Marshall, Mark Thomas2010-08-172010-08-172010-05https://hdl.handle.net/11299/93200University of Minnesota M.S. thesis. May 2010. Major: Cellular and Integrative physiology. Advisors: Paul A Iaizzo, PhD, Stephen A Katz, PhD. 1 computer file (PDF); v, 37 pages, appendix A. Ill. (some col.)Background: Concerns exist that ventricular pacing capture thresholds (VPCT) are modified by changing cardiac temperatures due to fluctuations in core body temperature or as caused by interactions between implantable pacing systems and heating caused by MRI scans. This project was designed to assess the effects of temperature on VPCT of the mammalian heart. Methods: Fresh ventricular specimens were obtained from healthy canine, healthy swine, and diseased human hearts. Isolated trabecula were suspended in temperature-controlled tissue baths containing oxygenated Krebs buffer. Small active fixation pacing leads delivered pacing pulses to each specimen. Baseline strength-duration curves were determined at Background: Concerns exist that ventricular pacing capture thresholds (VPCT) are modified by changing cardiac temperatures due to fluctuations in core body temperature or as caused by interactions between implantable pacing systems and heating caused by MRI scans. This project was designed to assess the effects of temperature on VPCT of the mammalian heart. Methods: Fresh ventricular specimens were obtained from healthy canine, healthy swine, and diseased human hearts. Isolated trabecula were suspended in temperature-controlled tissue baths containing oxygenated Krebs buffer. Small active fixation pacing leads delivered pacing pulses to each specimen. Baseline strength-duration curves were determined atBackground: Concerns exist that ventricular pacing capture thresholds (VPCT) are modified by changing cardiac temperatures due to fluctuations in core body temperature or as caused by interactions between implantable pacing systems and heating caused by MRI scans. This project was designed to assess the effects of temperature on VPCT of the mammalian heart. Methods: Fresh ventricular specimens were obtained from healthy canine, healthy swine, and diseased human hearts. Isolated trabecula were suspended in temperature-controlled tissue baths containing oxygenated Krebs buffer. Small active fixation pacing leads delivered pacing pulses to each specimen. Baseline strength-duration curves were determined at 37°C, then at randomized temperatures ranging from 35°C to 42°C. Final thresholds were repeated at 37°C to confirm baseline responses. All threshold data were normalized to a baseline average. Results: Both canine and swine trabeculae elicited significant decreases in thresholds (10-14%) at pacing stimulus durations (pulsewidths) of 0.02ms (p<0.01) and 0.10ms (p<0.05) between the temperatures of 38°C and 41°C, compared to baseline. Thresholds at 42°C trended back to baseline for both canine (NS) and swine trabeculae (p<0.05 compared to 38-41°C). Human trabeculae thresholds increased > 35% (p<.05) at 42°C relative to baseline with no significant differences at other temperatures. Conclusions: Temperature is a significant factor on pacing thresholds for mammalian ventricular myocardium. This data for the diseased human trabeculae indicates that cases where cardiac heating may occur (e.g. RF energy due to MRI scans), patients with marginal VPCT may lose proper function of an implanted pacing system.en-USCardiac temperaturesMammalian heartVentricular specimensTemperaturePacing stimulus durationsCellular and Integrative PhysiologyThesis or Dissertation