Regional myocardial sympathetic denervation predicts the risk of sudden cardiac arrest in ischemic cardiomyopathy.

Regional myocardial sympathetic denervation predicts the risk of sudden cardiac arrest in ischemic cardiomyopathy.
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DOI:
10.1016/j.jacc.2013.07.096
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发表时间:
2014-01-21
影响因子:
24
通讯作者:
Canty, John M., Jr.
Canty, John M., Jr.
中科院分区:
医学1区
文献类型:
--
作者:
Fallavollita, James A.;Heavey, Brendan M.;Luisi, Andrew J., Jr.;Michalek, Suzanne M.;Baldwa, Sunil;Mashtare, Terry L., Jr.;Hutson, Alan D.;deKemp, Robert A.;Haka, Michael S.;Sajjad, Munawwar;Cimato, Thomas R.;Curtis, Anne B.;Cain, Michael E.;Canty, John M., Jr.

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PAREPET(用正电子发射断层扫描预测心律失常事件)研究试图检验以下假设:量化心肌交感神经支配的不均匀性可以识别心脏骤停(SCA)风险最高的患者。左心室射血分数(LVEF)是识别有SCA风险且受益于植入式心脏除颤器(ICD)的患者的唯一参数。我们前瞻性入组了204例符合一级预防ICD条件的缺血性心肌病(LVEF ≤35%)受试者。正电子发射断层扫描(PET)用于定量心肌交感神经去神经(11 C-间羟麻黄碱[11 C-HED])、灌注(13 N-氨)和活力(胰岛素刺激的18 F-2-脱氧葡萄糖)。主要终点为SCA,定义为猝死或ICD因室颤或室性心动过速>240次/分而放电。随访4.1年后,病因特异性SCA为16.2%。冠状动脉容积(左心室[LV]的22 ± 7% vs. 19 ± 9%)和LVEF(24 ± 8% vs. 28 ± 9%)不是SCA的预测因子。相比之下,发生SCA的患者有更大量的交感神经去神经支配(33 ± 10% vs. LV的26 ± 11%; p = 0.001),反映了存活的去神经支配心肌。较低的三分之一的交感神经去神经有SCA率为1.2%/年和2.2%/年,而最高的三分之一有6.7%/年的速度。SCA的多变量预测因子为PET交感神经切除、左心室舒张末期容积指数、肌酐和无血管紧张素抑制。采用优化的临界点,所有4个风险因素的缺失识别为低风险(44%的队列; SCA <1%/年);而≥2个因素识别为高风险(20%的队列; SCA ~12%/年)。在缺血性心肌病中,使用11 C-HED PET评估交感神经去神经可预测SCA的病因特异性死亡率,与LVEF和梗死体积无关。这可能为识别最有可能从ICD中受益的患者提供了一种改进的方法。(使用正电子发射断层扫描[PAREPET]预测心律失常事件; NCT 01400334)
The PAREPET (Prediction of ARrhythmic Events with Positron Emission Tomography) study sought to test the hypothesis that quantifying inhomogeneity in myocardial sympathetic innervation could identify patients at highest risk for sudden cardiac arrest (SCA). Left ventricular ejection fraction (LVEF) is the only parameter identifying patients at risk of SCA who benefit from an implantable cardiac defibrillator (ICD). We prospectively enrolled 204 subjects with ischemic cardiomyopathy (LVEF ≤35%) eligible for primary prevention ICDs. Positron emission tomography (PET) was used to quantify myocardial sympathetic denervation (11C-meta-hydroxyephedrine [11C-HED]), perfusion (13N-ammonia) and viability (insulin-stimulated 18F-2-deoxyglucose). The primary endpoint was SCA defined as arrhythmic death or ICD discharge for ventricular fibrillation or ventricular tachycardia >240 beats/min. After 4.1 years follow-up, cause-specific SCA was 16.2%. Infarct volume (22 ± 7% vs. 19 ± 9% of left ventricle [LV]) and LVEF (24 ± 8% vs. 28 ± 9%) were not predictors of SCA. In contrast, patients developing SCA had greater amounts of sympathetic denervation (33 ± 10% vs. 26 ± 11% of LV; p = 0.001) reflecting viable, denervated myocardium. The lower tertiles of sympathetic denervation had SCA rates of 1.2%/year and 2.2%/year, whereas the highest tertile had a rate of 6.7%/year. Multivariate predictors of SCA were PET sympathetic denervation, left ventricular end-diastolic volume index, creatinine, and no angiotensin inhibition. With optimized cut-points, the absence of all 4 risk factors identified low risk (44% of cohort; SCA <1%/year); whereas ≥2 factors identified high risk (20% of cohort; SCA ~12%/year). In ischemic cardiomyopathy, sympathetic denervation assessed using 11C-HED PET predicts cause-specific mortality from SCA independently of LVEF and infarct volume. This may provide an improved approach for the identification of patients most likely to benefit from an ICD. (Prediction of ARrhythmic Events With Positron Emission Tomography [PAREPET]; NCT01400334)
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