Rostral ventrolateral medullary catecholaminergic neurones mediate irregular breathing pattern in volume overload heart failure rats

Congestion related to cardiac pressure and/or volume overload plays a central role in the pathophysiology, presentation, and prognosis of heart failure (HF). Most HF exacerbations are related to a progressive rise in cardiac filling pressures that precipitate pulmonary congestion and symptomatic decompensation. Furthermore, persistent symptoms and signs of congestion at discharge or among outpatients are strong predictors of an adverse outcome. Pulmonary congestion is also one of the most important diagnostic and therapeutic targets in chronic heart failure. The aim of this review is to analyze the importance of clinical, instrumental, and biochemical evaluation of congestion in HF by describing old and new tools. Lung ultrasonography (LUS) is an emerging method to assess pulmonary congestion. Accordingly, we describe the additive prognostic role of chest ultrasound with respect to traditional clinical and X-ray assessment in acute and chronic HF setting.

Download Full-text

Myocardial work index: a marker of left ventricular contractility in pressure‐induced or volume overload‐induced heart failure

ESC Heart Failure ◽

10.1002/ehf2.13314 ◽

2021 ◽

Author(s):

Bálint Károly Lakatos ◽

Mihály Ruppert ◽

Márton Tokodi ◽

Attila Oláh ◽

Szilveszter Braun ◽

...

Keyword(s):

Heart Failure ◽

Volume Overload ◽

Left Ventricular ◽

Ventricular Contractility ◽

Left Ventricular Contractility ◽

Work Index

Download Full-text

Evaluation of left ventricular function in an experimental model of congestive heart failure due to combined pressure and volume overload

Basic Research in Cardiology ◽

10.1007/bf01907105 ◽

1988 ◽

Vol 83 (1) ◽

pp. 58-64 ◽

Cited By ~ 8

Author(s):

K. Noma ◽

M. Brändle ◽

R. Jacob

Keyword(s):

Heart Failure ◽

Congestive Heart Failure ◽

Left Ventricular Function ◽

Ventricular Function ◽

Experimental Model ◽

Volume Overload ◽

Left Ventricular

Download Full-text

TVP1022 Attenuates Cardiac Remodeling and Kidney Dysfunction in Experimental Volume Overload-Induced Congestive Heart Failure

Circulation Heart Failure ◽

10.1161/circheartfailure.111.961037 ◽

2011 ◽

Vol 4 (4) ◽

pp. 463-473 ◽

Cited By ~ 8

Author(s):

Zaid A. Abassi ◽

Yaron D. Barac ◽

Sawa Kostin ◽

Ariel Roguin ◽

Elena Ovcharenko ◽

...

Keyword(s):

Heart Failure ◽

Congestive Heart Failure ◽

Cardiac Remodeling ◽

Volume Overload ◽

Kidney Dysfunction

Download Full-text

Pursuing the non-invasive assessment of cardiac contractility: the added value of pressure-area-strain loop analysis in volume overload-induced heart failure

European Heart Journal - Cardiovascular Imaging ◽

10.1093/ehjci/jeaa356.188 ◽

2021 ◽

Vol 22 (Supplement_1) ◽

Author(s):

M Tokodi ◽

BK Lakatos ◽

M Ruppert ◽

A Olah ◽

AA Sayour ◽

...

Keyword(s):

Heart Failure ◽

Mitral Valve ◽

Cardiac Contractility ◽

Volume Overload ◽

Left Ventricular ◽

Stroke Work ◽

Loading Conditions ◽

Innovation And Technology ◽

Pressure Area ◽

Area Strain

Abstract Funding Acknowledgements Type of funding sources: Public grant(s) – National budget only. Main funding source(s): This work was supported by the New National Excellence Programme (ÚNKP-19-3-I) of the Ministry for Innovation and Technology in Hungary, and the Artificial Intelligence Research Field Excellence Programme of the National Research, Development and Innovation Office of the Ministry of Innovation and Technology in Hungary. Background Global longitudinal strain (GLS) by speckle-tracking echocardiography (STE) is a sensitive parameter of left ventricular (LV) systolic function. Nevertheless, GLS is dependent on loading conditions. Through the analysis of pressure-strain loops, myocardial work was recently introduced and tested in different clinical scenarios. Myocardial work incorporates afterload, but still, it neglects changes in preload and LV geometry. Purpose Accordingly, our aim was to test our hypothesis that adding instantaneous LV size to myocardial work calculation can further mitigate the load-dependency of GLS, and therefore, a better correlation with intrinsic myocardial contractility can be achieved. Methods Volume overload-induced heart failure was established by an aortocaval fistula (ACF) in male Wistar rats (n = 12). Age-matched sham-operated animals served as controls (n = 12). STE was performed to assess GLS, which was immediately followed by invasive pressure-volume (P-V) analysis to assess LV pressure and to compute a gold-standard index of cardiac contractility (preload recruitable stroke work [PRSW]). Global myocardial work index (GMWI) was calculated from GLS and the invasively measured LV pressure. To compute GMWI indexed to LV area (GMWIA), the instantaneous power (calculated by multiplying the strain rate and the instantaneous LV pressure) was divided by the instantaneous LV area, and then it was integrated from mitral valve closure until mitral valve opening. Results LV ejection fraction did not differ significantly (ACF vs. controls: 59 ± 4 vs. 65 ± 9%, p = NS), whereas GLS (Figure 1A - representative animals) was slightly decreased in the ACF group (-13.2 ± 2.3 vs. -15.4 ± 1.9%, p < 0.05). In contrast, PRSW, GMWI (Figure 1B - representative animals) and GMWIA (Figure 1C - representative animals) were considerably reduced in ACF compared to controls (57 ± 13 vs. 111 ± 38mmHg, 1383 ± 382 vs. 1928 ± 281mmHg%, 11.6 ± 3.7 vs. 47.9 ± 22.8mmHg%/mm2, all p < 0.01). GLS showed moderate correlation with PRSW (r=-0.550, p < 0.01), whereas GMWI correlated more significantly, but still moderately with the invasively measured LV contractility (r = 0.681, p < 0.001). Correlation between the pressure-area-strain loop-derived GMWIA and P-V analysis-derived PRSW (Figure 1D) was found to be very strong (r = 0.924, p < 0.001). Conclusions In the case of LV volume overload-induced heart failure, our pressure-area-strain loop-derived metric reflected LV contractility better than GLS and even GMWI. Therefore, the incorporation of instantaneous LV size into myocardial work calculation represents a promising clinical tool to assess and monitor intrinsic myocardial function independently of loading conditions. Abstract Figure 1

