scholarly journals The Role of Natriuretic Peptides for the Diagnosis of Left Ventricular Dysfunction

2013 ◽  
Vol 2013 ◽  
pp. 1-10 ◽  
Author(s):  
Alberto Palazzuoli ◽  
Matteo Beltrami ◽  
Gaetano Ruocco ◽  
Marco Pellegrini ◽  
Ranuccio Nuti

Natriuretic peptides (NPs) are entered in current guidelines for heart failure (HF) diagnosis and management because of their high specificity and sensibility in screening patients with acute dyspnea. Due to their availability and relatively low cost, they became the first step examinations in HF patients evaluation at hospital admission together with clinical and chest radiography examination. NPs are released following any cardiac haemodynamic stress due to volume or pressure overload and should be considered as a mirror of cardiac condition helping in recognizing patients with poor outcome. Moreover, the exact role of NPs in early HF stages, in isolated diastolic dysfunction, and in general population is questioned. Several promising reports described their potential role; however, the wide cut-off definition, inclusion criteria, and intrinsic measurement biases do not actually consent to their clinical application in these settings. A multimodality strategy including both NPs and imaging studies appears to be the best strategy to define the cardiac dysfunction etiology and its severity as well as to identify patients with higher risk. In this review, we describe the current and potential role of NPs in patients with asymptomatic cardiac insufficiency, evaluating the requirement to obtain a better standardization for imaging as for laboratory criteria.

2013 ◽  
Vol 113 (suppl_1) ◽  
Author(s):  
Ludovic O Bénard ◽  
Daniel S Matasic ◽  
Mathilde Keck ◽  
Anne-Marie Lompré ◽  
Roger J Hajjar ◽  
...  

STromal Interaction Molecule 1 (STIM1), a membrane protein of the sarcoplasmic reticulum, has recently been proposed as a positive regulator of cardiomyocyte growth by promoting Ca2+ entry through the plasma membrane and the activation of Ca2+-mediated signaling pathways. We demonstrated that STIM1 silencing prevented the development of left ventricular hypertrophy (LVH) in rats after abdominal aortic banding. Our aim was to study the role of STIM1 during the transition from LVH to heart failure (HF). For experimental timeline, see figure. Transverse Aortic Constriction (TAC) was performed in C57Bl/6 mice. In vivo gene silencing was performed using recombinant Associated AdenoVirus 9 (AAV9). Mice were injected with saline or with AAV9 expressing shRNA control or against STIM1 (shSTIM1) (dose: 1e+11 viral genome), which decreased STIM1 cardiac expression by 70% compared to control. While cardiac parameters were similar between the TAC groups at weeks 3 and 6, shSTIM1 animals displayed a progressive and total reversion of LVH with LV walls thickness returning to values observed in sham mice at week 8. This reversion was associated with the development of significant LV dilation and severe contractile dysfunction, as assessed by echography. Hemodynamic analysis confirmed the altered contractile function and dilation of shSTIM1 animals. Immunohistochemistry showed a trend to more fibrosis. Despite hypertrophic stimuli, there was a significant reduction in cardiac myocytes cross-section area in shSTIM1-treated animals as compared to other TAC mice. This study showed that STIM1 is essential to maintain compensatory LVH and that its silencing accelerates the transition to HF.


2001 ◽  
Vol 31 (11) ◽  
pp. 1159
Author(s):  
Hainan Piao ◽  
Jin Sook Kwon ◽  
Hye Young Lee ◽  
Tae Jin Youn ◽  
Dong Woon Kim ◽  
...  

2009 ◽  
Vol 63 (5-6) ◽  
pp. 381-392
Author(s):  
Ljubica Spasojevic-Kosic

The endocrine role of the heart is evident in the secretion of noradrenaline and natriuretic peptides. The secretion of natriuretic peptides presents a useful mechanism for different conditions of cardiac dysfunction. Brain natriuretic peptide (BNP) has been accepted in human cardiology as a biomarker for cardiac insufficiency and coronary arterial disease. The specificity of the BNP structure is specie-specific, so that the testing of diagnostic and prognostic potential in dogs requires the existence of a test that is a homologue for that animal specie. The existence of an adequate method for measuring BNP concentration makes possible its implementation as a screening test in everyday clinical practice. .


Circulation ◽  
2014 ◽  
Vol 130 (suppl_2) ◽  
Author(s):  
Masayoshi Oikawa ◽  
Atsushi Kobayashi ◽  
Hiroyuki Yamauchi ◽  
Satoshi Suzuki ◽  
Akiomi Yoshihisa ◽  
...  

