李蔚.肥厚型心肌病患者心肌血流储备降低诱发左心室重构[J].内科急危重症杂志,2023,29(6):476-479
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| DOI：10.11768/nkjwzzzz20230608 |
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| 基金项目:四川省科技计划项目（No：2018SZ0231） |
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| 中文摘要: |
| 摘要 目的：研究心肌血流储备与肥厚型心肌病（HCM）患者左心室重构指数（LVRI）及左心室质量指数（LVMI）的关系。方法：收集98例HCM患者为研究组，另选取98例同期体检健康者为对照组。收集2组受试者基本资料和临床资料，采集静息状态常规心动图和心肌超声造影（MCE）图像，采集运动状态常规超声心动图及峰值期MCE图像，计算并分析2组受试者运动负荷后与静息状态的A×β的比值，即心肌血流储备值。采用Pearson法分析心肌血流储备与LVRI及LVMI的关系。结果：研究组患者室间隔490个节段中显影清晰有478个，其中非肥厚节段143个，肥厚节段335个。对照组室间隔490个节段中显影清晰有479个。研究组患者中纽约心功能分级（NYHA）为Ⅱ级、伴有胸闷、有药物治疗、有钙通道阻滞剂、有β受体阻滞剂治疗的患者数显著多于对照组（P均＜0.05）。研究组左心室收缩末期内径（LVESD）、左心室收缩末期容积（LVESV）、左心室舒张末期内径（LVEDD）、左心室舒张末期容积（LVEDV）、左心室射血分数（LVEF）、每搏输出量（SV）、二尖瓣舒张期血流E峰和A峰的比值（E/A）水平显著低于对照组；左心室后壁厚度（LVPWD）、舒张末期室间隔厚度（IVST）、LVMI及LVRI水平显著高于对照组（P均＜0.05）。研究组静息状态和负荷状态下MCE参数A值、β值和A×β值显著低于对照组；负荷状态下，研究组肥厚节段的MCE参数A值、β值和A×β值显著低于非肥厚节段（P均＜0.05）。运动负荷状态心肌灌注异常患者48例，静息状态心肌灌注异常患者32例，组间比较差异有统计学意义（t=5.407，P=0.020）。研究组患者的心肌血流储备显著低于对照组[(2.69±0.12) vs (3.07±0.22)，t=15.011，P<0.001]。研究组患者心肌血流储备与LVRI及LVMI呈负相关（P均＜0.05）。结论：HCM患者心肌血流储备的降低会导致LVMI及LVRI增加，诱发左心室重构。 |
| 英文摘要: |
| Abstract Objective: To study the relationship between myocardial blood flow reserve and left ventricular remodeling index (LVRI) and left ventricular mass index (LVMI) in patients with hypertrophic cardiomyopathy (HCM). Methods: A total of 98 patients with HCM were collected as the study group, and 98 healthy people were selected as the control group. The basic data and clinical data of two groups were collected, the resting conventional echocardiography and myocardial contrast echocardiography (MCE) images and the exercise conventional echocardiography and peak MCE images were obtained, and the ratio of Axβ after exercise load to Axβ at rest (the myocardial blood flow reserve value) was calculated and analyzed. Pearson method was used to analyze the relationship between myocardial blood flow reserve and LVRI and LVMI. Results: In the study group, 478 of 490 segments of interventricular septum were clearly developed, including 143 non-hypertrophic segments and 335 hypertrophic segments. In the control group, 479 of 490 segments of interventricular septum were clearly developed. In the study group, the number of patients with New York Heart Function Classification (NY-HA) grade II, chest tightness, medication, calcium channel blockers and beta blockers was significantly greater than that in the control group (all P< 0.05). The left ventricular end-systolic diameter (LVESD), left ventricular end-systolic volume (LVESV), left ventricular end-diastolic diameter (LVEDD), left ventricular output end-diastolic volume (LVEDV), left ventricular ejection fraction (LVEF), stroke output (SV) and the ratio of E peak to A peak of mitral diastolic blood flow (E/A) in the study group were significantly lower than those in the control group. The left ventricular posterior wall thickness (LVPWD), end-diastolic interventricular septum thickness (IVST), LVMI and LVRI levels in the study group were significantly higher than those in the control group (P< 0.05). The values of MCE parameters A,β and A×β in the study group were significantly lower than those in the control group at rest and under load. Under load, the MCE parameters A, β and A×β of the hypertrophic segment in the study group were significantly lower than those in the non-hypertrophic segment (P< 0.05). There were 48 patients with abnormal myocardial perfusion in exercise load state and 32 patients with abnormal myocardial perfusion in rest state, and the difference between the two groups was statistically significant (t=5.407, P=0.020). The myocardial blood flow reserve in the study group was significantly lower than that in the control group [(2.69±0.12) vs (3.07±0.22), t= 15.011, P< 0.001]. The myocardial blood flow reserve in the study group was negatively correlated with LVRI and LVMI (P< 0.05). Conclusion: The decrease of myocardial blood flow reserve in patients with hypertrophic cardiomyopathy will lead to the increase of LVMI and LVRI and induce left ventricular remodeling. |
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