JAMA：冠状动脉疾病患者局部心肌变薄与疤痕负荷有关

心血管CMR分析

局部左心室壁变薄被认为是透壁性心肌梗塞和瘢痕组织的表现。然而，最近的病例报道使用延迟增强心血管磁共振(CMR)成像技术揭示了室壁变薄可能存在于有限瘢痕负荷或无瘢痕负荷患者的可能性。

为了评估局部心肌壁变薄患者并明确瘢痕负荷和机能改善之间的关系，杜克大学心血管研究中心的Raymond J. Kim博士及其同事进行了深入研究，他们发现，CMR检查显示局部室壁变薄的CAD患者中，有18%瘢痕负荷有限，并与血管再通术后的收缩性改善及室壁变薄趋势的逆转相关。这些发现与现行假说不同，还需要进一步的研究予以证实。论文发表于国际权威杂志JAMA 2013年最新一期在线版上。

这一研究者发起的、前瞻性、3中心试验(IIR)自2000年八月份开始至2008年一月份结束，试验分成三个部分，第一部分对CMR检查证实为冠状动脉疾病(CAD)的患者予以评估，明确局部室壁变薄的发病率（定义为舒张末期室壁的厚度≤5.5 mm），第二部分明确室壁变薄的患者有无瘢痕的存在及其范围，第三部分评估冠状动脉重建术后的室壁变薄患者的心肌形态和收缩性的任何改变。本研究的主要结局为利用延迟增强CMR评估变薄区域的瘢痕负荷，并利用cine-CMR于血管再通术后对心肌形态及功能予以评估。

结果显示，在纳入试验的1055例连续CAD患者中，有201 (19% [95% CI, 17% to 21%])例发现局部室壁变薄。变薄区域平均跨越了34% (95% CI, 32% to 37% [SD, 15%])的LV表面面积。在上述区域，瘢痕范围为72% (95% CI, 69% to 76% [SD, 25%])，然而，18% (95% CI, 13% to 24%)的变薄区域瘢痕负荷有限(不到总变薄范围的50%)。在接受血管再通术的变薄患者中，经cine-CMR (n = 42)随访发现，变薄区域的瘢痕范围与局部(r = −0.72, P < .001)和全局(r = −0.53, P < .001)收缩性改善呈负相关。研究发现，瘢痕负荷有限的变薄区域的舒张末期室壁厚度在血管再通术后由4.4 mm (95% CI, 4.1 to 4.7)增加为7.5 mm (95% CI, 6.9 to 8.1) (P < .001)，从而逆转室壁变薄的趋势。多变量分析显示，瘢痕范围与收缩性改善(斜率系数, −0.03 [95% CI, −0.04 to −0.02]; P < .001)以及变薄趋势的逆转(斜率系数, −0.05 [95% CI, −0.06 to −0.04]; P < .001)有最强相关性。

研究人员由此得出结论，CMR检查显示局部室壁变薄的CAD患者中，有18%瘢痕负荷有限，并与血管再通术后的收缩性改善及室壁变薄趋势的逆转相关。这些发现与现行假说不同，还需要进一步的研究予以证实。

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IMPORTANCE:

Regional left ventricular (LV) wall thinning is believed to represent chronic transmural myocardial infarction and scar tissue. However, recent case reports using delayed-enhancement cardiovascular magnetic resonance (CMR) imaging raise the possibility that thinning may occur with little or no scarring.

OBJECTIVE:

To evaluate patients with regional myocardial wall thinning and to determine scar burden and potential for functional improvement.

DESIGN, SETTING, AND PATIENTS:

Investigator-initiated, prospective, 3-center study conducted from August 2000 through January 2008 in 3 parts to determine (1) in patients with known coronary artery disease (CAD) undergoing CMR viability assessment, the prevalence of regional wall thinning (end-diastolic wall thickness ≤5.5 mm), (2) in patients with thinning, the presence and extent of scar burden, and (3) in patients with thinning undergoing coronary revascularization, any changes in myocardial morphology and contractility. MAIN OUTCOMES AND MEASURES: Scar burden in thinned regions assessed using delayed-enhancement CMR and changes in myocardial morphology and function assessed using cine-CMR after revascularization.

RESULTS:

Of 1055 consecutive patients with CAD screened, 201 (19% [95% CI, 17% to 21%]) had regional wall thinning. Wall thinning spanned a mean of 34% (95% CI, 32% to 37% [SD, 15%]) of LV surface area. Within these regions, the extent of scarring was 72% (95% CI, 69% to 76% [SD, 25%]); however, 18% (95% CI, 13% to 24%) of thinned regions had limited scar burden (≤50% of total extent). Among patients with thinning undergoing revascularization and follow-up cine-CMR (n = 42), scar extent within the thinned region was inversely related to regional (r = -0.72, P < .001) and global (r = -0.53, P < .001) contractile improvement. End-diastolic wall thickness in thinned regions with limited scar burden increased from 4.4 mm (95% CI, 4.1 to 4.7) to 7.5 mm (95% CI, 6.9 to 8.1) after revascularization (P < .001), resulting in resolution of wall thinning. On multivariable analysis, scar extent had the strongest association with contractile improvement (slope coefficient, -0.03 [95% CI, -0.04 to -0.02]; P < .001) and reversal of thinning (slope coefficient, -0.05 [95% CI, -0.06 to -0.04]; P < .001).

CONCLUSIONS AND RELEVANCE:

Among patients with CAD referred for CMR and found to have regional wall thinning, limited scar burden was present in 18% and was associated with improved contractility and resolution of wall thinning after revascularization. These findings, which are not consistent with common assumptions, warrant further investigation.