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• W4244268505 abstract "Background Acute heart failure (AHF) is a heterogeneous syndrome that comprises the activation of multiple counter-regulatory processes including the immune and inflammatory pathways, which worsen the prognosis. Recent data have provided novel insights into the role of the immune and inflammatory systems in the pathogenesis of heart failure (HF), and low lymphocyte count has been proposed as an easily obtained marker of systemic inflammation that has shown a significant association with poor outcomes in this setting. Although the specific pathophysiological pathway underlying the occurrence of lymphocytopenia in HF remain incompletely understood, portal congestion has been involved into impaired leukocyte distribution and altered lymphocyte behavior. However, the associations between lymphocytopenia and ultrasound surrogates for portal congestion have never been reported in AHF. In the current study, we aimed to: characterize the clinical and biochemical variables associated with a low lymphocyte count on admission and at discharge in patients with AHF; assess the potential associations between lymphocyte count and ultrasound surrogates for portal congestion; and explore the relationships between lymphocyte count at discharge and long-term outcomes in AHF. Methods Clinical, biological and ultrasound assessments were prospectively obtained at the time of hospital admission and at discharge, after decongestive therapy. Patients were compared according to tertiles of absolute lymphocyte count at baseline (very low,<0.87; low,0.87-1.2; normal,>1.2 × 109/L). Right ventricular (RV) function was assessed using tricuspid annular plan systolic excursion (TAPSE). Doppler-derived portal vein pulsatility index (PVPI) was used as a surrogate for portal congestion. Results 103 patients with AHF were prospectively assessed. At baseline, mean absolute lymphocyte count was 1.1 ± 0.6 × 109/L, and 69% of patients had a lymphocyte count below local normal range (1.3 to 4.5 × 109/L). Patients with baseline very low lymphocyte count were older, had more advanced disease and higher PVPI when compared with those in the higher tertiles (all p<0.05). Very low lymphocyte count at baseline was associated with age (OR 1.098), PVPI (OR 1.026) and TAPSE (OR 0.865, all p<0.05). PVPI remained the only determinant of lymphocytopenia at the time of discharge (OR 1.033, p<0.05). In a Cox model, lymphocytopenia at discharge was significantly associated with all-cause of mortality (HR 4.796, p<0.05) after adjusting for age, sex, left ventricular ejection fraction and hemoglobin. Conclusions Low lymphocyte count in patients hospitalized for AHF is strongly associated with RV dysfunction and ultrasound markers of portal congestion. Whether this association supports the role of portal congestion as a pathophysiological mechanism directly involved in lymphocytopenia in AHF, or whether these two features only reflect a more advanced disease remains to be determined. Acute heart failure (AHF) is a heterogeneous syndrome that comprises the activation of multiple counter-regulatory processes including the immune and inflammatory pathways, which worsen the prognosis. Recent data have provided novel insights into the role of the immune and inflammatory systems in the pathogenesis of heart failure (HF), and low lymphocyte count has been proposed as an easily obtained marker of systemic inflammation that has shown a significant association with poor outcomes in this setting. Although the specific pathophysiological pathway underlying the occurrence of lymphocytopenia in HF remain incompletely understood, portal congestion has been involved into impaired leukocyte distribution and altered lymphocyte behavior. However, the associations between lymphocytopenia and ultrasound surrogates for portal congestion have never been reported in AHF. In the current study, we aimed to: characterize the clinical and biochemical variables associated with a low lymphocyte count on admission and at discharge in patients with AHF; assess the potential associations between lymphocyte count and ultrasound surrogates for portal congestion; and explore the relationships between lymphocyte count at discharge and long-term outcomes in AHF. Clinical, biological and ultrasound assessments were prospectively obtained at the time of hospital admission and at discharge, after decongestive therapy. Patients were compared according to tertiles of absolute lymphocyte count at baseline (very low,<0.87; low,0.87-1.2; normal,>1.2 × 109/L). Right ventricular (RV) function was assessed using tricuspid annular plan systolic excursion (TAPSE). Doppler-derived portal vein pulsatility index (PVPI) was used as a surrogate for portal congestion. 103 patients with AHF were prospectively assessed. At baseline, mean absolute lymphocyte count was 1.1 ± 0.6 × 109/L, and 69% of patients had a lymphocyte count below local normal range (1.3 to 4.5 × 109/L). Patients with baseline very low lymphocyte count were older, had more advanced disease and higher PVPI when compared with those in the higher tertiles (all p<0.05). Very low lymphocyte count at baseline was associated with age (OR 1.098), PVPI (OR 1.026) and TAPSE (OR 0.865, all p<0.05). PVPI remained the only determinant of lymphocytopenia at the time of discharge (OR 1.033, p<0.05). In a Cox model, lymphocytopenia at discharge was significantly associated with all-cause of mortality (HR 4.796, p<0.05) after adjusting for age, sex, left ventricular ejection fraction and hemoglobin. Low lymphocyte count in patients hospitalized for AHF is strongly associated with RV dysfunction and ultrasound markers of portal congestion. Whether this association supports the role of portal congestion as a pathophysiological mechanism directly involved in lymphocytopenia in AHF, or whether these two features only reflect a more advanced disease remains to be determined." @default.
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• W4244268505 date "2020-10-01" @default.
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• W4244268505 title "Lymphocytopenia During Hospitalization for Acute Heart Failure and Its Relationship with Portal Congestion and Right Ventricular Function" @default.
• W4244268505 doi "https://doi.org/10.1016/j.cardfail.2020.09.053" @default.
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