The consequences of implanting an automatic cardioverter defibrillator (ICD) on vehicle driving in France are poorly known. This retrospective study examined the behaviour at the wheel of ICD recipients who were recommended to abstain from driving for 3 to 6 months after device implantation.

The study population included 98 patients (mean age =59.5±14.8 years) followed for a mean of 24.9±23.9 months, who underwent ICD implant for ventricular Tachycardia (65% of patients), ventricular fibrillation (15%), syncope (8%), as part of a research protocol of myocardial cell transplantation (6%), or for primary prevention (5%). The underlying heart disease was ischemic in 59% of patients, dilated cardiomyopathy in 11%, hypertrophic cardiomyopathy in 8%, valvular in 6%, Brugada syndrome in 4%, right ventricular arrhythmogenic cardiomyopathy in 2%, and miscellaneous disorders in 9% of patients. Five patients died without post mortem interrogation of the ICD. Only 28% of drivers remembered, and 13% observed, the recommended driving limitations. However, 45% (the oldest) claimed to drive prudently. During follow-up, 47% of patients received an ICD shock. Their mean left ventricular ejection fraction was 34±14%, versus 43±18% in patients who received no ICD therapy (p =0.015). Syncope occurred in 16% who received ICD shocks. Shocks were delivered during driving in 6 patients, without consequent accident.

Despite their non-observance of recommended driving limitations, ICD recipients suffered few traffic accidents. Legislation in France should reproduce the guidelines issued by European professional societies and enacted by the British laws.

It is well known that atrial fibrillation (AF) tends to become permanent with time as illustrated by the fact that it becomes more difficult to maintain sinus rhythm when AF has been present for a long time. Atrial remodelling plays a part in this process and has been studied in experimental models. Atrial remodelling is defined as all the phenomena occurring during AF contributing to its maintenance. The persistence of AF induced by stimulation in the animal depends on the duration and the repetition of the atrial stimulation and it would appear that "AF induces AF". The tendency for AF to persist is associated with a shortening of the effective atrial refractory period with loss of its adaptation to the heart rate. The determining factor of both electrical and structural remodelling is the rapidity of the atrial rhythm of the AF itself. These phenomena lead to a type L calcium cellular overload as shown by its prevention or attenuation by the administration of verapamil, a calcium antagonist.

Electrical remodelling is accompanied by a structural remodelling in the experimental model of persistent AF over several weeks. Samples from the two atria examined by electronic microscopy show mitochondrial changes, an accumulation of glycogen, a deficit in myofibrils, a redistribution of the nuclear chromatim and a reduction of sarcoplasmic reticulum with changes in protein structure. This structural remodelling is a reaction of adaptation similar to that observed in hibernating myocardium during ischaemia and aims to prolong cellular viability by decreasing atrial contractility. Another aspect of structural remodelling is the activation of fibroblasts with formation of fibrosis with resulting heterogeneity of the conduction tissue. There is also an increase in converting enzyme and angiotensin II concentrations. Irbesartan, an angiotensin II antagonist, reduced fibroblast growth. This has clinical applications as shown by the reduction in the recurrences of AF after cardioversion when given in association with amiodarone. Persistent AF leads to left atrial dilatation with abnormal atrial contractility. Further studies are necessary to determine the effect of atrial remodelling which might also act on the foci responsible for inducing the AF.

Better understanding of atrial remodelling will contribute to the use of new pharmacological agents to prevent AF.   FULL TEXT PDF