Ventricular fibrillation and defibrillation in patients with implantable cardioverter defibrillators

Sammanfattning: Since the introduction of the implantable cardioverter defibrillator for humans with malignant ventricular arrhytmias in 1980, over 50, 000 patients world wide have received this device. The implantation procedure is simple and resembles the implantation of an ordinary pacemaker. There is, however, a risk of depressing the myocardial and cerebral function because of the repeated episodes of ventricular fibrillation and defibrillation instituted during the defibrillation threshold test performed to assure adequate device function. The overall objective of the present thesis was to study the cardiac and cerebral effects caused by repeated episodes of ventricular fibrillation and defibrillation. The effects on haemodynamic function, myocardial metabolism, release of markers of myocardial and endothelial cell injury, neurohumoral response and cerebral perfusion were assessed in humans. In an experimental model using pigs, haemodynamic effects of combined arrhythmic and electrical trauma were compared with that of defibrillation shocks alone. Between January 1991 and December 1995, 75 patients received a transvenous implantable cardioverter defibrillator. The overall survival at I year was 94 % and at 3 years 75 %. After I year 40 %, and after 3 years 55 % of the patients had experienced at least I appropriate defibrillation shock. The combined ischaemic and electrical trauma did not cause any systolic dysfunction, but did cause a significant impairment of diastolic filling, as reflected by a decrease in the E/A ratio. This result was reproduced in the animal study, where the diastolic filling and ventricular relaxation deteriorated transiently. Shocks delivered in sinus rhythm did not cause significant changes in diastolic filling. A decrease in coronary sinus blood flow was seen after induction of ventricular fibrillation, probably as an effect of decreased perfusion pressure over the coronary vascular bed, relieved by a short lasting postdefibrillation hyperaemia. In parallel, oxygen content and lactate increased shortly after ventricular fibrillation and defibrillation indicating a transient effect on myocardial metabolism. Defibrillation threshold tests with internal low energy DC shocks caused a significant increase in S-troponin T, CK-MBmass and S-myoglobin, suggestive of a minor myocardial cell injury. There was no evidence for an influence on the vascular endothelium, as assessed by endothelin release. After defibrillation,there was an increase in coronary sinus levels of neuropeptide Y and noradrenaline, indicating a locally increased sympathetic nerve activity as a response to hypoperfusion and exposure to defibrillation. There was also a release of histamine, which could indicate an ischaemia reperfusion induced effect on myocardial metabolism and impulse transmission. Short episodes of ventricular fibrillation did not induce any measurable effects on global and regional cerebral perfusion assessed by positron emission tomography 30 seconds and 10 minutes following restitution of sinus rhythm. There were no changes in the EEG during the procedure. In conclusion, transvenous implantation of cardioverter defibrillators, including threshold testing with 3 to 4 episodes of induced ventricular fibrillation and defibrillation, can be performed without any prolonged effects on myocardial or cerebral function.

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