QRS/T-wave and calcium alternans in a type I diabetic mouse model for spontaneous postmyocardial infarction ventricular tachycardia: A mechanism for the antiarrhythmic effect of statins.
QRS/T-wave and calcium alternans in a type I diabetic mouse model for spontaneous postmyocardial infarction ventricular tachycardia: A mechanism for the antiarrhythmic effect of statins.
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DOI：
10.1016/j.hrthm.2017.05.026
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发表时间：
2017-09
期刊：
影响因子：
5.5
通讯作者：
Galper JB
中科院分区：
文献类型：
--
作者：
Jin H;Welzig CM;Aronovitz M;Noubary F;Blanton R;Wang B;Rajab M;Albano A;Link MS;Noujaim SF;Park HJ;Galper JB
The incidence of sudden arrhythmic death is markedly increased in diabetics. Develop a mouse model for Post MI VT in the diabetic heart and determine the mechanism of an antiarrhythmic effect of statins. EKG transmitters were implanted in wild type (WT), placebo and pravastatin treated Type I diabetic Akita mice, MIs induced by coronary ligation, Ca2+ transients studied by optical mapping, Ca2+ transients and sparks in left VM (VM) by the Ionoptix system and confocal microscopy. Burst pacing of Akita mouse hearts resulted in rate related QRS/T-Wave alternans, which was attenuated in pravastatin treated mice. Post MI Akita mice developed QRS/T-wave alternans and VT, 2,820 ± 879 beats/mouse which decreased to 343 ± 115 in pravastatin treated mice, (n=13, P<0.05). Optical mapping demonstrated pacing induced VT originating in the peri-infarction zone and Ca2+ alternans, both attenuated in hearts of statin treated mice. Akita VM displayed: Ca2+ alternans, triggered activity, increased; Ca2+ transient decay time (Tau), incidence of Ca2+ sparks and cytosolic Ca2+ and decreased SR Ca2+ stores which were in part reversed in cells from statin treated mice. Homogenates of Akita ventricles demonstrated decreased SERCA2a/PLB ratio and increased ratio of protein phosphatase (PP-1) to the PP-1 inhibitor PPI-1 reversed in homogenates of pravastatin treated Akita mice. Pravastatin decreased the incidence of post MI VT and Ca2+ alternans in Akita mouse hearts in part via the reversal of abnormalities of Ca2+ handling via the PP-1/PPI-1 pathway.
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DOI：
10.1152/ajpheart.00313.2002
发表时间：
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影响因子：
4.8
作者：
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通讯作者：
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影响因子：
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DOI：
10.1111/j.1440-1681.2006.04440.x
发表时间：
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影响因子：
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