1. Figure 2 Lack of changes in current properties between myocytes
Figure 2 Lack of changes in current properties between myocytes. (A) Traces of I_CaL elicited by 10 mV incremental test pulses from –80 mV in myocytes with either large (left panel) or small (right panel) currents. Comparison of the current density–voltage relationships (B), activation and steady-state inactivation (C), in a group of current densities <2.5 pA/pF (open symbol) and >2.5 pA/pF (filled symbol). Each point is the mean ± SD of 10 myocytes.
From: Downregulation of the calcium current in human right atrial myocytes from patients in sinus rhythm but with a high risk of atrial fibrillation
Eur Heart J. 2008;29(9): doi: /eurheartj/ehn140
Eur Heart J | Published on behalf of the European Society of Cardiology. All rights reserved. © The Author For permissions please

2. Figure 1 Calcium current density varies between myocytes
Figure 1 Calcium current density varies between myocytes. (A) Distribution of I_CaL density recorded in 172 myocytes. Bars represent the number (n) of each of the I_CaL current density measurements, normalized to the total number of measurements. (B) Peak current amplitude and (C) current density plotted against membrane capacitance showing no significant correlation between the two parameters.
From: Downregulation of the calcium current in human right atrial myocytes from patients in sinus rhythm but with a high risk of atrial fibrillation
Eur Heart J. 2008;29(9): doi: /eurheartj/ehn140
Eur Heart J | Published on behalf of the European Society of Cardiology. All rights reserved. © The Author For permissions please

3. Figure 3 The density of I_CaL is homogeneous within a given sample. (A) The degree of identity between two I_CaL values recorded in myocytes isolated from the same sample is provided by plotting the difference between measures against their mean; the bias (mean difference ± SD) is indicated by lines. (B) Correlation between I_CaL measured from the same sample.
From: Downregulation of the calcium current in human right atrial myocytes from patients in sinus rhythm but with a high risk of atrial fibrillation
Eur Heart J. 2008;29(9): doi: /eurheartj/ehn140
Eur Heart J | Published on behalf of the European Society of Cardiology. All rights reserved. © The Author For permissions please

4. Figure 4 Density of peak I_CaL as a function of clinical parameters. MVD, mitral valve disease; EF, left ventricle ejection fraction; n, the number of patients; values are mean ± SEM.
From: Downregulation of the calcium current in human right atrial myocytes from patients in sinus rhythm but with a high risk of atrial fibrillation
Eur Heart J. 2008;29(9): doi: /eurheartj/ehn140
Eur Heart J | Published on behalf of the European Society of Cardiology. All rights reserved. © The Author For permissions please

5. Figure 5 The effect of the β-adrenergic agonist isoproterenol on I_CaL depends on current density. (A) Traces of I_CaL (300 ms test pulse from −80 mV to 0 mV) recorded in control conditions (open circle) and at the steady-state effect of 1 µM isoproterenol (solid circle, ISO) in myocytes showing a normal (left panel) or enhanced (right panel) response to isoproterenol. (B) Relation between percentage of increase in I_CaL upon 1 µM isoproterenol exposure and the peak I_CaL density measured just before the application of isoproterenol. (C) Concentration-dependent effect of isoproterenol on I_Ca recorded in patients with mitral valve disease or heart failure (solid circle) (n = 5) vs. patients with coronary artery disease and normal left ventricular function (open circle) (n = 5). (D) Percentage of increase in I_CaL upon application of 10 M of the phosphodiesterase inhibitor, IBMX.
From: Downregulation of the calcium current in human right atrial myocytes from patients in sinus rhythm but with a high risk of atrial fibrillation
Eur Heart J. 2008;29(9): doi: /eurheartj/ehn140
Eur Heart J | Published on behalf of the European Society of Cardiology. All rights reserved. © The Author For permissions please