Echocardiographic Assessment of Diastolic Heart Failure

2010 ◽  
Vol 6 (3) ◽  
pp. 13 ◽  
Author(s):  
Bogdan A Popescu ◽  
Carmen C Beladan ◽  
Carmen Ginghină ◽  
◽  
◽  
...  
Keyword(s):  
Heart Failure ◽  
Clinical Features ◽  
Diastolic Heart Failure ◽  
Left Ventricular ◽  
Diagnostic Modality ◽  
Mortality And Morbidity ◽  
Echocardiographic Parameters ◽  
Echocardiographic Assessment ◽  
Lv Diastolic Dysfunction

A normal ejection fraction (EF) is present in >50% of patients with clinical features of heart failure (HF). This entity has been referred to as HF with normal EF (HFNEF), or diastolic HF. The underlying pathophysiology of HFNEF is still under debate and this is reflected in the unsatisfactory results of pharmacological treatment and in the high mortality and morbidity rates, which are similar to those for systolic HF. By providing evidence of left ventricular (LV) diastolic dysfunction in patients with clinical features of HF and normal LVEF, echocardiography, the most practical and widely available diagnostic modality, can offer two of the three current diagnostic criteria for HFNEF. Moreover, abnormalities in LV myocardial deformation and torsional dynamics at rest and during exercise were recently demonstrated in HFNEF patients by echocardiography. Newer echocardiographic parameters may improve the understanding of this complex entity, but further studies are needed before using them in clinical practice for the diagnostic and therapeutic approach of patients with HFNEF. This article discusses the current echocardiographic approach to the diagnosis of diastolic HF, as well as the potential role of newer echo indices and modalities.

Link between diabetes and diastolic dysfunction and the diagnostic role of echocardiography

2009 ◽  
Vol 150 (45) ◽  
pp. 2060-2067 ◽  
Author(s):  
András Nagy ◽  
Zsuzsanna Cserép
Keyword(s):  
Heart Failure ◽  
Diastolic Dysfunction ◽  
Systolic Function ◽  
Diastolic Heart Failure ◽  
Systolic Dysfunction ◽  
Mitral Annulus ◽  
Left Ventricular ◽  
Diabetic Patients ◽  
Doppler Study

Diabetes mellitus, a disease that has been reaching epidemic proportions, is an important risk factor to the development of cardiovascular complication. The left ventricular diastolic dysfunction represents the earliest pre-clinical manifestation of diabetic cardiomyopathy, preceding systolic dysfunction and being able to evolve to symptomatic heart failure. In early stages, these changes appear reversible with tight metabolic control, but as pathologic processes become organized, the changes are irreversible and contribute to an excess risk of heart failure among diabetic patients. Doppler echocardiography provides reliable data in the stages of diastolic function, as well as for systolic function. Combination of pulsed tissue Doppler study of mitral annulus with transmitral inflow may be clinically valuable for obtaining information about left ventricular filling pressure and unmasking Doppler inflow pseudonormal pattern, a hinge point for the progression toward advanced heart failure. Subsequently we give an overview about diabetes and its complications, their clinical relevance and the role of echocardiography in detection of diastolic heart failure in diabetes.

P5443NOD2 knock down worsens diastolic dysfunction in murine angiotensin II-induced heart failure

2019 ◽  
Vol 40 (Supplement_1) ◽  
Author(s):  
I Mueller ◽  
J Lin ◽  
K Pappritz ◽  
C Tschoepe ◽  
S Van Linthout
Keyword(s):  
Heart Failure ◽  
Immune System ◽  
Angiotensin Ii ◽  
Ejection Fraction ◽  
Diastolic Dysfunction ◽  
Mrna Expression ◽  
Diastolic Heart Failure ◽  
Knock Down ◽  
Lv Diastolic Dysfunction

