The author reports no conflicts of interest for the published content.
In this month’s issue of
I recall caring for a patient many years ago who first was referred to me with atrial fibrillation, conduction disease, and mild cardiomyopathy. Similar to the patient described in this current case report,
My case at the time was quite sobering. Cardiac involvement in sarcoidosis can be fulminant and certainly points to active inflammation.
It seems to be that, for classical cardiac disorders that result in arrhythmias, we often forget about the atria. Certainly, this may be based on the incidence of the type of arrhythmia as we understand it today. For example, in cardiac sarcoid, the classical sequelae are conduction system disease, ventricular arrhythmias, and heart failure.
As the case by Lau et al. demonstrates, atrial fibrillation can be the first manifestation of cardiac sarcoidosis.
There are many systemic or cardiac diseases that result in both atrial and ventricular arrhythmias. Other infiltrative disorders such as cardiac amyloid
The coexistence of both ventricular and atrial arrhythmias are not unique to infiltrative disorders. The classical channelopathies, such as long QT syndrome or the Brugada syndrome, are associated with atrial fibrillation.
The case presented by Lau et al. illustrates several important lessons for the clinical electrophysiologist. First, disorders that create an arhythmogenic substrate in the ventricle may do so in the atria. It of course works both ways. A patient with cardiac sarcoidosis, which increases the risk of ventricular arrhythmias, may also have atrial arrhythmias. Conversely, a patient with cardiac sarcoidosis with atrial fibrillation may be at increased risk for ventricular arrhythmias. The presence of either kind of arrhythmia may be a marker of disease activity—in this case, noncaseating granulomas.
Secondly, with increasing resolution, we may be able to better delineate structural abnormalities associated with atrial fibrillation. Scar burden in the atria has been demonstrated as a factor that increases the likelihood of atrial fibrillation and to negatively affect ablation success.
Third, the assessment of disease activity (with both clinical events and diagnostic imaging) resulted in the present case undergoing effective treatment. Immunosuppressive therapy and/or perhaps antiarrhythmic drug treatment was effective at suppressing arrhythmia burden and, thus far, appears to slow down or halt disease progression.
In closing, one could argue that what’s bad for the ventricle, is bad for the atria. A disease that causes inflammation and scarring in the ventricle such as cardiac sarcoidosis can cause inflammation and scarring in the atria as well and result in atrial fibrillation. Disease activity in one may predict activity in the other. However, perhaps what’s good for the ventricle is also good for the atria. Treatment that halts the disease process in the ventricle may also suppress atrial fibrillation. It’s likely best that, when treating these disorders, we consider both possibilities.