Subclinical Cardiac Injury And Clinical Congestion

Abstract

<h3>Introduction</h3> Clinical congestion is associated with worse outcomes in patients with heart failure (HF). The pathophysiological mediators of this association remain uncertain. <h3>Hypothesis</h3> Detailed phenotyping of patients with HF, including clinical examination and measurement of invasive hemodynamics and cardiac biomarkers, will provide insights into the pathophysiology of clinical congestion. <h3>Methods</h3> In a prospective cohort of patients with HF and reduced LVEF, a clinical examination followed the same day by right heart catheterization and blood sampling for biomarker measurement was performed. A clinical congestion score was created based on JVP (cm H20 <10 = 0, 10-14 =1, >14 =2 points), bendopnea (0-1), S3 (0-1) and peripheral edema (0-2). Congestion tier was defined as Absent, Mild (1 point) or Moderate-Severe (≥ 2 points). Biomarker elevation was defined as high-sensitivity troponin T ≥52 ng/L or NT-proBNP ≥1000 pg/mL. Elevated right atrial pressure (RAP) was ≥10 mmHg and pulmonary capillary wedge pressure (PCWP) ≥22 mmHg. Univariate and multivariable analyses tested the association of biomarkers, RAP, and PCWP with clinical congestion. <h3>Results</h3> Of 154 subjects, 65 (42%) had no congestion, 35 mild (23%) and 54 (35%) moderate-severe. Increasing congestion tier was associated with NT-proBNP, troponin, RAP and PCWP (P<0.001 for each). Increasing congestion tier was associated with the combined presence of elevated troponin, NT-proBNP and PCWP (Figure). Only 22% of those with absent congestion had more than one of these findings, whereas 76% of those with moderate-severe congestion had at least 2 of them (p<0.001). In multivariable regression, elevated troponin was associated with the presence of clinical congestion (OR 2.8, 1.1-7.3, p=0.03) independently of RAP, PCWP, and NT-proBNP levels. <h3>Conclusions</h3> Increased ventricular filling pressures, elevated natriuretic peptide levels, and subclinical myocardial injury frequently coexist in patients with clinical congestion. Elevated troponin was associated with clinical congestion independently of ventricular filling pressures and natriuretic peptide levels, suggesting that subclinical cardiac injury contributes to the pathophysiology of clinical congestion.