Sharma Yash Paul, Gawalkar Atit A, Batta Akash, Shrimanth Yamasandi Siddegowda, Revaiah Pruthvi C, Karki Pragya, Chaudhary Vikas, Kasinadhuni Ganesh, Santosh Krishna, Bootla Dinakar, Kumar Sanjeev, Patel Nitin Kumar J, Sambyal Bharat Singh, Panda Prashant
Department of Cardiology, Post Graduate Institute of Medical Education and Research, Chandigarh, India.
Department of Internal Medicine, Post Graduate Institute of Medical Education and Research, Chandigarh, India.
J Family Med Prim Care. 2023 May;12(5):962-966. doi: 10.4103/jfmpc.jfmpc_1629_22. Epub 2023 May 31.
COVID-19 can cause severe pneumonia that can progress to multiple organ failure. It is believed that dysregulation of inflammation and cytokine storm, contributes to severe COVID-19. As inflammatory mediators play an important role in the pathogenesis of the severe disease, inflammatory markers like fever, leucocytosis, and C-reactive protein are known to predict severe disease. Various other biomarkers have been known to have prognostic value in patients with COVID-19 infection. Inflammation, both local and systemic plays an important role in the pathogenesis of acute coronary syndrome (ACS). Thus in this study, we aimed to compare and describe the various biomarkers, and mortality between patients admitted with COVID-19 infection and ACS patients without COVID-19 infection.
In a retrospective observational case-control study, a total of 108 patients admitted to our hospital during the month of May 2021 with COVID-19 were enrolled. Patients of the acute coronary syndrome (tested negative for COVID-19 infection) admitted during the same month were enrolled (including both the intensive care unit and ward) as controls.
The median age of patients with COVID was significantly lower than that of patients with acute coronary syndrome [49 years (IQR, 36-62 years) and 60 years (IQR, 52-66 years)]. Left ventricular ejection fraction was significantly higher among patients with COVID infection (58.5 ± 6.3% versus 36.9 ± 9.3%). The total leukocyte count was significantly higher among patients with COVID-19 compared to those with acute coronary syndrome [13200 per microliter (8625-17500) vs 9800 per microliter (8150-12150), < 0.001]. The blood urea level was significantly higher among patients with COVID infection [52.5 (IQR, 34.7-81.5) versus 20 (IQR, 16-31)]. Levels of C-reactive protein were significantly higher among patients with COVID [39 (IQR, 7.7-100) versus 2 (1.4-3.5)]. The mortality of patients hospitalized with COVID was 4 times higher than those with acute coronary syndrome [25.9% (28) versus 6.1% (6)]. Survivors of COVID-19 had higher hemoglobin levels than those who did not [12.5 g/dLvs 11.5 g/dL, = 0.03].
Elevated total leukocyte counts reflect underlying secondary bacterial infection among patients with COVID-19 and help initiate appropriate antibiotics. Depletion of intravascular volume reflected by an increased urea/creatinine ratio increases the risk of mortality and warrants aggressive measures of rehydration and albumin infusion.
新型冠状病毒肺炎(COVID-19)可导致严重肺炎,并可进展为多器官功能衰竭。据信,炎症失调和细胞因子风暴是导致重症COVID-19的原因。由于炎症介质在重症疾病的发病机制中起重要作用,发热、白细胞增多和C反应蛋白等炎症标志物可预测重症疾病。已知其他各种生物标志物对COVID-19感染患者具有预后价值。局部和全身炎症在急性冠状动脉综合征(ACS)的发病机制中起重要作用。因此,在本研究中,我们旨在比较和描述COVID-19感染患者与非COVID-19感染的ACS患者之间的各种生物标志物及死亡率。
在一项回顾性观察性病例对照研究中,纳入了2021年5月期间我院收治的108例COVID-19患者。同月收治的急性冠状动脉综合征患者(COVID-19感染检测阴性)(包括重症监护病房和病房患者)作为对照。
COVID患者的中位年龄显著低于急性冠状动脉综合征患者[49岁(四分位间距,36 - 62岁)和60岁(四分位间距,52 - 66岁)]。COVID感染患者的左心室射血分数显著更高(58.5±6.3%对36.9±9.3%)。与急性冠状动脉综合征患者相比,COVID-19患者的总白细胞计数显著更高[每微升13200(8625 - 17500)对每微升9800(8150 - 12150),P<0.001]。COVID感染患者的血尿素水平显著更高[52.5(四分位间距,34.7 - 81.5)对20(四分位间距,16 - 31)]。COVID患者的C反应蛋白水平显著更高[39(四分位间距,7.7 - 100)对2(1.4 - 3.5)]。COVID住院患者的死亡率比急性冠状动脉综合征患者高4倍[25.9%(28例)对6.1%(6例)]。COVID-19幸存者的血红蛋白水平高于未幸存者[12.5 g/dL对11.5 g/dL,P = 0.03]。
总白细胞计数升高反映COVID-19患者存在潜在的继发性细菌感染,并有助于启动适当的抗生素治疗。尿素/肌酐比值升高反映的血管内容量耗竭增加了死亡风险,需要采取积极的补液和输注白蛋白措施。