The Clinical Research, Investigation, and Systems Modeling of Acute Illness Center, University of Pittsburgh, Pittsburgh, Pennsylvania, United States of America.
PLoS One. 2011;6(8):e22847. doi: 10.1371/journal.pone.0022847. Epub 2011 Aug 10.
Acceleration of chronic diseases, particularly cardiovascular disease, may increase long-term mortality after community-acquired pneumonia (CAP), but underlying mechanisms are unknown. Persistence of the prothrombotic state that occurs during an acute infection may increase risk of subsequent atherothrombosis in patients with pre-existing cardiovascular disease and increase subsequent risk of death. We hypothesized that circulating hemostasis markers activated during CAP persist at hospital discharge, when patients appear to have recovered clinically, and are associated with higher mortality, particularly due to cardiovascular causes.
In a cohort of survivors of CAP hospitalization from 28 US sites, we measured D-Dimer, thrombin-antithrombin complexes [TAT], Factor IX, antithrombin, and plasminogen activator inhibitor-1 at hospital discharge, and determined 1-year all-cause and cardiovascular mortality.
Of 893 subjects, most did not have severe pneumonia (70.6% never developed severe sepsis) and only 13.4% required intensive care unit admission. At discharge, 88.4% of subjects had normal vital signs and appeared to have clinically recovered. D-dimer and TAT levels were elevated at discharge in 78.8% and 30.1% of all subjects, and in 51.3% and 25.3% of those without severe sepsis. Higher D-dimer and TAT levels were associated with higher risk of all-cause mortality (range of hazard ratios were 1.66-1.17, p = 0.0001 and 1.46-1.04, p = 0.001 after adjusting for demographics and comorbid illnesses) and cardiovascular mortality (p = 0.009 and 0.003 in competing risk analyses).
Elevations of TAT and D-dimer levels are common at hospital discharge in patients who appeared to have recovered clinically from pneumonia and are associated with higher risk of subsequent deaths, particularly due to cardiovascular disease.
慢性病的加速发展，尤其是心血管疾病，可能会增加社区获得性肺炎（CAP）后的长期死亡率，但潜在机制尚不清楚。在急性感染期间发生的促血栓形成状态的持续存在，可能会增加患有先前存在的心血管疾病的患者随后发生动脉血栓形成的风险，并增加随后因心血管原因导致死亡的风险。我们假设，在 CAP 住院患者出院时，即临床看似已康复时，循环止血标志物在 CAP 期间激活并持续存在，并且与更高的死亡率相关，尤其是心血管原因导致的死亡率。
在来自美国 28 个地点的 CAP 住院患者幸存者队列中，我们在出院时测量了 D-二聚体、凝血酶-抗凝血酶复合物[TAT]、因子 IX、抗凝血酶和纤溶酶原激活物抑制剂-1，并确定了 1 年全因和心血管死亡率。
在 893 名受试者中，大多数患者没有严重肺炎（70.6%从未发生严重败血症），只有 13.4%需要入住重症监护病房。出院时，88.4%的患者生命体征正常，临床看似已康复。所有受试者中有 78.8%和 30.1%在出院时 D-二聚体和 TAT 水平升高，无严重败血症的患者中有 51.3%和 25.3%升高。较高的 D-二聚体和 TAT 水平与全因死亡率（危险比范围为 1.66-1.17，p=0.0001 和 1.46-1.04，p=0.001，在调整了人口统计学和合并症后）和心血管死亡率（在竞争风险分析中 p=0.009 和 0.003）相关。
在临床看似已从肺炎康复的患者出院时，TAT 和 D-二聚体水平升高很常见，并且与随后死亡的风险增加相关，尤其是心血管疾病导致的死亡。
