1979)
  • EH Schuster et al.

    Early post-infarction angina

    N Engl J Med

    (1981)
  • P Theroux et al.

    Prognostic value of exercise testing soon after myocardial infarction

    N Engl J Med

    (1979)
  • Cited by (65)

    • Cardiac magnetic resonance imaging: Infarct size is an independent predictor of mortality in patients with coronary artery disease

      2011, Magnetic Resonance Imaging
      Citation Excerpt :

      Prior MI may serve as a substrate for reentrant tachyarrhythmias which can lead to ventricular fibrillation and sudden cardiac death [22,36,37]. Therefore, the volume of infarct may be a crucial determinant in the development of such arrhythmias related to sudden cardiac death, where the greater the infarct, the larger the substrate for the development of subsequent arrhythmias [20,23,38]. Indeed, Bello et al. [15] identified a value of 10% of left ventricular mass to be the critical substrate necessary to develop sustained ventricular arrhythmias in patients with CAD undergoing electrophysiological testing.

    • Quantitative Tissue Characterization of Infarct Core and Border Zone in Patients With Ischemic Cardiomyopathy by Magnetic Resonance Is Associated With Future Cardiovascular Events

      2010, Journal of the American College of Cardiology
      Citation Excerpt :

      They are descriptors of myocardial and electrical dysfunctions rather than specific physiologic markers to identify patients at risk for developing CVE (20). Prior studies have demonstrated that quantification of myocardial scar volume and percentage by CMR is superior to LVEDV, LVESV, and LVEF in prognosticating future CVE, particularly ventricular arrhythmia, in patients with ICM (8,18,22–25). This study confirms that the quantification of the total scar mass by CMR can be associated with the development of CVE in patients with ICM.

    View all citing articles on Scopus

    Supported by grants from the National Institutes of Health, Heart, Lung, and Blood Institute, HL-19782-06 and HL-05806-23, and by a Postdoctoral Fellowship of the Michigan Heart Association (Dr. Lynch).

    View full text