Impaired left ventricular function is associated with increased recovery time dispersion in patients with previous myocardial infarction☆
Article Outline
Abstract
Left ventricular (LV) dysfunction after myocardial infarction is associated with higher risk of serious ventricular arrhythmias and sudden death. We suspected that heterogeneity in ventricular repolarization contributes to these arrhythmias. To quantify this heterogeneity, we measured the recovery time (the interval between QRS onset and the time of maximum dV/dt in the ST-T segment) using an 87-lead body surface mapping electrocardiogram and estimated recovery time dispersion (the difference between maximum recovery time and minimum recovery time) in each lead. Differences between 110 patients with previous myocardial infarction and 31 healthy controls were compared. Recovery time dispersion [medians (25th, 75th percentiles)] was greatest in patients with a dilated LV {169 ms (154, 201) vs. 155 ms (137, 172), P < .005}, impaired ejection fraction {173 ms (155, 202) vs. 152 ms (138, 165), P < .0005} and LV dyskinesis {175 ms (159, 201) vs. 155 ms (137, 161), P < .0005}. This study suggests that LV dysfunction associated with myocardial infarction leads to heterogeneous ventricular repolarization and may provide the electrical substrate for ventricular arrhythmias.
Keywords: Repolarization abnormalities, previous myocardial infarction, impaired left ventricular function, recovery time, ventricular arrhythmias
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References
- Clinical, angiographic, and electrophysiologic findings in patients with aborted sudden death as compared with patients with sustained ventricular tachycardia after myocardial infarction. Circulation. 1985;71:1146
- Sudden death prevention in patients with advanced ventricular dysfunction. Circulation. 1993;88:2953
- Endocardial catheter mapping in patients in sinus rhythm: relationship to underlying heart disease and ventricular arrhythmias. Circulation. 1986;73:645
- The prognostic significance of quantitative signal-averaged variables relative to clinical variables, site of myocardial infarction, ejection fraction and ventricular premature beats: A prospective study. J Am Coll Cardiol. 1989;13:377
- . The role of local disparity in conduction and recovery time on ventricular vulnerability to fibrillation. Am Heart J. 1977;94:603
- Mechanism of ventricular arrhythmias caused by increased dispersion of repolarization. Eur Heart J. 1985;6:63
- Estimation of ventricular repolarization in man by monophasic action potential recording technique. Eur Heart J. 1985;6:71
- . QT dispersion and components of the QT interval in ischaemia and infarction. Br Heart J. 1995;73:32
- Reduction in QT interval dispersion by successful thrombolytic therapy in acute myocardial infarction. TEAM-2 Study Investigators. Circulation. 1994;90:94
- Enalapril reduces QTc dispersion in mild congestive heart failure secondary to coronary artery disease. Am J Cardiol. 1997;79:328
- . Correlation between in vivo transmembrane action potential durations and activation-recovery intervals from electrograms. Effects of interventions that alter repolarization time. Circulation. 1990;81:281
- Diagnostic value of recovery time measured by body surface mapping in patients with congenital long QT syndrome. Am J Cardiol. 1994;74:780
- Influence of epinephrine, propranolol, and atrial pacing on spatial distribution of recovery time measured by body surface mapping in congenital long QT syndrome. J Cardiovasc Electrophysiol. 1997;8:1102
- . Long-term recording of monophasic action potentials from human endocardium. Am J Cardiol. 1983;51:1629
- Heart rate variability and dispersion of QT interval in patients with vulnerability to ventricular tachycardia and ventricular fibrillation after previous myocardial infarction. J Am Coll Cardiol. 1997;30:1331
- Relation of QT dispersion to infarct size and left ventricular wall motion in anterior wall acute myocardial infarction. Am J Cardiol. 1999;83:1423
- Multivariate associates of QT dispersion in patients with acute myocardial infarction: Primacy of patency status of the infarct-related artery. TEAM-3 Investigators. Third trial of Thrombolysis with Eminase in Acute Myocardial Infarction. Am Heart J. 1998;135:1027
- . Concept of activation recovery interval and clinical usefulness of body surface recovery time and recovery time isochrone map. Nippon Rinsho. 1995;53:74
- Diverse mechanisms of unexpected cardiac arrest in advanced heart failure. Circulation. 1989;80:1675
- Role of neurohormonal mechanisms in determining survival in patients with severe chronic heart failure. Circulation. 1987;75:IV80
- Monophasic action potential recordings during acute changes in ventricular loading induced by the Valsalva manoeuvre. Br Heart J. 1992;67:221
- Repolarization abnormalities, arrhythmia and sudden death in canine tachycardia-induced cardiomyopathy. J Am Coll Cardiol. 1997;30:576
- Electrophysiologic substrate associated with pacing-induced heart failure in dogs: potential value of programmed stimulation in predicting sudden death. J Am Coll Cardiol. 1992;19:444
- Circadian variation of QT interval dispersion: Correlation with heart rate variability. J Electrocardiol. 1997;30:205
- . Correlation between refractory periods and activation-recovery intervals from electrograms: Effects of rate and adrenergic interventions. Circulation. 1985;72:1372
☆ Reprint requests: Hiroki Shimizu, MD, Department of Internal Medicine, Cardiovascular Division, Hyogo College of Medicine, 1-1, Mukogawa-cho, Nishinomiya, 663-8501, Japan; e-mail: hiroki@hyo-med.ac.jp.
PII: S0022-0736(02)30456-4
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