Hussein Ayman A, Niekoop Michelle, Dilsizian Vasken, Ghzally Yousra, Abdulghani Mohammed, Asoglu Ramazan, Chen Wengen, Smith Mark, See Vincent, Shorofsky Stephen R, Dickfeld Timm-Michael
Section of Cardiac Pacing and Electrophysiology, Cleveland Clinic, Cleveland, OH, USA.
Division of Cardiology, University of Maryland School of Medicine, 22 S Greene St, Baltimore, MD, 21201, USA.
J Interv Card Electrophysiol. 2017 Apr;48(3):247-254. doi: 10.1007/s10840-016-0219-1. Epub 2017 Jan 25.
Hibernating myocardium (HM) is associated with sudden cardiac death (SCD). Little is known about the electrophysiological properties of HM and the basis of its association with SCD. We aimed to electrophysiologically characterize HM in patients with ventricular tachycardia (VT).
Endocardial voltage mapping, metabolic FDG-positron emission tomography (PET) and perfusion Rb, Tl, or Tc scans were performed in 61 ischemic heart disease patients with VT. Hibernating areas were identified which was followed by three-dimensional PET reconstructions and integration with voltage maps to allow hybrid metabolic-electro-anatomic assessment of the arrhythmogenic substrate.
Of 61 patients with ischemic heart disease and refractory VT, 7 were found to have hibernating myocardium (13%). A total of 303 voltage points were obtained within hibernating myocardium (8.2 points per 10 cm) and displayed abnormal voltage in 48.5 and 78.3% of bipolar and unipolar recordings, respectively, with significant heterogeneity of bipolar (p < 0.0001) and unipolar voltage measurements (p = 0.0004). Hibernating areas in 6 of 7 patients contained all three categories of bipolar voltage-defined scar (<0.5 mV), border zone (0.5-1.5 mV), and normal myocardium (>1.5 mV). The characteristics of local electrograms were also assessed and found abnormal in most recordings (76.6, 10.2% fractionated, 5.3% isolated potentials). Exit sites of clinical VTs were determined in 6 patients, of which 3 were located within hibernating myocardium.
Hibernating myocardium displays abnormal and heterogeneous electrical properties and seems to contribute to the substrate of VT. These observations may underlie the vulnerability to reentry and SCD in patients with hypoperfused yet viable myocardium.
冬眠心肌（HM）与心源性猝死（SCD）相关。关于HM的电生理特性及其与SCD关联的基础知之甚少。我们旨在对室性心动过速（VT）患者的HM进行电生理特征分析。
对61例患有VT的缺血性心脏病患者进行心内膜电压标测、代谢性氟脱氧葡萄糖正电子发射断层扫描（PET）以及灌注铷、铊或锝扫描。识别出冬眠区域，随后进行三维PET重建并与电压图整合，以对致心律失常基质进行混合代谢 - 电解剖评估。
在61例患有缺血性心脏病和难治性VT的患者中，发现7例有冬眠心肌（13%）。在冬眠心肌内共获得303个电压点（每10 cm有8.2个点），双极和单极记录中分别有48.5%和78.3%显示异常电压，双极（p < 0.0001）和单极电压测量存在显著异质性（p = 0.0004）。7例患者中有6例的冬眠区域包含双极电压定义的所有三类瘢痕（<0.5 mV）、边界区（0.5 - 1.5 mV）和正常心肌（>1.5 mV）。还评估了局部电图的特征，发现大多数记录异常（76.6%，10.2%呈碎裂，5.3%为孤立电位）。确定了6例患者临床VT的出口部位，其中3例位于冬眠心肌内。
冬眠心肌表现出异常和异质性的电特性，似乎是VT基质的一部分。这些观察结果可能是灌注不足但仍存活心肌患者发生折返和SCD易感性的基础。
