Key result
High cDPP3 levels in cardiogenic shock linked to ~40% greater short-term mortality risk.
Why the study?
Acute heart failure has high mortality and incompletely understood pathophysiology, prompting evaluation of the role of circulating dipeptidyl peptidase 3 in cardiogenic shock and heart failure models.
Are circulating DPP3 levels associated with mortality in cardiogenic shock, and does DPP3 inhibition improve haemodynamics in acute heart failure?
Population
174 patients in cardiogenic shock and mouse models
Comparison
High vs lower cDPP3 levels, and cDPP3 inhibition vs controls in mice
Design
Clinical cohort study and preclinical animal experiment
Authors
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High cDPP3 may aid risk stratification in cardiogenic shock; hypothesis-generating for DPP3 inhibition in acute heart failure.
Cohort (n=174)
Are circulating DPP3 levels associated with mortality in cardiogenic shock, and does DPP3 inhibition improve haemodynamics in acute heart failure?
Effect estimate: HR 1.4 (95% CI 1.1-1.8)
Circulating DPP3 is a novel myocardial depressant factor associated with mortality in cardiogenic shock, and its inhibition represents a potential new therapeutic target for severe heart failure.
Deniau et al. (2019) conducted a cohort in Cardiogenic shock (n=174). High circulating Dipeptidyl Peptidase 3 (cDPP3) levels was evaluated on Short-term mortality risk (HR 1.4, 95% CI 1.1-1.8). High circulating Dipeptidyl Peptidase 3 (cDPP3) levels in cardiogenic shock patients were associated with an increased short-term mortality risk (HR 1.4; 95% CI 1.1-1.8).
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