Today we discussed a complex case of dyspnea that was partly due to tachycardia induced cardiomyopathy, or what is broadly termed arrhythmia induced cardiomyopathy (AIC). These patients typically present with 1-2 weeks of a sustained tachyarrhythmia (usually atrial fibrillation, as in our patient) and then new LV dysfunction in the absence of other underlying causes. AIC is a bit of an odd bird, in that the underlying pathogenesis is not all that intuitive.
1. What is the natural history/pathogenesis of AIC? Difficult question to answer, however there are defined steps that are known primarily from animal studies (see figure). In general there are two phases to AIC: the remodeling phase and the failure phase. During the remodeling phase (lasts from 1-3 weeks), the LV dilates as a compensatory response. Together with this dilatation, the RAAS system is upregulated, calcium handing becomes dysfunctional, and normal architecture of the ECM is lost. At some point, the system decompensates, and filling pressures become abnormal, leading to congestion. Contemporary wisdom places the minimum time needed to develop AIC at around 2 weeks, and the minimum heart rate at 120, though these numbers are extrapolated from animal studies.
2. How to treat AIC? First, treat the arrhythmia, then once the rhythm is controlled, usual heart failure therapy. Most will correct fully with rate/rhythm control.
For more reading on this topic, refer to the excellent JACC review from 2015: JACC 2015; 66: 1714-1728.