Virginia Commonwealth University, Richmond VA; McGuire VA Medical Center, Richmond VA.
Minneapolis VA Medical Center, Minneapolis MN.
Clinics (Sao Paulo). 2024 Aug 27;79:100473. doi: 10.1016/j.clinsp.2024.100473. eCollection 2024.
The prevalence of COVID-19 as the primary diagnosis among hospitalized patients with myocardial injury has increased during the pandemic and targeting elevated oxidant stress and inflammatory biomarkers may offer a potential role for novel therapies to improve outcomes.
At a single VA Medical Center from January 1 through December 31, 2021, troponin assays from patients being evaluated in the Emergency Room for consideration of admission were analyzed and peak levels from each patient were considered abnormal if exceeding the Upper Reference Limit (URL). Among admitted patients with an elevated troponin level, ICD-10 diagnoses were categorized, biomarker elevations were recorded, and independent predictors of death in patients with COVID-19 were determined at a median of 6-months following admission.
Of 998 patients, 399 (40 %) had a negative troponin and were not included in the analysis. Additional patients with an elevated troponin were also excluded, either because they were not admitted (n = 68) or had a final diagnosis of Type 1 MI (n = 117). Of the remaining 414 patients with an elevated peak troponin, COVID-19 was the primary diagnosis in 43 patients (10 %) and was the 4 most common diagnosis of patients admitted with myocardial injury behind congestive heart failure, sepsis, and COPD or pneumonia. At a median of 6-months following admission, 18 (42 %) of the COVID-19 patients had died and independent predictors of death (Odd Ratio: Confidence Intervals) were age (1.18: 1.06‒1.37), Troponin level (Log 10 transformed) (16.54: 2.30‒266.65) and C-Reactive Protein (CRP) (1.30: 1.10‒1.65).
Newly diagnosed COVID-19 during the pandemic was a common cause of elevated troponin in hospitalized patients without a Type 1 MI. Age, peak troponin level and peak CRP level were independent predictors of poor outcomes and suggest a need to target these cardiac biomarkers, potentially with novel antioxidant or anti-inflammatory therapies.
在大流行期间，COVID-19 作为住院心肌损伤患者的主要诊断，其发病率有所增加，针对氧化应激和炎症生物标志物升高，可能为改善预后提供新的治疗方法。
在 2021 年 1 月 1 日至 12 月 31 日期间，在一家退伍军人事务部医疗中心，对在急诊室接受评估以考虑入院的患者进行了肌钙蛋白检测，每位患者的峰值水平如果超过上参考限 (URL)，则被认为异常。在因肌钙蛋白升高而入院的患者中，根据 ICD-10 诊断进行分类，记录生物标志物升高情况，并在入院后中位数为 6 个月时确定 COVID-19 患者死亡的独立预测因素。
在 998 例患者中，399 例（40%）肌钙蛋白阴性，未纳入分析。还排除了肌钙蛋白升高的其他患者，要么因为未入院（n=68），要么因为最终诊断为 1 型心肌梗死（n=117）。在剩余的 414 例肌钙蛋白峰值升高的患者中，COVID-19 是 43 例（10%）患者的主要诊断，是因充血性心力衰竭、败血症和 COPD 或肺炎而入院的心肌损伤患者的第四大常见诊断。在入院后中位数为 6 个月时，18 例（42%）COVID-19 患者死亡，死亡的独立预测因素（优势比：置信区间）为年龄（1.18：1.06-1.37）、肌钙蛋白水平（对数 10 转换）（16.54：2.30-266.65）和 C 反应蛋白（CRP）（1.30：1.10-1.65）。
在大流行期间新诊断的 COVID-19 是住院患者肌钙蛋白升高且无 1 型心肌梗死的常见原因。年龄、峰值肌钙蛋白水平和峰值 CRP 水平是预后不良的独立预测因素，表明需要针对这些心脏生物标志物进行治疗，可能需要使用新型抗氧化或抗炎治疗方法。
