Letter to the editor: Corticosteroids and AF

Cardiology Review® OnlineAugust 2008
Volume 25
Issue 8

Corticosteroids and AF

Halonen and colleagues (March 2008) detailed very interesting results regarding the use of specific doses of corticosteroids following coronary artery bypass graft (CABG) surgery, aortic valve replacement (AVR), or combined CABG surgery and AVR.1,2 I commend them on their findings and Dr Rashba for his eloquent commentary.3 I would simply like to point out a few caveats regarding this study.

Numerous studies have highlighted the pleiotropic effects of HMG-CoA reductase inhibitors, specifically, the ability of statins as a class to decrease the levels of C-reactive protein and other markers of inflammation.4,5 Furthermore, statins have been proposed to influence mechanisms contributing to myocardial remodeling, including inhibiting matrix metalloproteinases.6 Numerous studies point to the antiarrhythmic effects of statin therapy, and, specifically, on the incidence of the development of postoperative atrial fibrillation (AF).7 Furthermore, patients in the AVR or the CABG surgery and AVR arms most certainly would have received statin therapy, given the beneficial results of statins on the progression of aortic stenosis/sclerosis.8 Other important details not mentioned in the Halonen study were the intraoperative transesophageal echocardiographic determinations. It is known that potential substrate for the development of AF includes anatomic derangements of the atria and ventricles, such as left atrial enlargement, increased left ventricular wall thickness, and reduced left ventricular fractional shortening. Certainly, those individuals undergoing AVR alone or combined CABG surgery and AVR would have had intraoperative studies to determine the integrity and positioning of the valve, as well as other morphologic and functional measurements.

The metabolic demands of the patients in this study were alluded to by the dose of metoprolol given; however, specific mention of patients with thyroid disease was absent. Finally, postoperative pain leading to increased adrenergic drive was not specifically addressed. This has important bearing given the recent cohort study borne from ASFIT (AF Suppression Trials) I, II, and III, showing that perioperative nonsteroidal anti-inflammatory drug use can decrease the odds of developing postcardiothoracic surgery atrial fibrillation.9

The findings of the Halonen study provide further insight into how postoperative AF develops; however, conventional therapies (eg, statins) and diagnostic evaluation (eg, echocardiograms) must not be neglected when treating or investigating the potential causes of postoperative AF. Halonen and colleagues do not mention whether such interventions were accounted for in their study; thus, one must be cautious in attributing the decreased incidence of the development of postoperative AF in their cohort to the administration of corticosteroids.

Saadi A. Siddiqi, DO

Cardiology Hospitalist

Hartford, CT

Editor’s note: Despite numerous attempts, the editors were unable to elicit a response from Dr Halonen to this letter.

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