Myocardial injury, neurohormonal activation and inflammation after internal atrial defibrillation

The effects of patient-activated atrial defibrillation on subclinical myocardial injury are unknown. Using biochemical markers, this study assessed the effect of a single internal atrial shock delivered by the implantable atrial defibrillator on myocardial damage, neurohormonal activation and inflammation.

Twelve patients were implanted with a dual chamber defibrillator for the sole indication of drug refractory symptomatic persistent atrial fibrillation (AF). All had maximum defibrillation energy programmed to maximise the first shock success rate. Creatine kinase isoenzyme, troponin T, cortisol, catecholamines, C-reactive protein and brain natriuretic peptide were measured (i) during sinus rhythm, (ii) 8 h after onset of spontaneously occurring AF (before cardioversion) and (iii) 8 h following successful patient activated cardioversion.

There was no change in creatine kinase, troponin T, cortisol or C-reactive protein during AF or following internal cardioversion. Brain natriuretic peptide levels rose from a median value of 56 pg/ml during sinus rhythm (inter-quartile range 14-92 pg/ml) to 133 pg/ml during AF (30-262 pg/ml), p=0.002. There was a decrease 8 h after cardioversion to baseline (52 and 40-189 pg/ml), p=0.01. There were increases in serum adrenaline and noradrenaline levels during AF from 0.43 (0.12-0.61) to 0.58 pg/ml (0.39-0.80 pg/ml), p=0.002 and from 2.06 (1.61-2.59) to 2.83 nmol/l (2.43-3.46 nmol/l), p=0.02, respectively. These figures reverted to baseline levels 8 h post-cardioversion.

Internal atrial defibrillation does not result in myocardial injury. The onset of AF results in sympathetic activation and increased brain natriuretic peptide levels, which resolve following restoration of sinus rhythm.