Yalçin Hulya, Valenta Ines, Yalçin Fatih, Corona-Villalobos Celia, Vasquez Nestor, Ra Joshua, Kucukler Nagehan, Tahari Abdel, Pozios Iraklis, Zhou Yun, Pomper Martin, Abraham Theodore P, Schindler Thomas H, Abraham M Roselle
Department of Medicine, Hypertrophic Cardiomyopathy Center of Excellence, Johns Hopkins University, Baltimore, Maryland.
Department of Radiology, Johns Hopkins University, Baltimore, Maryland.
Am J Cardiol. 2016 Dec 15;118(12):1908-1915. doi: 10.1016/j.amjcard.2016.08.085. Epub 2016 Sep 15.
Vasodilator-induced transient left ventricular (LV) cavity dilation by positron emission tomography (PET) is common in patients with hypertrophic cardiomyopathy (HC). Because most patients with PET-LV cavity dilation lack obstructive epicardial coronary artery disease, we hypothesized that vasodilator-induced subendocardial hypoperfusion resulting from microvascular dysfunction underlies this result. To test this hypothesis, we quantified myocardial blood flow (MBF) (subepicardial, subendocardial, and global MBF) and left ventricular ejection fraction (LVEF) in 104 patients with HC without significant coronary artery disease, using NH-PET. Patients with HC were divided into 2 groups, based on the presence/absence of LV cavity dilation (LVvolume/LVvolume >1.13). Transient PET-LV cavity dilation was evident in 52% of patients with HC. LV mass, stress left ventricular outflow tract gradient, mitral E/E', late gadolinium enhancement, and prevalence of ischemic ST-T changes after vasodilator were significantly higher in patients with HC with LV cavity dilation. Baseline LVEF was similar in the 2 groups, but LV cavity dilation patients had lower stress-LVEF (43 ± 11 vs 53 ± 10; p <0.001), lower stress-MBF in the subendocardial region (1.6 ± 0.7 vs 2.3 ± 1.0 ml/min/g; p <0.001), and greater regional perfusion abnormalities (summed difference score: 7.0 ± 6.1 vs 3.9 ± 4.3; p = 0.004). The transmural perfusion gradient, an indicator of subendocardial perfusion, was similar at rest in the 2 groups. Notably, LV cavity dilation patients had lower stress-transmural perfusion gradients (0.85 ± 0.22, LV cavity dilation vs 1.09 ± 0.39, LV cavity dilation; p <0.001), indicating vasodilator-induced subendocardial hypoperfusion. The stress-transmural perfusion gradient, global myocardial flow reserve, and stress-LVEF were associated with LV cavity dilation. In conclusion, diffuse subendocardial hypoperfusion and myocardial ischemia resulting from microvascular dysfunction contribute to development of transient LV cavity dilation in HC.
在肥厚型心肌病（HC）患者中，通过正电子发射断层扫描（PET）检测到血管扩张剂诱发的短暂性左心室（LV）腔扩张很常见。由于大多数PET-LV腔扩张患者不存在阻塞性心外膜冠状动脉疾病，我们推测微血管功能障碍导致的血管扩张剂诱发的心内膜下灌注不足是这一结果的基础。为了验证这一假设，我们使用NH-PET对104例无明显冠状动脉疾病的HC患者的心肌血流量（MBF）（心外膜下、心内膜下和整体MBF）和左心室射血分数（LVEF）进行了量化。根据是否存在LV腔扩张（LV容积/LV容积>1.13），将HC患者分为两组。52%的HC患者出现短暂性PET-LV腔扩张。有LV腔扩张的HC患者的左心室质量、应激性左心室流出道梯度、二尖瓣E/E'、延迟钆增强以及血管扩张剂后缺血性ST-T改变的发生率显著更高。两组的基线LVEF相似，但有LV腔扩张的患者应激性LVEF较低（43±11对53±10；p<0.001），心内膜下区域的应激性MBF较低（1.6±0.7对2.3±1.0 ml/min/g；p<0.001），且区域灌注异常更大（总和差异评分：7.0±6.1对3.9±4.3；p = 0.004）。两组静息时作为心内膜下灌注指标的透壁灌注梯度相似。值得注意的是，有LV腔扩张的患者应激性透壁灌注梯度较低（0.85±0.22，有LV腔扩张组对1.09±0.39，无LV腔扩张组；p<0.001），表明血管扩张剂诱发的心内膜下灌注不足。应激性透壁灌注梯度、整体心肌血流储备和应激性LVEF与LV腔扩张相关。总之，微血管功能障碍导致的弥漫性心内膜下灌注不足和心肌缺血促成了HC患者短暂性LV腔扩张的发生。
