March 31, 2007AJP Heart and Circulatory Physiology
Effect of intracellular Ca2+ and action potential duration on L-type Ca2+ channel inactivation and recovery from inactivation in rabbit cardiac myocytes
Key result
Long action potential duration and slower intracellular Ca2+ decline lead to cumulative inactivation limiting I(Ca) at high heart rates, potentially contributing to negative FFR in heart failure.
Why the study?
Does prolonged action potential duration and altered intracellular Ca2+ affect L-type Ca2+ channel inactivation and recovery in rabbit cardiac myocytes?
Population
Rabbit cardiac myocytes
Comparison
Exposure to different diastolic intracellular… vs Normal/lower diastolic Ca2+ concentrations and…
Design
Preclinical
Authors
Discussion
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Implication
May explain rate-dependent contractile impairment in HF; hypothesis-generating in rabbit myocytes, requires human validation.
Structured PICO
Does prolonged action potential duration and altered intracellular Ca2+ affect L-type Ca2+ channel inactivation and recovery in rabbit cardiac myocytes?
P
Population
Rabbit cardiac myocytes
I
Intervention
Exposure to different diastolic intracellular Ca2+ concentrations (up to 600 nM) and various action potential durations (APDs) simulating heart failure
C
Comparator
Normal/lower diastolic Ca2+ concentrations (<600 nM) and shorter APDs
O
Outcome
L-type Ca2+ current (I(Ca)) inactivation and recovery from inactivationsurrogate
Prolonged action potential duration and slower intracellular calcium decline limit calcium current availability at high heart rates, potentially contributing to the negative force-frequency relationship seen in heart failure.
Cite This Study
Altamirano et al. (2007) studied Heart failure (simulated). Different diastolic [Ca2+]i and action potential durations vs. Normal/baseline conditions was evaluated on I(Ca) inactivation and recovery from inactivation. Long action potential duration and slower intracellular Ca2+ decline lead to cumulative inactivation limiting I(Ca) at high heart rates, potentially contributing to negative FFR in heart failure.