This article refers to 'Biologically active adrenomedullin as a marker for residual congestion and early rehospitalization in patients hospitalized for acute heart failure: Data from STRONG-HF' by G. Voordes et al., published in this issue on pages 1480-1492. That what does not kill us makes us stronger. Friedrich Nietzsche Congestion in heart failure results from fluid accumulation and/or elevated filling pressures due to impaired cardiac function. These processes lead to symptoms like dyspnoea, oedema, and fatigue, significantly impacting patients' well-being and prognosis. Biomarkers, including natriuretic peptides like B-type natriuretic peptide (BNP) and N-terminal proBNP (NT-proBNP), are valuable tools in heart failure management, reflecting cardiac stress and aiding in diagnosis and risk assessment. Emerging biomarkers such as carbohydrate antigen 125 (CA125), galectin-3, and soluble ST2 provide additional perspectives on extravascular congestion, myocardial fibrosis, stress, and renal function, enriching our understanding of the multifaceted pathophysiologic processes contributing to heart failure. 1 Adrenomedullin (ADM), specifically bio-ADM, is derived from the cleavage of pre-ADM to an active form via amidation. ADM is crucial in maintaining vascular integrity and regulating vascular tone and permeability. It diffuses across the vascular barrier, stabilizing vascular endothelial cells and inducing vasodilatation in vascular smooth muscle cells. In heart failure and sepsis, conditions marked by endothelial dysfunction, elevated plasma bio-ADM levels may represent a compensatory mechanism to prevent vascular leakage. 2In this issue of the Journal, Voordes et al. 3 set out to explore the potential of bio-ADM in evaluating residual congestion and predicting early rehospitalization in acute heart failure patients, utilizing the comprehensive dataset from the STRONG-HF study. The STRONG-HF trial showed that high-intensity care (HIC) focused on simultaneous and/or rapid sequence initiation andThe opinions expressed in this article are not necessarily those of the Editors of the European Journal of Heart Failure or of the European Society of Cardiology.