Dietary omega-3 fatty acids and susceptibility to ventricular fibrillation: lack of protection and a proarrhythmic effect.

Dietary omega-3 fatty acids and susceptibility to ventricular fibrillation: lack of protection and a proarrhythmic effect.
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DOI:
10.1161/circep.111.966739
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发表时间:
2012-06-01
期刊:
Circulation. Arrhythmia and electrophysiology
影响因子:
--
通讯作者:
Schwartz PJ
Schwartz PJ
中科院分区:
其他
文献类型:
--
作者:
Billman GE;Carnes CA;Adamson PB;Vanoli E;Schwartz PJ

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最近的临床研究,评估补充欧米茄-3多不饱和脂肪酸(n-3 PUFA)对心脏性猝死的影响,产生了相互矛盾的结果。我们的目的是澄清这个问题,使用一个建立的和临床相关的犬心脏性猝死模型。在76只心肌梗死(MI)愈合的犬(来自两项独立研究)的运动试验的最后一分钟,使用2分钟的左旋支动脉闭塞评价了心室颤动(VF)的易感性; 44只发生VF(易感,VF+),32只未发生VF(抵抗,VF-)。然后将这些犬随机分配至安慰剂组(1 g/天,玉米油; 15 VF+,11 VF-)或n-3 PUFA组(1-4 g/天,二十二碳六烯酸+二十碳五烯酸乙酯,29 VF+,21 VF-)。还用n-3 PUFA(4 g/天)处理7只假手术(无MI)犬。治疗后(3个月)重复运动+缺血试验。日粮n-3 PUFAs使红细胞和左心室n-3 PUFA水平显著升高(P<0.01)。9只MI后犬(安慰剂组5只,n-3 PUFA组4只)和2只假手术组犬在3个月治疗期间突然死亡。n-3 PUFA治疗未能预防VF+犬的心律失常(安慰剂组降低27%,n-3 PUFA组降低24%,P=0.5646),但在VF−动物中诱导VT/VF(n-3 PUFA组33%,安慰剂组0%,P=0.0442)。尽管心脏组织n-3 PUFA含量大幅增加,但饮食n-3 PUFA不能预防缺血诱导的VF,实际上增加了非梗死和低风险MI后犬的心律失常易感性。
Recent clinical studies that evaluated the effects of supplemental omega-3 polyunsaturated fatty acids (n-3 PUFAs) on sudden cardiac death have yielded conflicting results. Our aim was to clarify this issue using an established and clinical relevant canine model of sudden cardiac death. Susceptibility to ventricular fibrillation (VF) was evaluated using a 2 minute left circumflex artery occlusion during the last minute of an exercise test in 76 dogs (from two independent studies) with healed myocardial infarctions (MI); 44 developed VF (susceptible, VF+) while 32 did not (resistant, VF−). These dogs were then randomly assigned to either placebo (1 g/day, corn oil; 15 VF+, 11 VF−) or n-3 PUFA (1–4 g/day, docosahexaenoic acid + eicosapentaenoic acid ethyl esters, 29 VF+, 21 VF−) groups. Seven sham (no-MI) dogs were also treated with n-3 PUFA (4 g/day). After treatment (3 months), the exercise + ischemia test was repeated. Dietary n-3 PUFAs produced significant (P<0.01) increases in red blood cell and left ventricular n-3 PUFA levels. Nine post MI (5 placebo vs. 4 n-3 PUFA) and 2 sham dogs died suddenly during the 3-month treatment period. The n-3 PUFA treatment failed to prevent arrhythmias in VF+ dogs (decreased in 27% placebo vs. 24% n-3 PUFA, P=0.5646) but induced VT/VF in VF− animals (n-3 PUFA 33% vs. placebo 0%, P=0.0442). Despite large increases in cardiac tissue n-3 PUFA content, dietary n-3 PUFAs did not prevent ischemia-induced VF and actually increased arrhythmia susceptibility in both non-infarcted and low risk post-MI dogs.