Does end-organ dysfunction precede or follow cardiogenic shock in acute decompensated heart failure? The two-faced Janus. Letter regarding the article ‘Epidemiology, pathophysiology and contemporary management of cardiogenic shock — a position statement from the Heart Failure Association (HFA) of the European Society of Cardiology (ESC)’

We read with great interest the position statement of the Heart Failure Association of the European Society of Cardiology on the management of cardiogenic shock (CS).¹ The section regarding organ dysfunction elegantly explains the pathophysiologic correlation between organ injury and CS, that is admirably represented in Figure 2. Notwithstanding, we believe that the temporal progression of organ dysfunction in this scenario may be more complex than summarized in this document, which states that end-organ damage comes during overt stage C CS.¹

We agree that organ dysfunction usually presents after the occurrence of overt CS when this complicates sudden acute events such as acute myocardial infarction or fulminant myocarditis. However, this progression may be debated in the context of acute decompensated heart failure (ADHF). A previous work by our group showed that in ADHF patients with baseline systolic blood pressure (SBP) >100 mmHg (mean SBP 104.3 ± 26.1 mmHg) and lactate <2 mmol/L, end-organ injury not only was present earlier than overt CS manifestation, but also helped predict worsening heart failure and potential evolution into CS during index hospitalization.² Indeed, cold profile assessments including laboratory markers of renal and hepatic injury outperformed a pure clinical profile assessment in the prediction of worsening heart failure during index hospitalization.^{2, 3} Moreover, the addition of ammonia as a marker of intestinal damage in ADHF further improved the accuracy of cold profile in predicting a composite of cardiac death, urgent heart transplantation and urgent mechanical circulatory support at 3 months.⁴ In this population, end-organ injury reflects venous congestion in the presence of marginal cardiac output as well as poor end-organ functional reserve, neurohormonal activation and inflammation, even in the absence of overt hypoperfusion, and several studies showed this predicts worse prognosis.⁵

In conclusion, in ADHF patients, end-organ damage often precedes overt CS (stages A–B) and the assessment of ‘subclinical hypoperfusion’ could help predict evolution into CS, facilitating timely identification and treatment of patients at risk. Future research on this issue is needed.