Changes in Ultrastructural Calcium Distribution in Goat Atria During Atrial Fibrillation,

It has been suggested that Ca2+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 Ca2+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 Ca2+distribution was observed, with regular deposits along the sarcolemma (an average of 3.4 deposits per μ m at a regular distance). The number of sarcolemma-bound Ca2+deposits substantially increased after 1 and 2 weeks of atrial fibrillation. After this period the amount of Ca2+precipitate decreased at 4 and 8 weeks, and became below control level at 16 weeks. A similar time-related redistribution of Ca2+occurred in mitochondria. Whereas mitochondria from control goats displayed very few Ca2+deposits (average 4.0 deposits per μ m2), their number markedly increased after 1 and 2 weeks of atrial fibrillation, which indicates cellular Ca2+overload. From 4 weeks, Ca2+deposits reached control levels and were below control level after 16 weeks of atrial fibrillation (2.5 deposits per μ m2). Our findings are consistent with the previously observed Ca2+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 Ca2+homeostasis, thereby avoiding Ca2+overload. This protection against Ca2+overload co-occurs with dedifferentiation like cellular remodeling.