Department of Clinical Science, University of Bergen, PO box 7804, N-5020 Bergen, Norway.
Department of Clinical Science, University of Bergen, PO box 7804, N-5020 Bergen, Norway; Department of Heart Disease, Haukeland University Hospital, PO box 1400, N-5021 Bergen, Norway.
Int J Cardiol. 2019 Jul 1;286:1-6. doi: 10.1016/j.ijcard.2019.03.059. Epub 2019 Mar 28.
The underlying mechanisms causing myocardial ischemia in non-obstructive coronary artery disease (CAD) are still unclear. We explored whether left ventricular hypertrophy (LVH) was associated with myocardial ischemia in patients with stable angina and non-obstructive CAD.
132 patients (mean age 63 ± 8 years, 56% women) with stable angina and non-obstructive CAD diagnosed as <50% stenosis by coronary computed tomography angiography (CCTA) underwent myocardial contrast stress echocardiography. Left ventricular (LV) hypertrophy (LVH) was identified by LV mass index >46.7 g/m in women and >49.2 g/m in men. Patients were grouped according to presence or absence of myocardial ischemia by myocardial contrast stress echocardiography. The number of LV segments with ischemia at peak stress was taken as a measure of the extent of myocardial ischemia.
Myocardial ischemia was found in 52% of patients, with on average 5 ± 3 ischemic LV segments per patient. The group with myocardial ischemia had higher prevalence of LVH (23 vs. 10%, p = 0.035), while age, sex and prevalence of hypertension did not differ between groups (all p > 0.05). In multivariable regression analyses, LVH was associated with presence of myocardial ischemia (odds ratio 3.27, 95% confidence interval [1.11-9.60], p = 0.031), and larger extent of myocardial ischemia (β = 0.22, p = 0.012), independent of confounders including age, hypertension, obesity, hypercholesterolemia, calcium score and segment involvement score by CCTA.
LVH was independently associated with both presence and extent of myocardial ischemia in patients with stable angina and non-obstructive CAD by CCTA. These results suggest LVH as an independent contributor to myocardial ischemia in non-obstructive CAD.
ClinicalTrials.gov, identifier NCT018535271.
非阻塞性冠状动脉疾病（CAD）引起心肌缺血的潜在机制仍不清楚。我们探讨了左心室肥厚（LVH）与稳定型心绞痛和非阻塞性 CAD 患者心肌缺血的关系。
132 名（平均年龄 63±8 岁，56%为女性）经冠状动脉计算机断层扫描血管造影（CCTA）诊断为狭窄<50%的稳定型心绞痛和非阻塞性 CAD 患者接受心肌对比应激超声心动图检查。左心室（LV）肥厚（LVH）通过 LV 质量指数（女性>46.7 g/m，男性>49.2 g/m）确定。根据心肌对比应激超声心动图是否存在心肌缺血，将患者分为两组。峰值应激时存在缺血的 LV 节段数作为心肌缺血程度的衡量标准。
52%的患者存在心肌缺血，平均每位患者有 5±3 个缺血性 LV 节段。存在心肌缺血的患者 LVH 发生率更高（23%比 10%，p=0.035），而年龄、性别和高血压患病率在两组间无差异（均 p>0.05）。多变量回归分析显示，LVH 与心肌缺血的存在相关（比值比 3.27，95%置信区间 [1.11-9.60]，p=0.031），与更大程度的心肌缺血相关（β=0.22，p=0.012），独立于年龄、高血压、肥胖、高胆固醇血症、钙评分和 CCTA 节段受累评分等混杂因素。
LVH 与 CCTA 诊断的稳定型心绞痛和非阻塞性 CAD 患者心肌缺血的存在和程度均独立相关。这些结果表明 LVH 是非阻塞性 CAD 心肌缺血的一个独立因素。
ClinicalTrials.gov，标识符 NCT018535271。
