Hyponatraemia in heart failure: time for new solutions?

Heart ◽  
2021 ◽  
pp. heartjnl-2021-320277
Author(s):  
Agnieszka Kapłon-Cieślicka ◽  
Anzhela Soloveva ◽  
Yura Mareev ◽  
Irina Cabac-Pogorevici ◽  
Frederik Hendrik Verbrugge ◽  
...  
Keyword(s):  
Heart Failure ◽  
Failure Time ◽  
Advanced Disease ◽  
Volume Overload ◽  
Angiotensin Receptor ◽  
Water Restriction ◽  
Mortality And Morbidity ◽  
Sodium Glucose Cotransporter ◽  
Potential Benefits ◽  
Dilutional Hyponatraemia

Hyponatraemia is very common in heart failure (HF), especially in decompensated patients. It is associated with increased mortality and morbidity and considered a marker of advanced disease. Recognition of hyponatraemia and its causes may help guide treatment strategy. Historically, therapy has primarily focused on water restriction, decongestion with loop diuretics in case of volume overload (dilutional hyponatraemia) and sodium repletion in case of depletion. In this review, we summarise the potential benefits of established and emerging HF therapies on sodium homeostasis, with a focus on dual vasopressin antagonists, angiotensin receptor-neprilysin inhibitors, sodium-glucose cotransporter 2 inhibitors and hypertonic saline, and propose a potential therapeutic approach for hyponatraemia in HF.

scholarly journals CRT in Patients with Heart Failure: Time Course of Perfusion and Wall Motion Changes

2010 ◽  
Vol 2010 ◽  
pp. 1-5 ◽  
Author(s):  
Alessia Gimelli ◽  
Paolo Frumento ◽  
Guido Valle ◽  
Mario Stanislao ◽  
Umberto Startari ◽  
...  
Keyword(s):  
Heart Failure ◽  
Time Course ◽  
Wall Motion ◽  
Failure Time ◽  
Nyha Class ◽  
Volume Overload ◽  
Regional Wall Motion ◽  
Regional Wall ◽  
End Diastolic Volume ◽  
Reverse Remodelling

In patients treated with CRT no data relative to the relationship between regional wall motion and perfusion and reverse remodelling of the left ventricle at short and medium term followup were available. To this aim, 36 heart failure patients were studied by G-SPECT before (T0), within 2 months (T1) and 6 months (T2) after CRT. A clinical followup was completed for 36 months. In 30/36 patients there was an improvement of NYHA Class at T1 that persisted at T2. G-SPECT showed significant improvement of perfusion at T1 in 92% of patients without further changes at T2. A reduction of LV volumes, an increase of EF and an improvement of regional wall motion and thickening were observed at T1 versus baseline, with only minor changes at T2. Moreover, baseline extension of perfusion defects was scarcely correlated with improvement after CRT. Finally, end diastolic volume, perfusion defect and diabetes mellitus were independent predictors of survival. The main effects of CRT on regional myocardial perfusion and wall motion are obtained within 2 months. Volume overload modulates recovery of ventricular function independently of reperfusion and, with extension of perfusion abnormalities and diabetes were independent predictors of survival during followup.

Sodium–Glucose Cotransporter Inhibitors Reduce Mortality and Morbidity in Patients With Heart Failure

2021 ◽  
Vol Publish Ahead of Print ◽  
Author(s):  
Massimiliano Camilli ◽  
Marco Lombardi ◽  
Juan G. Chiabrando ◽  
Andrea Zito ◽  
Marco G. Del Buono ◽  
...  
Keyword(s):  
Heart Failure ◽  
Mortality And Morbidity ◽  
Sodium Glucose Cotransporter ◽  
Patients With Heart Failure

scholarly journals Left Ventricular SGLT1 Protein Expression Correlates with the Extent of Myocardial Nitro-Oxidative Stress in Rats with Pressure and Volume Overload-Induced Heart Failure

Antioxidants ◽  
2021 ◽  
Vol 10 (8) ◽  
pp. 1190
Author(s):  
Alex Ali Sayour ◽  
Mihály Ruppert ◽  
Attila Oláh ◽  
Kálmán Benke ◽  
Bálint András Barta ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Heart Failure ◽  
Protein Expression ◽  
Volume Overload ◽  
Left Ventricular ◽  
Diabetic Rat ◽  
Strong Positive Correlation ◽  
Sodium Glucose Cotransporter ◽  
Hemodynamic Overload

Myocardial sodium-glucose cotransporter 1 (SGLT1) has been shown to be upregulated in humans with heart failure (HF) with or without diabetes. In vitro studies have linked SGLT1 to increased nitro-oxidative stress in cardiomyocytes. We aimed to assess the relation between left ventricular (LV) SGLT1 expression and the extent of nitro-oxidative stress in two non-diabetic rat models of chronic heart failure (HF) evoked by either pressure (TAC, n = 12) or volume overload (ACF, n = 12). Sham-operated animals (Sham-T and Sham-A, both n = 12) served as controls. Both TAC and ACF induced characteristic LV structural and functional remodeling. Western blotting revealed that LV SGLT1 protein expression was significantly upregulated in both HF models (both p < 0.01), whereas the phosphorylation of ERK1/2 was decreased only in ACF; AMPKα activity was significantly reduced in both models. The protein expression of the Nox4 NADPH oxidase isoform was increased in both TAC and ACF compared with respective controls (both p < 0.01), showing a strong positive correlation with SGLT1 expression (r = 0.855, p < 0.001; and r = 0.798, p = 0.001, respectively). Furthermore, SGLT1 protein expression positively correlated with the extent of myocardial nitro-oxidative stress in failing hearts assessed by 3-nitrotyrosin (r = 0.818, p = 0.006) and 4-hydroxy-2-nonenal (r = 0.733, p = 0.020) immunostaining. Therefore, LV SGLT1 protein expression was upregulated irrespective of the nature of chronic hemodynamic overload, and correlated significantly with the expression of Nox4 and with the level of myocardial nitro-oxidative stress, suggesting a pathophysiological role of SGLT1 in HF.

Sign in / Sign up

Export Citation Format

Share Document