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Mild hypothermia (33°C) increases the inducibility of atrial fibrillation: An in vivo large animal model study
Author(s) -
Manninger Martin,
Alogna Alessio,
Zweiker David,
Zirngast Birgit,
Reiter Stefan,
Herbst Viktoria,
Maechler Heinrich,
Pieske Burkert M.,
Heinzel Frank R.,
Brussee Helmut,
Post Heiner,
Scherr Daniel
Publication year - 2018
Publication title -
pacing and clinical electrophysiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.686
H-Index - 101
eISSN - 1540-8159
pISSN - 0147-8389
DOI - 10.1111/pace.13351
Subject(s) - medicine , hypothermia , cardiology , sinus rhythm , atrial fibrillation , anesthesia , ventricular fibrillation , heart rate , qrs complex , myocardial infarction , atrium (architecture) , blood pressure
Objective Application of therapeutic mild hypothermia in patients after resuscitation, often accompanied by myocardial infarction, cardiogenic shock, and systemic inflammation may impact on cardiac rhythm. We therefore tested susceptibility to atrial arrhythmias during hyperthermia (HT, 40.5°C), normothermia (NT, 38.0°C), and mild hypothermia (MH, 33.0°C). Methods Nine healthy, anesthetized closed‐chest landrace pigs were instrumented with a quadripolar stimulation catheter in the high right atrium and a decapolar catheter in the coronary sinus. Twelve‐lead surface electrograms were recorded and core body temperature was altered to HT, NT, and MH using external warming or intravascular cooling. Repetitive measurements of effective atrial refractory period (AERP), atrial fibrillation (AF) inducibility, and electrocardiogram (ECG) parameters at different heart rates were performed. Results During MH, AERP was significantly longer while the inducibility of AF was significantly higher compared to NT and HT (median [range]: HT 18 (0, 80)%; NT 25 (0, 80)%; MH 68 (0, 100)%; P < 0.05 MH vs NT+HT). Mean AF duration did not differ between groups. Arterial potassium levels decreased with falling temperatures (HT: 4.2 ± 0.1 mmol/L; NT: 4.0 ± 0.2 mmol/L; MH: 3.5 ± 0.1 mmol/L; P < 0.001). Surface ECGs during MH showed reduced spontaneous heart rate (HT: 99 ± 13 beats/min; NT: 87 ± 15 beats/min; MH: 66 ± 10 beats/min; P < 0.05), increased PQ, stim‐Q, and QT intervals (P < 0.01) but no change in QRS duration or time from peak to end of the T wave interval. Conclusion Our data imply that MH represents an arrhythmic substrate rendering the atria more susceptible to AF although conduction times as well as refractory periods are increased. Further investigations on potential electrophysiological limits of therapeutic cooling in patients are required.