Kozàkovà Michaela, Morizzo Carmela, Ferrannini Ele, Palombo Carlo
Department of Internal Medicine, University of Pisa School of Medicine, Pisa, Italy.
J Hypertens. 2003 Jul;21(7):1407-14. doi: 10.1097/00004872-200307000-00032.
High pulsatile load is associated with structural alterations of the heart and arteries, which may cause changes in the coronary circulation and predispose to myocardial ischemia. This study was designed to investigate the relationships of coronary vasodilator capacity and exercise-induced myocardial ischemia to pulsatile and steady components of office blood pressure.
Eighty-two untreated, middle-aged hypertensive patients without coronary artery stenosis and 23 normotensive volunteers, underwent exercise electrocardiogram test and standard and transesophageal echocardiography to assess the occurrence of myocardial ischemia, left ventricular (LV) mass and geometry, total arterial compliance and coronary vasodilator capacity.
In the hypertensive population, minimum coronary resistance (MCR) was significantly higher (P < 0.01) in the top as compared to all three lower pulse pressure (PP) quartiles (1.10 +/- 0.19, 1.21 +/- 0.23, 1.20 +/- 0.26 and 1.43 +/- 0.26 mmHg s/cm). An additional increase in MCR also occurred in the top quartile of systolic blood pressure (SBP), but not across quartiles of mean blood pressure. In regression analysis, MCR increased with PP, SBP and LV wall thickness and decreased with total arterial compliance. As compared to hypertensive patients with a negative exercise test for myocardial ischemia (n = 30), those with a positive test (n = 20) had higher MCR (1.12 +/- 0.22 versus 1.39 +/- 0.29 mmHg s/cm, P < 0.01) and lower total arterial compliance (96 +/- 22 versus 81 +/- 16%, P < 0.01).
In untreated middle-aged hypertensive patients, coronary vasodilator capacity declines with increasing office PP and SBP. A decreased arterial compliance and increased LV wall thickness appear to be major alterations underlying this relationship. Exercise-induced myocardial ischemia is associated with higher MCR and lower arterial compliance.
高搏动负荷与心脏和动脉的结构改变有关，这可能导致冠状动脉循环变化并易引发心肌缺血。本研究旨在探讨冠状动脉扩张能力和运动诱发的心肌缺血与诊室血压的搏动和稳定成分之间的关系。
82名未经治疗的中年高血压患者（无冠状动脉狭窄）和23名血压正常的志愿者接受了运动心电图测试以及标准和经食管超声心动图检查，以评估心肌缺血的发生情况、左心室（LV）质量和几何形状、总动脉顺应性以及冠状动脉扩张能力。
在高血压人群中，最高四分位数组的最小冠状动脉阻力（MCR）显著高于所有三个较低脉压（PP）四分位数组（分别为1.10±0.19、1.21±0.23、1.20±0.26和1.43±0.26 mmHg·s/cm，P<0.01）。收缩压（SBP）最高四分位数组的MCR也有额外增加，但平均血压四分位数组之间未出现这种情况。回归分析显示，MCR随PP、SBP和LV壁厚度增加而升高，随总动脉顺应性降低而降低。与运动试验心肌缺血阴性的高血压患者（n = 30）相比，试验阳性的患者（n = 20）MCR更高（1.12±0.22与1.39±0.29 mmHg·s/cm，P<0.01），总动脉顺应性更低（96±22%与81±16%，P<0.01）。
在未经治疗的中年高血压患者中，冠状动脉扩张能力随诊室PP和SBP升高而下降。动脉顺应性降低和LV壁厚度增加似乎是这种关系的主要潜在改变。运动诱发的心肌缺血与更高的MCR和更低的动脉顺应性相关。
