Key result
In diseased human trabeculae, pacing thresholds increased by >35% at 42°C compared to baseline (P<0.05), indicating potential risk of pacing loss during cardiac heating.
Why the study?
Does temperature variation affect ventricular pacing capture thresholds in mammalian myocardium?
Does temperature variation affect ventricular pacing capture thresholds in mammalian myocardium?
Elevated temperatures up to 42°C significantly increase pacing thresholds in diseased human myocardium, highlighting a potential risk for loss of capture during MRI scans or febrile events.
Ex vivo data suggest possible VPCT shifts with temperature; leaves open whether MRI-conditional devices need adjusted thresholds in vivo.
BACKGROUND: Human core body temperature can fluctuate between 36 degrees C (sleep) and 42 degrees C (intense exercise). Also, efforts are underway to develop implantable pacing systems that minimize heating during magnetic resonance imaging (MRI) scans (i.e., MRI safe). Concerns exist that ventricular pacing capture thresholds (VPCT) are modified by changing cardiac temperatures. 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 trabeculae 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 degrees C, then at randomized temperatures ranging from 35 degrees C to 42 degrees C. Final thresholds were repeated at 37 degrees 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 0.02 ms (P < 0.01) and 0.10 ms (P < 0.05) between the temperatures of 38 degrees C and 41 degrees C, compared to baseline. Thresholds at 42 degrees C trended back to baseline for both canine (NS) and swine trabeculae (P < 0.05 compared to 38 degrees C-41 degrees C). Human trabeculae thresholds increased >35% (P < 0.05) at 42 degrees C relative to baseline with no significant differences at other temperatures. CONCLUSIONS: Temperature is a significant factor on pacing thresholds for mammalian ventricular myocardium. Our data for the diseased human trabeculae indicate that cases where cardiac heating may occur (e.g., radiofrequency energy due to MRI scans, febrile events), patients without adequate VPCT safety margin may be at higher risk of loss of proper function of an implanted pacing or defibrillation system.
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Marshall et al. (2010) studied Diseased human hearts (and healthy canine/swine). Temperature changes (35°C to 42°C) vs. 37°C (baseline) was evaluated on Ventricular pacing capture thresholds (VPCT) (p=< 0.05). In diseased human trabeculae, pacing thresholds increased by >35% at 42°C compared to baseline (P<0.05), indicating potential risk of pacing loss during cardiac heating.
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