Heart Institute, Cedars-Sinai Medical Center, Los Angeles, CA (B.K.T., B.T.J., K.R., C.T., A.U.-E., S.S.C.) ; Cleveland Clinic Foundation, Cleveland OH (B.K.T.).
J Am Heart Assoc. 2012 Jun;1(3):e001511. doi: 10.1161/JAHA.112.001511. Epub 2012 Jun 22.
Concentric left ventricular hypertrophy (LVH) is independently associated with increased risk of sudden cardiac death (SCD). Some animal models of LVH display specific alterations of the myocardial interstitium that could increase myocardial vulnerability to ventricular arrhythmias, but these merit evaluation in humans with LVH and SCD.
Twelve consecutive patients with isolated LVH and SCD (LVH+SCD) in the absence of hypertrophic cardiomyopathy, coronary disease, or other cardiac structural abnormality were ascertained in the Oregon Sudden Unexpected Death Study. Detailed postmortem comparisons were conducted with 18 controls who had isolated LVH and unnatural deaths (Control Group A) and 6 controls who had structurally normal hearts and unnatural deaths (Control Group B). Postmortem left ventricular myocardial sections were obtained for measurement of collagen volume fraction, characterization of gap junctions, and quantification of collagen subtypes. Heart weight normalized to body weight was higher in LVH+SCD cases (6.9±1.2 g/kg) than in Control Group A (5.3±1.4 g/kg) and Control Group B (4.2±0.3 g/kg); P=0.001. Collagen volume fraction was also higher in LVH+SCD cases (3.1±0.4) than in Control Group A (2.3±0.4) and Control Group B (1.6±0.3); P=0.0002. The relative amount of collagen III was significantly higher in LVH+SCD cases (33.0±4.4%) than in Control Group A (20.9±4.3%) and Control Group B (13.4±3.5%); P=0.0001. There was an overall increase in the number of connexin 43-labeled gap junctions with increasing myocyte size. No subject was found to have high-risk hypertrophic cardiomyopathy mutations.
In addition to the expected increase in myocardial mass and overall collagen content, SCD with isolated LVH was associated with relative abundance of type III collagen, a novel finding that warrants further mechanistic evaluation. (J Am Heart Assoc. 2012;1:e001511 doi: 10.1161/JAHA.111.001511.).
同心性左心室肥厚（LVH）与心源性猝死（SCD）风险增加独立相关。一些 LVH 的动物模型显示心肌间质的特定改变，这可能增加心肌对室性心律失常的易感性，但这些在 LVH 和 SCD 的人类中需要进行评估。
在俄勒冈州猝发意外死亡研究中，确定了 12 例连续的孤立性 LVH 和 SCD（LVH+SCD）而无肥厚型心肌病、冠心病或其他心脏结构性异常的患者。与 18 例具有孤立性 LVH 和非自然死亡的对照（对照组 A）和 6 例具有正常心脏结构和非自然死亡的对照（对照组 B）进行了详细的死后比较。获得死后左心室心肌切片，用于测量胶原容积分数、间隙连接的特征以及胶原亚型的定量。LVH+SCD 病例的左心室重量与体重的比值高于对照组 A（6.9±1.2 g/kg）和对照组 B（4.2±0.3 g/kg）；P=0.001。LVH+SCD 病例的胶原容积分数（3.1±0.4）也高于对照组 A（2.3±0.4）和对照组 B（1.6±0.3）；P=0.0002。LVH+SCD 病例的 III 型胶原相对量（33.0±4.4%）明显高于对照组 A（20.9±4.3%）和对照组 B（13.4±3.5%）；P=0.0001。随着心肌细胞大小的增加，连接蛋白 43 标记的间隙连接数量总体上增加。未发现具有高危肥厚型心肌病突变的患者。
除了预期的心肌质量和整体胶原含量增加外，孤立性 LVH 伴 SCD 还与 III 型胶原的相对丰度相关，这是一个新的发现，需要进一步进行机制评估。（美国心脏协会杂志。2012;1:e001511 doi: 10.1161/JAHA.111.001511。）
Zotero 插件
