Atrial fibrillation and cardiac rehabilitation: an overview.

Background: Atrial fibrillation (AF) is the most common cardiac arrhythmia, and its frequency will only continue to increase in the future. Despite available drug and electrophysical treatments, death and functional restrictions due to AF are still common. More comprehensive standards of care are therefore needed.Purpose: After a foreword regarding the link between physical activity and AF, this article aims to give to the clinician an overview of the benefits he may expect or not when including patients suffering from AF in a cardiac rehabilitation programme.Method: We selected prospective, randomised controlled trials published during the past 10 years and referenced in the PubMed Database evaluating the safety of rehabilitation and/or its impact on AF incidence or tolerance, and tried to summarise them to propose a narrative review.Conclusion: Cardiac rehabilitation, along with moderate and regular physical activity, has been proven to reduce the time in arrhythmia of patients with paroxysmal and persistent AF. In chronic AF, cardiac rehabilitation may decrease the resting ventricular response rate in patients and therefore improve symptoms linked to arrhythmia. These studies have managed to demonstrate cardiac rehabilitation as a safe and manageable option for AF patients, without serious risk of additional side effects. Its efficiency to limit the occurrence of serious undesirable outcomes, such as mortality and hospitalisation, has not been adequately demonstrated, likely due to the small scale of most studies and lack of long-term follow-up. Large-scale and long-term studies are thus desirable.

Platelet inhibition with tirofiban early during percutaneous coronary intervention: dosing revisited.

Platelet inhibition is central to the efficacy of the intravenous glycoprotein IIb/IIIa receptor inhibitors. Differences in the degree of platelet inhibition achieved with these agents may account for the disparity in clinical efficacy noted in recently completed clinical trials. The purpose of this study was to evaluate ex vivo platelet inhibition with tirofiban in patients admitted with acute coronary syndrome and who were referred for percutaneous coronary interventions. Twenty-five patients were studied. Ten patients received tirofiban 10 microg/kg bolus and 0.15 microg/kg infusion for 16 hr. Platelet inhibition was determined at 5, 15, 30, 45, 60, and 120 min after tirofiban, by light transmission aggregometry (LTA), rapid platelet function assay (RPFA), and platelet works (PW). The average platelet inhibition using RPFA with PPACK, was 87% at 5 min, then decreased to a nadir of 72% at 30 min and recovered back to > 80% at 60 min and onward. Similar trends were noted with RPFA-citrate, PW, and LTA. Ca-chelating anticoagulants (EDTA and citrate) overestimated platelet inhibition at all time points. Dose adjustment was done by increasing the bolus (15 microg/kg) in five patients, increasing the maintenance dose (0.2 microg/kg/min) in five patients, and increasing both the bolus and the maintenance dose in another five patients. Platelet inhibition tested by all the above methods was consistently over 90% when both the bolus and maintenance doses were increased. No increased incidence of major bleeding was noted at this adjusted dose. The current dosing of tirofiban may be inadequate to achieve appropriate platelet inhibition during PCI in patients admitted with acute coronary syndrome and receiving tirofiban immediately before the procedure in the cardiac catheterization laboratory. Dose adjustment may be needed to maximize platelet inhibition early during PCI.