Changes in ultrastructural calcium distribution in goat atria during atrial fibrillation

It has been suggested that Ca(2+)content of atrial cardiomyocytes is increased at the onset of atrial fibrillation (AF). Whether this phenomenon is transient is currently unknown. Therefore, in this study the time-related changes in Ca(2+)location in atrial myocytes from goats with chronic AF have been investigated. The distribution of calcium was assessed with the electron microscope using the cytochemical phosphate-pyroantimonate and oxalate-pyroantimonate methods in atrial biopsies from goats in sinus rhythm and goats with 1-16 weeks of burst-pacing-induced AF. In atrial myocytes from control goats in sinus rhythm, a normal Ca(2+)distribution was observed, with regular deposits along the sarcolemma (an average of 3.4 deposits per microm at a regular distance). The number of sarcolemma-bound Ca(2+)deposits substantially increased after 1 and 2 weeks of atrial fibrillation. After this period the amount of Ca(2+)precipitate decreased at 4 and 8 weeks, and became below control level at 16 weeks. A similar time-related redistribution of Ca(2+)occurred in mitochondria. Whereas mitochondria from control goats displayed very few Ca(2+)deposits (average 4.0 deposits per micro m(2)), their number markedly increased after 1 and 2 weeks of atrial fibrillation, which indicates cellular Ca(2+)overload. From 4 weeks, Ca(2+)deposits reached control levels and were below control level after 16 weeks of atrial fibrillation (2.5 deposits per microm(2)). Our findings are consistent with the previously observed Ca(2+)overload early after the onset of atrial fibrillation. The present study shows that this overload persists for at least 2 weeks, after which the cardiomyocytes apparently adapt to a new Ca(2+)homeostasis, thereby avoiding Ca(2+)overload. This protection against Ca(2+)overload co-occurs with dedifferentiation like cellular remodeling.