{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,27]],"date-time":"2026-10-27T21:27:50Z","timestamp":1793136470109,"version":"4.5.0"},"reference-count":74,"publisher":"Ovid Technologies (Wolters Kluwer Health)","issue":"5","content-domain":{"domain":["www.ahajournals.org"],"crossmark-restriction":true},"short-container-title":["Circulation Research"],"published-print":{"date-parts":[[2015,2,27]]},"abstract":"<jats:sec>\n            <jats:title>\n              <jats:underline>Rationale:<\/jats:underline>\n            <\/jats:title>\n            <jats:p>\n              Alternans is a risk factor for cardiac arrhythmia, including atrial fibrillation. At the cellular level alternans manifests as beat-to-beat alternations in contraction, action potential duration (APD), and magnitude of the Ca\n              <jats:sup>2+<\/jats:sup>\n              transient (CaT). Electromechanical and CaT alternans are highly correlated, however, it has remained controversial whether the primary cause of alternans is a disturbance of cellular Ca\n              <jats:sup>2+<\/jats:sup>\n              signaling or electrical membrane properties.\n            <\/jats:p>\n          <\/jats:sec>\n          <jats:sec>\n            <jats:title>\n              <jats:underline>Objective:<\/jats:underline>\n            <\/jats:title>\n            <jats:p>\n              To determine whether a primary failure of intracellular Ca\n              <jats:sup>2+<\/jats:sup>\n              regulation or disturbances in membrane potential and AP regulation are responsible for the occurrence of alternans in atrial myocytes.\n            <\/jats:p>\n          <\/jats:sec>\n          <jats:sec>\n            <jats:title>\n              <jats:underline>Methods and Results:<\/jats:underline>\n            <\/jats:title>\n            <jats:p>\n              Pacing-induced APD and CaT alternans were studied in single rabbit atrial and ventricular myocytes using combined [Ca\n              <jats:sup>2+<\/jats:sup>\n              ]i and electrophysiological measurements. In current-clamp experiments, APD and CaT alternans strongly correlated in time and magnitude. CaT alternans was observed without alternation in L-type Ca\n              <jats:sup>2+<\/jats:sup>\n              current, however, elimination of intracellular Ca\n              <jats:sup>2+<\/jats:sup>\n              release abolished APD alternans, indicating that [Ca\n              <jats:sup>2+<\/jats:sup>\n              ]i dynamics have a profound effect on the occurrence of CaT alternans. Trains of 2 distinctive voltage commands in form of APs recorded during large and small alternans CaTs were applied to voltage-clamped cells. CaT alternans was observed with and without alternation in the voltage command shape. During alternans AP-clamp large CaTs coincided with both long and short AP waveforms, indicating that CaT alternans develop irrespective of AP dynamics.\n            <\/jats:p>\n          <\/jats:sec>\n          <jats:sec>\n            <jats:title>\n              <jats:underline>Conclusions:<\/jats:underline>\n            <\/jats:title>\n            <jats:p>\n              The primary mechanism underlying alternans in atrial cells, similarly to ventricular cells, resides in a disturbance of Ca\n              <jats:sup>2+<\/jats:sup>\n              signaling, whereas APD alternans are a secondary consequence, mediated by Ca\n              <jats:sup>2+<\/jats:sup>\n              -dependent AP modulation.\n            <\/jats:p>\n          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