Markus Marcello Ricardo Paulista, Stritzke Jan, Lieb Wolfgang, Mayer Björn, Luchner Andreas, Döring Angela, Keil Ulrich, Hense Hans-Werner, Schunkert Heribert
Medical Clinic II, University of Lübeck Medical School, Lübeck, Germany.
J Hypertens. 2008 Oct;26(10):2040-9. doi: 10.1097/HJH.0b013e328308da55.
It is unclear whether persistent prehypertension causes structural or functional alterations of the heart.
We examined echocardiographic data of 1005 adults from a population-based survey at baseline in 1994/1995 and at follow-up in 2004/2005. We compared individuals who had either persistently normal (<120 mmHg systolic and <80 mmHg diastolic, n = 142) or prehypertensive blood pressure (120-139 mmHg or 80-89 mmHg, n = 119) at both examinations using multivariate regression modeling.
Over 10 years, left ventricular end-diastolic diameters were stable and did not differ between the two groups. However, the prehypertensive blood pressure group displayed more pronounced ageing-related increases of left ventricular wall thickness (+4.7 versus +11.9%, P < 0.001) and left ventricular mass (+8.6 versus +15.7%, P = 0.006). Prehypertension was associated with a raised incidence of left ventricular concentric remodeling (adjusted odds ratio 10.7, 95% confidence interval 2.82-40.4) and left ventricular hypertrophy (adjusted odds ratio 5.33, 1.58-17.9). The ratio of early and late diastolic peak transmitral flow velocities (E/A) decreased by 7.7% in the normal blood pressure versus 15.7% in the prehypertensive blood pressure group (P = 0.003) and at follow-up the ratio of early diastolic peak transmitral flow and early diastolic peak myocardial relaxation velocities (E/EM) was higher (9.1 versus 8.5, P = 0.031) and left atrial size was larger (36.5 versus 35.3 mm, P = 0.024) in the prehypertensive blood pressure group. Finally, the adjusted odds ratio for incident diastolic dysfunction was 2.52 (1.01-6.31) for the prehypertensive blood pressure group.
Persistent prehypertension accelerates the development of hypertrophy and diastolic dysfunction of the heart.
持续性高血压前期是否会导致心脏结构或功能改变尚不清楚。
我们检查了1005名成年人的超声心动图数据，这些数据来自1994/1995年的一项基于人群的基线调查以及2004/2005年的随访调查。我们使用多变量回归模型比较了在两次检查中收缩压持续正常（<120 mmHg且舒张压<80 mmHg，n = 142）或处于高血压前期血压（120 - 139 mmHg或80 - 89 mmHg，n = 119）的个体。
在10年期间，左心室舒张末期直径稳定，两组之间无差异。然而，高血压前期血压组左心室壁厚度与年龄相关的增加更为明显（分别为 +4.7% 与 +11.9%，P < 0.001），左心室质量增加也更显著（分别为 +8.6% 与 +15.7%，P = 0.006）。高血压前期与左心室向心性重构的发生率升高相关（调整后的优势比为10.7，95%置信区间为2.82 - 40.4）以及左心室肥厚（调整后的优势比为5.33，1.58 - 17.9）。正常血压组舒张期二尖瓣血流早期和晚期峰值流速之比（E/A）下降了7.7%，而高血压前期血压组下降了15.7%（P = 0.003），并且在随访时，高血压前期血压组舒张期二尖瓣血流早期峰值与舒张期心肌早期松弛速度之比（E/EM）更高（9.1对8.5，P = 0.031），左心房大小更大（36.5对35.3 mm，P = 0.024）。最后，高血压前期血压组发生舒张功能障碍的调整后优势比为2.52（1.01 - 6.31）。
持续性高血压前期会加速心脏肥厚和舒张功能障碍的发展。
