Thibodeau Jennifer T, Pham David D, Kelly Samuel A, Ayers Colby R, Garg Sonia, Grodin Justin L, Drazner Mark H
Division of Cardiology, Department of Internal Medicine, University of Texas Southwestern Medical Center, Dallas, Texas.
Division of Cardiology, Department of Internal Medicine, University of Texas Southwestern Medical Center, Dallas, Texas.
J Card Fail. 2022 Mar;28(3):422-430. doi: 10.1016/j.cardfail.2021.09.002. Epub 2021 Sep 14.
Clinical congestion is associated with adverse outcomes in patients with heart failure. The pathophysiological mediators of this association remain uncertain.
We prospectively enrolled a cohort of patients with heart failure and reduced left ventricular ejection fraction and performed a detailed clinical examination followed on the same day by an invasive right heart catheterization and blood sampling for biomarkers. High-sensitivity troponin T and N-terminal pro-B-type natriuretic peptide (NT-proBNP) levels were measured. A clinical congestion score was calculated based on jugular venous pressure (cm H0 <10 = 0, 10-14 = 1, >14 = 2 points), bendopnea (0 vs 1), a third heart sound (0 vs 1), or peripheral edema (0-2). Congestion was categorized into tiers as absent (0 points), mild (1 point), or moderate to severe (≥ 2 points). We tested for associations of high-sensitivity troponin T, NT-proBNP, and elevated ventricular filling pressures with clinical congestion in both univariate and multivariable analyses. Of 153 participants, 65 (42%) had absent, 35 mild (23%), and 53 (35%) had moderate to severe clinical congestion. Congestion tier was associated with higher NT-proBNP and hs-troponin levels, and the right atrial pressure and pulmonary capillary wedge pressure (P < .001 for each). Increased congestion tier was also associated with the coexistent presence of elevated troponin T (≥52 ng/L), NT-proBNP (≥1000 pg/mL), and pulmonary capillary wedge pressure (≥22 mm Hg). Specifically, 78% of those with absent clinical congestion had 0 to 1 of these findings, whereas 75% of those with moderate-severe congestion had 2 or all 3 of these abnormalities (P < .001). An elevated hs-troponin was associated with mild or greater clinical congestion (odds ratio 3, 95% confidence interval 1.2-7.5, P = .02) in multivariable analysis adjusting for potential confounders including the right atrial pressure, pulmonary capillary wedge pressure, and NT-proBNP levels.
Clinical congestion is a phenotype in which there is a high coexistent presence of elevated ventricular filling pressures, elevated natriuretic peptide levels, and subclinical myocardial injury. An elevated troponin was associated with clinical congestion in multivariable models that adjusted for ventricular filling pressures and natriuretic peptide levels. These data strengthen the evidence base for an association of elevated troponin with clinical congestion, suggesting that subclinical myocardial injury may be an important contributor to the pathophysiology of the congested state.
临床充血与心力衰竭患者的不良预后相关。这种关联的病理生理介质仍不确定。
我们前瞻性纳入了一组左心室射血分数降低的心力衰竭患者，进行了详细的临床检查，随后于同一天进行有创右心导管检查并采集血样检测生物标志物。测量了高敏肌钙蛋白T和N末端B型利钠肽原（NT-proBNP）水平。根据颈静脉压（厘米水柱<10 = 0分，10 - 14 = 1分，>14 = 2分）、端坐呼吸（0分与1分）、第三心音（0分与1分）或外周水肿（0 - 2分）计算临床充血评分。充血分为无（0分）、轻度（1分）或中度至重度（≥2分）几个等级。我们在单变量和多变量分析中测试了高敏肌钙蛋白T、NT-proBNP以及升高的心室充盈压与临床充血之间的关联。153名参与者中，65名（42%）无充血，35名轻度充血（23%），53名（35%）有中度至重度临床充血。充血等级与较高的NT-proBNP和高敏肌钙蛋白水平以及右心房压和肺毛细血管楔压相关（每项P <.001）。充血等级增加还与肌钙蛋白T升高（≥52 ng/L）、NT-proBNP升高（≥1000 pg/mL）和肺毛细血管楔压升高（≥22 mmHg）同时存在有关。具体而言，无临床充血者中78%有0至1项这些表现，而中度至重度充血者中75%有2项或全部3项这些异常（P <.001）。在对包括右心房压、肺毛细血管楔压和NT-proBNP水平等潜在混杂因素进行调整的多变量分析中，高敏肌钙蛋白升高与轻度或更严重的临床充血相关（比值比3，95%置信区间1.2 - 7.5，P =.02）。
临床充血是一种表型，其中心室充盈压升高、利钠肽水平升高和亚临床心肌损伤同时存在的情况很常见。在对心室充盈压和利钠肽水平进行调整的多变量模型中，肌钙蛋白升高与临床充血相关。这些数据加强了肌钙蛋白升高与临床充血关联的证据基础，表明亚临床心肌损伤可能是充血状态病理生理学的一个重要促成因素。
