Is there a correlation between ventricular fibrillation cycle length and electrophysiological and anatomic properties of the canine left ventricle?

• Published in: American journal of physiology. Heart and circulatory physiology 2004-08, Vol.287 (2), p.H823-H832
• Main Authors: Taneja, Taresh, Horvath, George, Racker, Darlene K, Johnson, David, Goldberger, Jeffrey, Kadish, Alan
• Format: Article
• Language: English
• Subjects: Animals; Chronic Disease; Dogs; Electric Stimulation; Electrocardiography; Heart - innervation; Myocardial Infarction - complications; Myocardial Infarction - etiology; Myocardial Infarction - physiopathology; Myocardium - pathology; Necrosis; Refractory Period, Electrophysiological; Time Factors; Ventricular Dysfunction, Left - etiology; Ventricular Dysfunction, Left - physiopathology; Ventricular Fibrillation - complications; Ventricular Fibrillation - etiology; Ventricular Fibrillation - pathology; Ventricular Fibrillation - physiopathology
• ISSN: 0363-6135; 1522-1539
• DOI: 10.1152/ajpheart.00795.2003

Division of Cardiology, Department of Medicine, Feinberg Cardiovascular Research Institute, Northwestern University, Chicago, Illinois 60611 Submitted 18 August 2003 ; accepted in final form 11 March 2004 We hypothesized that myocardial infarction-related alterations in ventricular fibrillation (VF) cycle length (VFCL) would correlate with changes in local cardiac electrophysiological and anatomic properties. An electrophysiological study was performed in normal, subacute, and chronic infarction mongrel dogs. VF was induced by programmed electrical stimulation and mean and minimum early and late VFCL was determined and correlated with local electrophysiological and anatomic properties. Effective refractory period (ERP), activation recovery time (ART), ERP/ART ratio, threshold, and ERP and ART dispersion were determined at 112 sites on the anterior left ventricle. Wave front progression was analyzed over a 2-s period. The extent of local tissue necrosis and of myocardial fiber disarray was also evaluated. The early mean VFCL was significantly longer in the subacute infarction (149 ± 35 ms) and chronic infarction dogs (129 ± 18 ms) compared with control dogs (102 ± 15 ms; P < 0.0001 for both comparisons) as was the early minimum VFCL with similar trends seen during late VF. Complete epicardial reentrant circuits were significantly more common in normal dogs (4.3 ± 2.4, 22.4% of cycles) than in subacute (0.75 ± 0.96, 5.3% of cycles, P < 0.05 vs. normal) and chronic infarction dogs (1.3 ± 1.3, 7.5% of cycles, P < 0.05 vs. normal). There was a poor correlation between the mean and minimum early and late VFCL and local electrophysiological and anatomic properties ( R 2 < 0.2 for all comparisons) with a much better correlation between average mean and minimum VFCL (over the entire plaque) and global ERP and ART dispersion during early and late VF. In conclusion, VFCL in normal and infarcted myocardium shows a poor correlation with local ventricular electrophysiological and anatomic properties measured in sinus rhythm. However, there was a much better correlation between the average VFCL with global dispersion of repolarization. The lack of correlation between local VFCL and refractoriness and the infrequent occurrence of epicardial reentry suggests that intramural reentry may be the primary mechanism of VF in this model. Address for reprint requests and other correspondence: A. Kadish, Feinberg Pavilion, Suite 8-536, 251 E. Huron, Chicago, IL 60611 (E-mail: a-kad