Download Full-text

Biomarkers for the diagnosis and management of heart failure

Heart Failure Reviews ◽

10.1007/s10741-021-10105-w ◽

2021 ◽

Author(s):

Vincenzo Castiglione ◽

Alberto Aimo ◽

Giuseppe Vergaro ◽

Luigi Saccaro ◽

Claudio Passino ◽

...

Keyword(s):

Heart Failure ◽

Risk Stratification ◽

Adverse Outcome ◽

Volume Overload ◽

High Sensitivity ◽

Circulating Biomarkers ◽

Diagnosis And Management ◽

Conflicting Evidence ◽

Galectin 3

AbstractHeart failure (HF) is a significant cause of morbidity and mortality worldwide. Circulating biomarkers reflecting pathophysiological pathways involved in HF development and progression may assist clinicians in early diagnosis and management of HF patients. Natriuretic peptides (NPs) are cardioprotective hormones released by cardiomyocytes in response to pressure or volume overload. The roles of B-type NP (BNP) and N-terminal pro-B-type NP (NT-proBNP) for diagnosis and risk stratification in HF have been extensively demonstrated, and these biomarkers are emerging tools for population screening and as guides to the start of treatment in subclinical HF. On the contrary, conflicting evidence exists on the role of NPs as a guide to HF therapy. Among the other biomarkers, high-sensitivity troponins and soluble suppression of tumorigenesis-2 are the most promising biomarkers for risk stratification, with independent value to NPs. Other biomarkers evaluated as predictors of adverse outcome are galectin-3, growth differentiation factor 15, mid-regional pro-adrenomedullin, and makers of renal dysfunction. Multi-marker scores and genomic, transcriptomic, proteomic, and metabolomic analyses could further refine HF management.

Download Full-text

Abstract 375: Mechanotransduction via Titin’s N2B Element Contributes to Cardiac Remodeling

Circulation Research ◽

10.1161/res.117.suppl_1.375 ◽

2015 ◽

Vol 117 (suppl_1) ◽

Author(s):

Mathew Bull ◽

Pooja Nair ◽

Joshua Strom ◽

Michael Gotthardt ◽

Henk Granzier

Keyword(s):

Heart Failure ◽

Cardiac Remodeling ◽

Mapk Pathway ◽

Hot Spot ◽

Pressure Overload ◽

Volume Overload ◽

Mitogen Activated Protein Kinase ◽

Stress And Strain ◽

Knock Out ◽

Voluntary Running

Pathological remodeling is responsible for the functional deficits characteristic of heart failure patients. Understanding mechanotransduction is limited, but holds potential to provide novel therapeutic targets to treat patients with heart failure, especially those with diastolic dysfunction and preserved ejection fraction (HFpEF). Titin is the largest known protein and is abundant in muscle. It is the main contributor of passive stiffness in the heart and functions as a molecular mechano-sensor for stress and strain in the myocyte. Titin is composed of four distinct regions, (N-terminal Z-line, I-band, A-band, and C-terminal M-line), and acts as a molecular spring that is responsible for the assembly and maintenance of ultrastructure in the sarcomere. The elastic N2B element found in titin’s I-band region has been proposed as a mechano-sensor and signaling “hot spot” in the sarcomere. This study investigates the role of titin’s cardiac specific N2B element as sensor for stress and strain induced remodeling in the heart. The previously published N2B knock out (KO) mouse was subjected to a variety of stressors including transverse aortic constriction (TAC), aorto-caval fistula (ACF), chronic swimming, voluntary running and isoproterenol injections. Through chronic pathologic stress, pressure overload (TAC) and chronic volume overload (ACF), we found that the N2B element is necessary for the response to volume overload but not pressure overload as determined by changes in cardiac remodeling. Furthermore, the response to exercise either by chronic swimming or voluntary running was reduced in the N2B KO mouse. Finally, unlike the wild-type (WT) mouse, the N2B KO mouse did not respond to isoproterenol injections with hypertrophic remodeling. Ongoing work to elucidate the molecular pathways involving the N2B element and response to stress, is focused on its binding protein Four-and-a-half-LIM domains 2 (FHL2) and the mitogen activated protein kinase (MAPK) pathway. Taken together our data suggest that the N2B element contributes significantly to mechanotransduction in the heart.

Download Full-text