Berg David D, Alviar Carlos L, Bhatt Ankeet S, Baird-Zars Vivian M, Barnett Christopher F, Daniels Lori B, Defilippis Andrew P, Fagundes Antonio, Katrapati Praneeth, Kenigsberg Benjamin B, Guo Jianping, Keller Norma, Lopes Mathew S, Mody Anika, Papolos Alexander I, Phreaner Nicholas, Sedighi Romteen, Sinha Shashank S, Toomu Sandeep, Varshney Anubodh S, Morrow David A, Bohula Erin A
Levine Cardiac Intensive Care Unit, Cardiovascular Division, Department of Medicine, Brigham and Women's Hospital, Harvard Medical School, Boston, Massachusetts.
The Leon H. Charney Division of Cardiovascular Medicine, New York University Langone Medical Center, New York, New York.
J Card Fail. 2022 Apr;28(4):675-681. doi: 10.1016/j.cardfail.2021.12.020. Epub 2022 Jan 17.
Acute heart failure (HF) is an important complication of coronavirus disease 2019 (COVID-19) and has been hypothesized to relate to inflammatory activation.
We evaluated consecutive intensive care unit (ICU) admissions for COVID-19 across 6 centers in the Critical Care Cardiology Trials Network, identifying patients with vs without acute HF. Acute HF was subclassified as de novo vs acute-on-chronic, based on the absence or presence of prior HF. Clinical features, biomarker profiles and outcomes were compared.
Of 901 admissions to an ICU due to COVID-19, 80 (8.9%) had acute HF, including 18 (2.0%) with classic cardiogenic shock (CS) and 37 (4.1%) with vasodilatory CS. The majority (n = 45) were de novo HF presentations. Compared to patients without acute HF, those with acute HF had higher cardiac troponin and natriuretic peptide levels and similar inflammatory biomarkers; patients with de novo HF had the highest cardiac troponin levels. Notably, among patients critically ill with COVID-19, illness severity (median Sequential Organ Failure Assessment, 8 [IQR, 5-10] vs 6 [4-9]; P = 0.025) and mortality rates (43.8% vs 32.4%; P = 0.040) were modestly higher in patients with vs those without acute HF.
Among patients critically ill with COVID-19, acute HF is distinguished more by biomarkers of myocardial injury and hemodynamic stress than by biomarkers of inflammation.
急性心力衰竭（HF）是2019冠状病毒病（COVID-19）的重要并发症，据推测与炎症激活有关。
我们评估了危重症心脏病试验网络中6个中心因COVID-19连续入住重症监护病房（ICU）的患者，确定有或无急性HF的患者。根据既往有无HF，将急性HF分为新发与慢性急性发作。比较临床特征、生物标志物谱和结局。
在901例因COVID-19入住ICU的患者中，80例（8.9%）发生急性HF，其中18例（2.0%）为典型心源性休克（CS），37例（4.1%）为血管扩张性CS。大多数（n = 45）为新发HF表现。与无急性HF的患者相比，有急性HF的患者心肌肌钙蛋白和利钠肽水平更高，炎症生物标志物相似；新发HF患者的心肌肌钙蛋白水平最高。值得注意的是，在COVID-19危重症患者中，有急性HF的患者疾病严重程度（序贯器官衰竭评估中位数，8 [四分位间距，5 - 10] 对6 [4 - 9]；P = 0.025）和死亡率（43.8%对32.4%；P = 0.040）略高于无急性HF的患者。
在COVID-19危重症患者中，急性HF更多地由心肌损伤和血流动力学应激的生物标志物而非炎症生物标志物来区分。