Background: High mitral inflow E velocity to tissue Doppler e’ ratio (E/e’) is implicated as increased left ventricular (LV) filling pressure, but it is not always consistent with clinical findings. Early (E) and late (A) diastolic filling velocity ratio (E/A) is also used to evaluate LV diastolic function and filling pressure, but the usefulness of combined assessment of E/e’ and E/A is not fully understood. Methods: We retrospectively analyzed 1266 patients who underwent echocardiography to assess cardiac function between January 2013 to March 2014 in our hospital. The patients were grouped based on the values of E/e’ (low E/e’<15, high E/e’≥15) and E/A (low E/A≤0.8, high E/A>0.8). Results: First, we analyzed a role of E/A in the setting of high E/e’ condition. The low E/A with high E/e’ group (n=95) displayed lower tricuspid regurgitant pressure gradient (TRPG, 22 [16-28] mmHg vs. 29 [23-38] mmHg, P<0.01) and smaller inferior vena cava (IVC) diameter (12 [10-15] mm vs. 14 [11-17] mm, P<0.01) than the high E/A with high E/e’ group (n=136), suggesting that low E/A indicated controlled fluid retention even with high E/e’. We next investigated the role of E/e’ in the situation of low E/A state. Compared to the low E/A with low E/e’ group (n=584), the low E/A with high E/e’ group showed similar TRPG (22 [16-28] mmHg vs. 21 [17-26] mmHg, ns), similar IVC diameter (12 [10-15] mm vs. 12 [10-15] mm, ns), but larger LV end-diastolic diameter (48 [42-52] mm vs. 45 [40-50] mm, P<0.01), larger left atrial volume (53 [38-67] ml vs. 41 [29-54] ml, P<0.01), lower LV ejection fraction (59 [47-66]% vs. 63 [57-67]%, P<0.01), and slower LV systolic velocity (5.9 [4.9-7.3] cm/s vs. 7.8 [6.5-9.5] cm/s, P<0.01), indicating that high E/e’ was a predictor of LV remodeling and dysfunction in the situation of low E/A condition. Conclusions: The low E/A indicated controlled fluid retention regardless of E/e’ value. A high E/e’ reflected LV remodeling and dysfunction. Thus, we conclude that combined assessment of E/e’ and E/A is useful to interpret cardiac condition.


1996 ◽  
Vol 18 (8) ◽  
pp. 1051-1071 ◽  
Author(s):  
C. J. Charles ◽  
R. J. Kaaja ◽  
E. A. Espiner ◽  
M. G. Nicholls ◽  
C. J. Pemberton ◽  
...  

Circulation ◽  
2020 ◽  
Vol 141 (3) ◽  
pp. 199-216 ◽  
Author(s):  
Fiona Bartoli ◽  
Marc A. Bailey ◽  
Baptiste Rode ◽  
Philippe Mateo ◽  
Fabrice Antigny ◽  
...  

Background: Orai1 is a critical ion channel subunit, best recognized as a mediator of store-operated Ca 2+ entry (SOCE) in nonexcitable cells. SOCE has recently emerged as a key contributor of cardiac hypertrophy and heart failure but the relevance of Orai1 is still unclear. Methods: To test the role of these Orai1 channels in the cardiac pathophysiology, a transgenic mouse was generated with cardiomyocyte-specific expression of an ion pore-disruptive Orai1 R91W mutant (C-dnO1). Synthetic chemistry and channel screening strategies were used to develop 4-(2,5-dimethoxyphenyl)-N-[(pyridin-4-yl)methyl]aniline (hereafter referred to as JPIII), a small-molecule Orai1 channel inhibitor suitable for in vivo delivery. Results: Adult mice subjected to transverse aortic constriction (TAC) developed cardiac hypertrophy and reduced ventricular function associated with increased Orai1 expression and Orai1-dependent SOCE (assessed by Mn 2+ influx). C-dnO1 mice displayed normal cardiac electromechanical function and cellular excitation-contraction coupling despite reduced Orai1-dependent SOCE. Five weeks after TAC, C-dnO1 mice were protected from systolic dysfunction (assessed by preserved left ventricular fractional shortening and ejection fraction) even if increased cardiac mass and prohypertrophic markers induction were observed. This is correlated with a protection from TAC-induced cellular Ca 2+ signaling alterations (increased SOCE, decreased [Ca 2+ ] i transients amplitude and decay rate, lower SR Ca 2+ load and depressed cellular contractility) and SERCA2a downregulation in ventricular cardiomyocytes from C-dnO1 mice, associated with blunted Pyk2 signaling. There was also less fibrosis in heart sections from C-dnO1 mice after TAC. Moreover, 3 weeks treatment with JPIII following 5 weeks of TAC confirmed the translational relevance of an Orai1 inhibition strategy during hypertrophic insult. Conclusions: The findings suggest a key role of cardiac Orai1 channels and the potential for Orai1 channel inhibitors as inotropic therapies for maintaining contractility reserve after hypertrophic stress.


2018 ◽  
Vol 120 ◽  
pp. 13
Author(s):  
M. Ruppert ◽  
S. Korkmaz-Icöz ◽  
S. Loganathan ◽  
W. Jiang ◽  
L. Lehmann ◽  
...  

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