Key result
Chronic heart failure is linked to ~25 percentage points lower SVR response to phenylephrine.
Why the study?
Patients with chronic HF are at increased risk of vasoplegia after cardiac surgery, potentially because neurohormonal activation in HF alters vascular regulation, motivating comparison of perioperative vasoresponsiveness in patients with and without HF.
Does chronic heart failure impair perioperative vasoresponsiveness to phenylephrine, nitroglycerin, and vasopressin in patients undergoing cardiac surgery with cardiopulmonary bypass?
Observational (n=36)
Does chronic heart failure impair perioperative vasoresponsiveness to phenylephrine, nitroglycerin, and vasopressin in patients undergoing cardiac surgery with cardiopulmonary bypass?
Patients with chronic heart failure undergoing cardiac surgery exhibit impaired α1-adrenergic vasoresponsiveness to phenylephrine but preserved or greater ex vivo responsiveness to vasopressin, supporting the potential earlier use of vasopressin for postoperative hypotension in this population.
Answers are grounded in this paper and cite their sources.
Reduced phenylephrine responsiveness in HF patients may heighten perioperative vasoplegia risk; leaves open optimal vasopressor selection in this population.
Background: Patients with chronic heart failure (HF) are at increased risk of vasoplegia after cardiac surgery, potentially because neurohormonal activation in the context of HF alters vascular regulation. Methods: We compared perioperative vasoresponsiveness in patients with and without HF undergoing cardiac surgery with cardiopulmonary bypass (CPB). Patients were prospectively enrolled, and changes in systemic vascular resistance (ΔSVR) after phenylephrine and nitroglycerin were measured perioperatively (in vivo). Ex vivo vasoreactivity to phenylephrine and vasopressin was tested in 40 biopsies. Results: In vivo and ex vivo analyses included 36 and 13 patients (10 controls and 3 HF patients), respectively. At baseline, phenylephrine increased SVR by 26% in HF patients (estimated marginal mean, 95% CI 16–35%) versus 51% in controls (95% CI 38–64%; p = 0.002). This attenuated response persisted during CPB, and ex vivo observations suggested a similar pattern. Responsiveness to nitroglycerin was unchanged. Lower post-CPB ΔSVR was associated with greater norepinephrine use during the first postoperative day (β = −346.6, 95% CI −541.2 to −151.9; R2 = 0.291). Conversely, HF patients showed greater ex vivo responsiveness to vasopressin. Conclusions: HF is associated with marked impairment of α1-adrenergic vasoresponsiveness, indicating impaired α1-adrenergic signaling. Preserved vasopressin responsiveness may support its earlier use for postoperative hypotension in these patients.
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Papazisi et al. (2026) conducted an observational in Chronic heart failure in patients undergoing cardiac surgery with cardiopulmonary bypass (n=36). Chronic heart failure vs. Patients without chronic heart failure (controls) was evaluated on Baseline percentage increase in systemic vascular resistance (ΔSVR) after phenylephrine (p=0.002). Chronic heart failure was associated with an attenuated baseline SVR increase to phenylephrine during cardiac surgery compared with controls.
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