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Another interesting afib research article October 30, 2003 10:50AM |
Registered: 8 years ago Posts: 18,890 |
Atrial L-type Ca2+ currents and human atrial fibrillation.
Van Wagoner DR, Pond AL, Lamorgese M, Rossie SS, McCarthy PM, Nerbonne JM.
Department of Cardiology and Kaufman Center for Heart Failure, The Cleveland Clinic Foundation, Cleveland, Ohio 44195, USA. vanwagd@ccf.org
Chronic atrial fibrillation (AF) is characterized by decreased atrial contractility, shortened action potential duration, and decreased accommodation of action potential duration to changes in activation rate.
Studies on experimental animal models of AF implicate a reduction in L-type Ca2+ current (I(Ca)) density in these changes. To evaluate the effect of AF on human I(Ca), we compared I(Ca) in atrial myocytes isolated from 42 patients in normal sinus rhythm at the time of cardiac surgery with that of 11 chronic AF patients.
I(Ca) was significantly reduced in the myocytes of patients with chronic AF (mean -3.35+/-0.5 pA/pF versus -9.13+/-1. 0 pA/pF in the controls), with no difference between groups in the voltage dependence of activation or steady-state inactivation. Although I(Ca) was lower in myocytes from the chronic AF patients, their response to maximal beta-adrenergic stimulation was not impaired.
Postoperative AF frequently follows cardiac surgery. Half of the patients in the control group (19/38) of this study experienced postoperative AF. Whereas chronic AF is characterized by reduced atrial I(Ca), the patients with the greatest I(Ca) had an increased incidence of postoperative AF, independent of patient age or diagnosis.
This observation is consistent with the concept that calcium overload may be an important factor in the initiation of AF.
The reduction in functional I(Ca) density in myocytes from the atria of chronic AF patients may thus be an adaptive response to the arrhythmia-induced calcium overload.
Circ Res. 1999 Sep 3;85(5):428-36.
Van Wagoner DR, Pond AL, Lamorgese M, Rossie SS, McCarthy PM, Nerbonne JM.
Department of Cardiology and Kaufman Center for Heart Failure, The Cleveland Clinic Foundation, Cleveland, Ohio 44195, USA. vanwagd@ccf.org
Chronic atrial fibrillation (AF) is characterized by decreased atrial contractility, shortened action potential duration, and decreased accommodation of action potential duration to changes in activation rate.
Studies on experimental animal models of AF implicate a reduction in L-type Ca2+ current (I(Ca)) density in these changes. To evaluate the effect of AF on human I(Ca), we compared I(Ca) in atrial myocytes isolated from 42 patients in normal sinus rhythm at the time of cardiac surgery with that of 11 chronic AF patients.
I(Ca) was significantly reduced in the myocytes of patients with chronic AF (mean -3.35+/-0.5 pA/pF versus -9.13+/-1. 0 pA/pF in the controls), with no difference between groups in the voltage dependence of activation or steady-state inactivation. Although I(Ca) was lower in myocytes from the chronic AF patients, their response to maximal beta-adrenergic stimulation was not impaired.
Postoperative AF frequently follows cardiac surgery. Half of the patients in the control group (19/38) of this study experienced postoperative AF. Whereas chronic AF is characterized by reduced atrial I(Ca), the patients with the greatest I(Ca) had an increased incidence of postoperative AF, independent of patient age or diagnosis.
This observation is consistent with the concept that calcium overload may be an important factor in the initiation of AF.
The reduction in functional I(Ca) density in myocytes from the atria of chronic AF patients may thus be an adaptive response to the arrhythmia-induced calcium overload.
Circ Res. 1999 Sep 3;85(5):428-36.
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Newman
Re: Another interesting afib research article October 30, 2003 09:30PM |
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Shannon
Re: Another interesting afib research article October 31, 2003 11:27AM |
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Re: Another interesting afib research article November 01, 2003 05:19AM |
Registered: 8 years ago Posts: 18,890 |
Newman - My interpretation is based on the last two paragraphs....
This observation is consistent with the concept that calcium overload may be an important factor in the initiation of AF.
The reduction in functional I(Ca) density in myocytes from the atria of chronic AF patients may thus be an adaptive response to the arrhythmia-induced calcium overload.
...which I take to mean what we have commented on before, too much intracellular calcium is not good. It is excitotoxic for afib.
Other than dietary sources of calcium, afibbers should be very cautious about consuming supplemental calcium.
When there is too much serum calcium - that is what goes unused or required intracellularly - the rest floats around and gets deposited in tissue
(atherosclerosis) or on bone (spurs) and kidney stones.
I was just pleased to see another documentation about excess calcium being "not a good thing."
Jackie
This observation is consistent with the concept that calcium overload may be an important factor in the initiation of AF.
The reduction in functional I(Ca) density in myocytes from the atria of chronic AF patients may thus be an adaptive response to the arrhythmia-induced calcium overload.
...which I take to mean what we have commented on before, too much intracellular calcium is not good. It is excitotoxic for afib.
Other than dietary sources of calcium, afibbers should be very cautious about consuming supplemental calcium.
When there is too much serum calcium - that is what goes unused or required intracellularly - the rest floats around and gets deposited in tissue
(atherosclerosis) or on bone (spurs) and kidney stones.
I was just pleased to see another documentation about excess calcium being "not a good thing."
Jackie
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