Biochemical or clinical heart failure, not so simple

This article refers to ‘Characterization of NT-proBNP in a large cohort COVID-19 patients’ by J. Caro-Codón et al., published this issue on pages 456–464. Everything must be made as simple possible. But not simpler Albert Einstein In the Journal, study al.1 brings up how clinical use natriuretic peptides (NPs) has evolved and powerful meaningful these biomarkers are. The story started with description (1950s) dense ‘granules’ atrial myocardium, vaguely reminiscent glandular tissue. 1981, de Bold al.2 found potent vasodilatory response extracts from myocardium rats; purified substance was named NP.3 1988, second member family [brain NP (BNP)] described porcine brains thereafter ventricular myocardium4; currently B-type NP, including active form (BNP) inactive amino-terminal fragment (NT-proBNP). heart emerged hormonal organ that secretes presence failure (HF), self-protective pressure volume overload; and, importantly, higher concentration, worse prognosis.5 I run into BNP 1999, while searching for better prognosticator could overcome limitations catecholamines evaluation candidates transplantation. such far times, measurement time-consuming based radioimmunoassay techniques. development rapid automated electrochemiluminescence immunoassays gave great impulse NPs biomarkers. early 2000s, several studies showed utility diagnosis HF patients dyspnoea acute settings.6, 7 However, predominance negative predictive value led recommendation using rule out suspicion HF. reflects there are elevated concentrations explained unsolved pathophysiological hampered wide acceptance their incorporation laboratory settings. Indeed, were definitely included diagnostic algorithms until 2012 guidelines,8 subsequent surveys predominantly restricted clinicians.9, 10 describes practice regarding who attended emergency room tertiary hospital 2020, during first wave coronavirus disease 2019 (COVID-19) pandemic Europe. comment is physicians charge measured less than 13% (n = 396) all admitted patients. Although main symptom at presentation dyspnoea, determination delayed median 4 days after admission. Moreover, decision clearly biased more severe condition, lower oxygen saturation, risk (older age, proportion males, cardiovascular comorbidities, biochemical parameters inflammatory markers). Therefore, primarily used an aid suggested guidelines. deserves almost half (48.5%) determinations above age-adjusted rule-out values, indicating strong disagreement final rate clinically diagnosed (11.7%). As pivotal studies, levels synonymous but prognosis, irrespective diagnosis: why?. It well established mainly produced cardiomyocytes defence different cardiac stresses. stimuli mechanical stretch, overload, also hypoxia, ischaemia, vascular dysfunction, neurohormonal hyperactivity inflammation (e.g. COVID-19).11-14 sensors inform ‘suffering’ primary non-cardiac diseases (Figure 1). differs concept ‘damage’ reflected troponin elevation indeed, both complementary prognosticators.15 case should help us realize lucky we have well-tuned biomarkers, working sensitive involvement initially diseases. Elevated circulating troponins detected reports.16, 17 Their allowed identify frequency complications, provided understanding new life-threatening disease. most challenging question is: why insist clinically-based HF, when amazing sensors? population presented what correct?: 11% physician-dependent criteria or 48% (NP) criteria? From my own view, had involvement, probably consider two concepts: (11.7%) (48%). prognosis altered markers supports ‘biochemical HF’ real entity explore further epidemiological therapeutic perspective. Finally, shows awkward still moving field NPs: simplicity ruling difficulty interpreting values. introduction represents major advance management now move beyond idea ‘clinical towards exploring frontiers under Conflict interest: D.A.P.F. served advisory board and/or received speaker honoraria Novartis, Servier, AstraZeneca, Vifor, Pfizer, Abbott Roche Diagnostics.