Multichannel telemetry system to study mechanisms of sudden death in a canine model of coronary microembolization-induced heart failure

J. Wang, M. Knecht, G. H. Yi, M. M. Scheinman, J. Sackner-Bernstein, S. Popilskis, H. Levin, C. Alfemess, M. Packer

Research output: Contribution to journalArticlepeer-review

Abstract

Previous studies have reached conflicting conclusions regarding the role of fatal arrhythmia or cardiac mechanical failure in predicting sudden death (SD) in heart failure (HF) To determine the cause which proceeded SD, dogs were chronically instrumented for daily coronary microembolization (EMBO) resulting in HF and for continuously monitoring of ECGs, MAP, LVP, LV dimension and myocardium segment length using telemetry technique. HF is documented by hemodynamic measurement 35±8 days after the first coronary EMBO as the follows (*p<0.05 from control): Control Heart Failure LV systolic Pressure (mmgH) 134±4 93± 1* LV end-diastolic Pressure (mmHg) 5± 1 20± 1* LVdP/dt(mmHg/s) 3094±I18 1670±61* Mean Arterial Pressure (mmHg) 99±1 83±4* Heart Rate (b/min) 79±6 I29±4* In three dogs, arrhythmias occurred 14±2.3 days after the first EMBO. Both ventricular arrhythmia which was observed for 14± 1.3 days to 15±4.1 hours prior to SD, and atrial fibrillation which was observed 18±3 days before SD, were detected. One dog developed junctional tachycardia (rate: 168 b/min) 20 minutes before SD Bradyarrhytnmia was observed before and during SD in 2/3 animals. In all 3 animals hemodynamic deterioration triggered SD because ECG activity was lasted 17±4.2 min after the cardiac pump failure. These results suggested that the ECG records using holler during SD in patients with HF may mislead to a conclusion of the SD due to fatal arrhythmia since hemodynarnics was not monitored.

Original languageEnglish (US)
Pages (from-to)A33
JournalFASEB Journal
Volume10
Issue number3
StatePublished - Dec 1 1996

ASJC Scopus subject areas

  • Biotechnology
  • Biochemistry
  • Molecular Biology
  • Genetics

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