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Continuous Telemetry from a Chronic Canine Model of Sudden Cardiac Death
Author(s) -
KILLINGSWORTH CHERYL R.,
RITSCHER DAVID E.,
WALCOTT GREGORY P.,
ROLLINS DENNIS L.,
IDEKER RAYMOND E.,
SMITH WILLIAM M.
Publication year - 2000
Publication title -
journal of cardiovascular electrophysiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.193
H-Index - 138
eISSN - 1540-8167
pISSN - 1045-3873
DOI - 10.1046/j.1540-8167.2000.01333.x
Subject(s) - medicine , cardiology , ventricular fibrillation , ventricle , endocardium , sudden death , sudden cardiac death , circumflex , bradycardia , myocardial infarction , artery , telemetry , anesthesia , heart rate , blood pressure , engineering , aerospace engineering
Continuous Telemetry in a Dog Model of Sudden Death. Introduction : We sought to develop a continuously telemetered animal model of sudden cardiac death (SCD) to study the role of existing infarcts and acute ischemia in fatal arrhythmias. Methods and Results : A telemetry system capable of recording eight channels of electrophysiologic data continuously and chronically has been developed. To demonstrate the use of this technology in an animal model of sudden death. 12 anesthetized dogs were instrumented with eight electrodes located in endocardium of the right side of the heart, epicardium of the left ventricle (LV), or in the subcutaneous tissues. The left anterior descending (LAD) coronary artery was occluded for 90 minutes and reperfused to produce LV infarction. A copper wire was placed in the left circumflex (LCX) coronary artery to cause intimal injury in a second arterial bed. The telemetry unit recorded deaths in seven animals between 19 to 64 hours after surgery. Five animals that did not experience SCD by the fifth postoperative day served as controls. There were three modes of SCD: complex ventricular ectopy that degenerated into ventricular fibrillation VF (n = 4); normal sinus rhythm that suddenly degenerated into VF (n = 1); and bradycardia (RK intervals > 1.000 msec) that lasted >3 minutes and preceded VF (n = 2). ST segment changes were significantly greater in the LCX‐bed electrograms for tachyarrhythmic compared to bradyarrhythmic deaths (mean ± SD; 4.0 ± 3.4 mV and 0.2 ± 0.8 mV, respectively). Fast Fourier transform showed the peak frequency of VF 10 seconds after onset was significantly higher in the five dogs with initial tachyarrhythmic compared with the VF that followed profound bradycardia (6.5 ± 3.1 Hz and 3.7 ± 0.6 Hz. respectively). Computer‐assisted planimetry of postmortem heart slices revealed that infarcts in the two dogs with bradycardie events were larger (19.7%± 2.2% of the LV and septal mass) than in the five dogs with tachyarrhythmias (7.7%± 2.4%) or in the five control dogs (11.9%± 8.1%). Conclusion : It is possible to record via telemetry the events leading to SCD in an animal model. Continuous telemetry monitoring demoastrated that both tachyarrhythmias and bradyarrhythmias ultimately resulted in VF in an animal model of SCD. Animals with tachyarrhythmic deaths had greater ischemia in the LCX bed, smaller preexisting infarcts, and higher VF peak frequency than animals with bradyarrhythmic deaths.