Winzap Patric A, Kraler Simon, Obeid Slayman, Wenzl Florian A, Templin Christian, Klingenberg Roland, von Eckardstein Arnold, Roffi Marco, Muller Olivier, Räber Lorenz, Lüscher Thomas F
Center for Molecular Cardiology, University of Zurich, Wagistrasse, Schlieren 8952, Switzerland.
Cardiology, Cantonal Hospital Aarau, Aarau, Switzerland.
Eur Heart J Acute Cardiovasc Care. 2023 Jul 7;12(7):437-450. doi: 10.1093/ehjacc/zuad047.
Outcomes after acute coronary syndromes (ACS) are determined by baseline risk profiles, including initial systolic blood pressure (sBP) levels. Herein, we aimed to characterize ACS patients stratified by initial sBP levels and study their relation to inflammation, myocardial injury and post-ACS outcomes.
We analysed 4724 prospectively recruited ACS patients according to invasively assessed sBP (<100, 100-139, and ≥140 mmHg) at admission. Biomarkers of systemic inflammation [high-sensitivity C-reactive protein (hs-CRP)] and myocardial injury [high-sensitivity cardiac troponin T (hs-cTnT)] were measured centrally. Major adverse cardiovascular events (MACE; composite measure of non-fatal myocardial infarction, non-fatal stroke, and cardiovascular death) were externally adjudicated. Leukocyte counts, hs-CRP, hs-cTnT, and creatine kinase (CK) levels decreased from low to high sBP strata (ptrend < 0.001). Patients with sBP < 100 mmHg developed more often cardiogenic shock (CS; P < 0.001), and had a 1.7-fold increased multivariable-adjusted MACE risk at 30 days (HR 1.68, 95% CI 1.05-2.69, P = 0.031) which did not persist at one year (HR 1.38, 95% CI 0.92-2.05, P = 0.117). Those with sBP < 100 mmHg and CS showed a higher leukocyte count (P < 0.001), an increased neutrophil-to-lymphocyte-ratio (P = 0.031), and higher hs-cTnT and CK levels relative to those without CS (P < 0.001 and P = 0.002, respectively), whereas hs-CRP levels did not differ. Patients who developed CS had a 3.6- and 2.9-fold increased MACE risk at 30 days (HR 3.58, 95% CI 1.77-7.24, P < 0.001) and at one year (HR 2.94 95% CI, 1.57-5.53, P < 0.001), which was intriguingely attenuated after controlling for distinct inflammatory profiles.
In patients with ACS, proxies of systemic inflammation and myocardial injury are inversely associated with initial sBP levels, with highest biomarker levels observed in those <100 mmHg. If linked to high levels of cellular inflammation, these patients are prone to develop CS and are at high MACE and mortality risk.
急性冠状动脉综合征（ACS）后的预后由基线风险特征决定，包括初始收缩压（sBP）水平。在此，我们旨在对根据初始sBP水平分层的ACS患者进行特征描述，并研究其与炎症、心肌损伤及ACS后预后的关系。
我们根据入院时通过有创评估的sBP（<100、100 - 139和≥140 mmHg）对4724例前瞻性招募的ACS患者进行分析。集中检测全身炎症生物标志物[高敏C反应蛋白（hs-CRP）]和心肌损伤生物标志物[高敏心肌肌钙蛋白T（hs-cTnT）]。主要不良心血管事件（MACE；非致命性心肌梗死、非致命性卒中及心血管死亡的综合指标）由外部判定。白细胞计数、hs-CRP、hs-cTnT和肌酸激酶（CK）水平从低sBP分层到高sBP分层逐渐降低（ptrend < 0.001）。sBP < 100 mmHg的患者更常发生心源性休克（CS；P < 0.001），在30天时多变量调整后的MACE风险增加1.7倍（HR 1.68，95%CI 1.05 - 2.69，P = 0.031），但在1年时未持续存在（HR 1.38，95%CI 0.92 - 2.05，P = 0.117）。与无CS的患者相比，sBP < 100 mmHg且发生CS的患者白细胞计数更高（P < 0.001），中性粒细胞与淋巴细胞比值增加（P = 0.031），hs-cTnT和CK水平更高（分别为P < 0.001和P = 0.002），而hs-CRP水平无差异。发生CS的患者在30天时MACE风险增加3.6倍，在1年时增加2.9倍（HR 3.58，95%CI 1.77 - 7.24，P < 0.001；HR 2.94，95%CI 1.57 - 5.53，P < 0.001），有趣的是，在控制了不同的炎症特征后这种风险有所降低。
在ACS患者中，全身炎症和心肌损伤指标与初始sBP水平呈负相关，在sBP < 100 mmHg的患者中观察到最高的生物标志物水平。如果与高水平的细胞炎症相关，这些患者易于发生CS，且MACE和死亡风险较高。
