Lehmann Nils, Erbel Raimund, Mahabadi Amir A, Kälsch Hagen, Möhlenkamp Stefan, Moebus Susanne, Stang Andreas, Roggenbuck Ulla, Strucksberg Karl-Heinz, Führer-Sakel Dagmar, Dragano Nico, Budde Thomas, Seibel Rainer, Grönemeyer Dietrich, Jöckel Karl-Heinz
aInstitute for Medical Informatics, Biometry & Epidemiology bDepartment of Cardiology cInstitute of Clinical Chemistry and Laboratory Medicine, University Clinic Essen, Essen dDepartment of Cardiology, Krankenhaus Bethanien, Moers, Germany eDepartment of Epidemiology, Boston University, Massachusetts, USA fInstitute of Medical Sociology, University Clinic Düsseldorf, Düsseldorf gAlfried Krupp Hospital Essen, Essen hDiagnosticum, Mülheim iInstitute of Diagnostic and Interventional Radiology, University Witten/Herdecke, Witten, Germany *Nils Lehmann and Raimund Erbel contributed equally to the article.
J Hypertens. 2016 Nov;34(11):2233-42. doi: 10.1097/HJH.0000000000001080.
To determine the role of hypertension for coronary artery calcification (CAC) progression.
The population-based Heinz Nixdorf Recall study recruited 4814 participants from a German urban population in 2000-2003. CAC was measured using electron-beam computed tomography at baseline and after 5 years. The present analyses refer to 3481 participants with repeat scan (coronary heart disease until 5 years excluded, age at baseline 45-74 years, and 53.1% women). Blood pressure (BP), Framingham risk factors, and antihypertensive medication were recorded at baseline. BP was staged according to Joint National Committee 7 guidelines. Participants under antihypertensive medication were classified as stage 2. CAC at 5 years was predicted from baseline using our dedicated, publicly available algorithm. CAC progression was accordingly classified as slow, expected, or rapid.
Normotension was found in 20.5%, prehypertension in 27.2%, stage 1 hypertension in 15.8%, and stage 2 (ST2) in 36.5%. The frequency of rapid progression increases with BP stage (normotension: 16.7% to ST2: 21.1%, P = 0.004). Risk factor adjusted relative risk [RR (95% confidence interval), reference: normotension] of rapid progression was for prehypertension: 1.22 (0.98;1.51), stage 1: 1.29 (1.01;1.65), and ST2: 1.45 (1.17;1.79). Risk factor adjusted measures of CAC progression per 10 mmHg SBP were already elevated in women with BP below 140/90 mmHg: CAC onset, RR = 1.22 (1.07;1.40), rapid progression, RR = 1.17 (1.05;1.31), 5-year CAC progression, 6.7% (0.5;13.4). In men below 140/90 mmHg, only RR of rapid progression was considerably increased [RR = 1.11 (0.96;1.29)].
CAC progression, a sign of ongoing target organ damage, is already accelerated in prehypertensive patients, a substantial proportion of our urban population.
确定高血压在冠状动脉钙化（CAC）进展中的作用。
基于人群的海因茨·尼克斯多夫召回研究在2000年至2003年期间从德国城市人口中招募了4814名参与者。在基线和5年后使用电子束计算机断层扫描测量CAC。目前的分析涉及3481名进行了重复扫描的参与者（排除5年内患冠心病者，基线年龄45 - 74岁，女性占53.1%）。在基线时记录血压（BP）、弗雷明汉危险因素和抗高血压药物使用情况。BP根据美国国家联合委员会第7版指南进行分级。正在使用抗高血压药物的参与者被归类为2期。使用我们专门的、公开可用的算法从基线预测5年时的CAC。相应地，CAC进展被分类为缓慢、预期或快速。
血压正常者占20.5%，高血压前期者占27.2%，1期高血压者占15.8%，2期（ST2）高血压者占36.5%。快速进展的频率随血压分级增加（血压正常：16.7%至ST2：21.1%，P = 0.004）。快速进展的危险因素调整相对风险[RR（95%置信区间），参考：血压正常]，高血压前期为：1.22（0.98；1.51），1期为：1.29（1.01；1.65），ST2为：1.45（1.17；1.79）。在收缩压低于140/90 mmHg的女性中，每10 mmHg收缩压的危险因素调整后的CAC进展测量值已经升高：CAC起始，RR = 1.22（1.07；1.40），快速进展，RR = 1.17（1.05；1.31），5年CAC进展，6.7%（0.5；13.4）。在收缩压低于140/90 mmHg的男性中，只有快速进展的RR显著增加[RR = 1.11（0.96；1.29）]。
CAC进展是持续靶器官损害的标志，在高血压前期患者（我们城市人口的很大一部分）中已经加速。
