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目的 探讨高血压病患者是否存在心肌微血管病变以及其与疾病严重程度和心肌肥厚的关系。方法 应用心肌对比超声心动图 ,静注含氟碳气体声振白蛋白微泡造影剂 (全氟显 )后 ,采用间断谐波成像技术测量静息时和注射潘生丁后心肌的A、β和A·β值 ,并计算出A、β比值和冠脉微血管的血流储备 (CMVFR)。 结果 高血压病患者静息时的A、β和A·β值均较对照组增高 (P >0 0 5) ,而注射潘生丁后明显降低 (P <0 0 1 ) ,A、β比值以及CMVFR显著降低(P <0 0 5和 0 0 1 ) ;随着高血压病情的加重 ,A和A·β值增高 ,A比值和CMVFR下降 ,A和A·β值与SBP、DBP显著正相关 (P <0 0 1 )、CMVFR与DBP负相关 (P <0 0 5) ;高血压左室肥厚 (LVH)患者静息状态的A、β和A·β值较无肥厚者增加 ,A、β比值和CMVFR下降 ;A和A·β与LVM和LVMI显著相关 (P <0 0 1 ) ;CMVFR与室间隔厚度负相关(P <0 0 5)。结论 高血压病患者静息时的心肌微循环血流量增加、心肌微血管储备功能和非内皮依赖性的血管扩张能力明显受损、心肌毛细血管密度明显减少 ,并且随着疾病的进展而加重 ;高血压LVH患者较无LVH者的微血管功能受损程度更严重
Objective To investigate the presence or absence of myocardial microangiopathy in hypertensive patients and its relationship with disease severity and cardiac hypertrophy. Methods After myocardial contrast echocardiography, intravenous injection of fluorocarbon gas to albumin microbubble contrast medium (perfluorinated), we used interrupted harmonic imaging to measure the myocardial A, β and A at rest and after injection of dipyridamole · Β values, and calculate the A, β ratio and coronary microvascular blood flow reserve (CMVFR). Results The levels of A, β and A · β at rest in hypertension patients were significantly higher than those in controls (P 0 05), but significantly lower after injection of dipyridamole (P 0 01), A and β ratios and CMVFR (P <0.05 and 0.01). With the aggravation of hypertension, A and A · β increased, A decreased and CMVFR decreased, and A and A · β had significant positive correlation with SBP and DBP (P <0.01). CMVFR was negatively correlated with DBP (P <0.05). A, β and A · β at rest in hypertensive patients with left ventricular hypertrophy were significantly higher than those without hypertrophy Ratio and CMVFR decreased; A and A · β were significantly correlated with LVM and LVMI (P <0.01); CMVFR was negatively correlated with interventricular septum thickness (P <0.05). Conclusion Hypertension patients with myocardial microcirculation at rest increased blood flow, myocardial microvascular reserve function and non-endothelium-dependent vasodilatation was significantly impaired, myocardial capillary density was significantly reduced, and with the progress of the disease aggravate; high Blood pressure LVH patients with LVH less impaired microvascular function more serious