Characterisation of haemodynamic and metabolic abnormalities in the heart failure spectrum: the role of combined cardiopulmonary and exercise echocardiography stress test

Author(s):  
Nicola R. Pugliese ◽  
Nicolò De Biase ◽  
Alessio Balletti ◽  
Francesco Filidei ◽  
Alessandra Pieroni ◽  
...  
2021 ◽  
Vol 14 (6) ◽  
Author(s):  
Pedro Caravaca Pérez ◽  
Jorge Nuche ◽  
Laura Morán Fernández ◽  
David Lora ◽  
Zorba Blázquez-Bermejo ◽  
...  

Background: Poor natriuresis has been associated with a poorer response to diuretic treatment and worse prognosis in acute heart failure. Recommendations on how and when to measure urinary sodium (UNa) are lacking. We aim to evaluate UNa quantification after a furosemide stress test (FST) capacity to predict appropriate decongestion during acute heart failure hospitalization. Methods: Patients underwent an FST on day-1 of admission, and UNa was measured 2 hours after, dividing patients into low or high UNa based on the sample median value. A semiquantitative composite congestive score (CCS; 0–9) and NT pro-BNP (N-terminal pro-B-type natriuretic peptide) quantification were assessed before the FST and at day 5 after the FST. Results: Median UNa after FST in the 65 patients included was 113 (97–122) mmol/L. At day 5, a lower proportion of patients with a low UNa reached a 30% decrease in NT-proBNP levels (21 [66%] for low UNa versus 31 [94%] for high UNa; P =0.005) and an appropriate grade of decongestion (CCS<3) (20 [62%] for low UNa versus 32 [97%] for high UNa; P <0.001). A UNa>83 mmol/L 2 hours after FST had a 96% sensitivity to predict an NT-proBNP reduction ≥30% and 95% to predict a CCS<3 at day 5. Low UNa patients presented a lower cumulative diuresis and weight loss and presented more often with prolonged hospitalization, worsening heart failure, and readmission because of acute heart failure or death at 6 months. Conclusions: Low natriuresis after an FST identified patients at a higher risk of an inadequate diuretic response and an inappropriate decongestion. FST-guided diuretic treatment might help to improve decongestion, shorten hospitalizations, and to reduce adverse outcomes.


Author(s):  
Pedro Caravaca Pérez ◽  
Jorge Nuche ◽  
Juan Carlos López-Azor ◽  
Rafael Salguero-Bodes ◽  
Fernando Arribas Ynsaurriaga ◽  
...  

2021 ◽  
Vol 26 (2) ◽  
pp. 4147
Author(s):  
E. N. Pavlyukova ◽  
D. A. Kuzhel

Heart failure (HF) with preserved ejection fraction (HFpEF) is currently the most common type of this condition, especially among elderly patients. Despite the preserved left ventricular (LV) and a moderate increase in natriuretic peptide, patients  with HFpEF have the same out-of-hospital mortality as those with HF with reduced ejection fraction (HFrEF). Diagnosis of HFpEF is difficult due to nonspecific symptoms, expensive blood tests, and questionable rest echocardiographic data on diastolic function. In addition, the reason for poor diagnosis of HfpEF in clinical practice may be old age and comorbidities, which can also cause nonspecific symptoms of moderate chronic shortness of breath, weakness, and palpitations. The consequence is the detection of HFpEF only in every fourth patient with an acute or chronic heart failure. The use of simplified clinical diagnostic protocols along with a non-invasive ultrasound stress test can help overcome the existing problems in the diagnosis of HFpEF.


2020 ◽  
Vol 134 (1) ◽  
pp. 71-72
Author(s):  
Naseer Ahmed ◽  
Masooma Naseem ◽  
Javeria Farooq

Abstract Recently, we have read with great interest the article published by Ibarrola et al. (Clin. Sci. (Lond.) (2018) 132, 1471–1485), which used proteomics and immunodetection methods to show that Galectin-3 (Gal-3) down-regulated the antioxidant peroxiredoxin-4 (Prx-4) in cardiac fibroblasts. Authors concluded that ‘antioxidant activity of Prx-4 had been identified as a protein down-regulated by Gal-3. Moreover, Gal-3 induced a decrease in total antioxidant capacity which resulted in a consequent increase in peroxide levels and oxidative stress markers in cardiac fibroblasts.’ We would like to point out some results stated in the article that need further investigation and more detailed discussion to clarify certain factors involved in the protective role of Prx-4 in heart failure.


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