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 mu 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 mu m(2)), 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 mu m(2)). 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 Ca(2+)homeostasis, thereby avoiding Ca(2+)overload. This protection against Ca(2+)overload co-occurs with dedifferentiation like cellular remodeling. (C) 2000 Academic Press.