Abstract Background Heart failure with preserved ejection fraction (HFpEF) is associated with cardiac inflammatory responses, indicating a potential role of the immune system in the pathology of diastolic dysfunction. The cytoplasmatic pattern recognition receptor, nucleotide binding oligomerization domain 2 (NOD2) belongs to the innate immune system and induces among others the NLRP3 inflammasome, known to be involved in myocarditis and coronary heart disease. Purpose The aim of this study was to explore the role of NOD2 in Angiotensin II (AngII)-induced diastolic heart failure. Methods In NOD2−/− knock down and C57Bl6/j-wild type (WT) mice, diastolic dysfunction was induced by subcutaneous administration of 1.4mg/kg*day–1 AngII. Twenty-one days after first AngII administration, left ventricular (LV) function was evaluated by pressure tip catheter. Cardiac fibrosis, inflammation, and the expression of NOD2 and the NLRP3 component Apoptosis-associated speck like protein containing a caspase recruitment domain (ASC) were determined via immunohistochemistry, real-time PCR or Western Blot. Results LV NOD2 mRNA expression was 2.3-fold (p<0.0005) and 1.9-fold (p<0.0005) lower in NOD2−/− control and NOD2−/− AngII mice compared to their respective WT littermates. In parallel, LV protein expression of the downstream NLRP3 component Apoptosis-associated speck like protein containing a caspase recruitment domain (ASC) was 1.5-fold (p<0.05) lower in NOD2−/− AngII mice versus WT AngII mice, whereas LV protein IL-1β levels were unchanged. LV diastolic dysfunction was more pronounced in NOD2−/− AngII mice versus WT AngII mice, as displayed by a 19% (p<0.05) increased LV relaxation time and 24% (p<0.057) impaired dP/dtmin, with no changes in the ejection fraction (EF: NOD2−/− AngII 72.5%±5.4 versus WT AngII 65.6±3.5). In parallel, LV presence of CD68-positive cells was 1.8-fold (p<0.05) higher in NOD2−/− AngII compared to WT AngII mice. Concomitantly, NOD2−/− AngII mice displayed 1.3-fold (p<0.05) and 1.7-fold (p<0.05) higher LV mRNA expression of the chemokine macrophage inflammatory protein (MIP)-2 and monocyte chemotactant protein (MCP)-1 compared to WT AngII mice, respectively. Furthermore, cardiac interstitial fibrosis in NOD2−/− mice with AngII-induced diastolic dysperformance was more pronounced versus the WT AngII group, as indicated by a 2.0-fold (p<0.0005), 2.0-fold, and 1.6-fold (p<0.05) higher LV ColI/ColIII ratio, and TGF-β and TIMP-1 mRNA expression, respectively. Conclusion NOD2−/− deteriorates LV diastolic dysfunction and worsens pathophysiological key mechanisms in mice with AngII-induced diastolic heart failure.

scholarly journals Therapy potential for the correction of cardiovascular disturbances in diabetes mellitus

2012 ◽  
Vol 11 (4) ◽  
pp. 59-64
Author(s):  
I. P. Tatarchenko ◽  
N. V. Pozdnyakova ◽  
A. G. Mordovina ◽  
O. I. Morozova ◽  
E. V. Rubleva
Keyword(s):  
Diabetes Mellitus ◽  
Heart Failure ◽  
Diastolic Heart Failure ◽  
Left Ventricular ◽  
Functional Class ◽  
Angiotensin Ii Receptor ◽  
Vasomotor Activity ◽  
Lv Diastolic Dysfunction ◽  
And Function ◽  
Arterial Endothelium

Aim. To study the dynamics of left ventricular (LV) structure and function, as well as vasomotor activity of arterial endothelium, in patients with Type 2 diabetes mellitus (DM-2) and diastolic heart failure (DHF) who are treated with an angiotensin II receptor antagonist olmesartan. Material and methods. The study included 56 patients (26 men and 30 women; mean age 58,2±5,3 years) with NYHA Functional Class I-II chronic heart failure (CHF), diastolic LV dysfunction (abnormal relaxation), and LV ejection fraction (EF) >50%. Other inclusion criteria were DM-2 duration <15 years and per os glucoselowering treatment. Results. The major pathogenetic mechanisms of LV diastolic dysfunction and endothelial dysfunction in DM-2 are linked to the development of central sympathetic hyperactivation and activation of the tissue reninangiotensin system. Conclusion. After 30 weeks of olmesartan therapy, LV structure and geometry, LV diastolic function, and vasomotor activity of arterial endothelium had improved, which was expected to reduce the risk of myocardial ischemia.

Abstract 15352: Plasma Levels of BNP are Lower in Patients With Heart failure With Preserved EF (HFpEF) as Compared With Those With Reduced EF (HFrEF)

Circulation ◽  
2015 ◽  
Vol 132 (suppl_3) ◽  
Author(s):  
Eisaku Harada ◽  
Yuji Mizuno ◽  
Makoto Shono ◽  
Hiroyuki Maeda ◽  
Naotsugu Yano ◽  
...  
Keyword(s):  
Heart Failure ◽  
Plasma Levels ◽  
Left Atrial ◽  
Female Gender ◽  
Posterior Wall ◽  
Left Ventricular ◽  
Posterior Wall Thickness ◽  
Lv Mass ◽  
Echocardiographic Parameters

Introduction: Heart failure with preserved ejection fraction (HFpEF) is increasing in prevalence and causes substantial morbidity, mortality, and resource utilization in the aging population. The plasma level of B-type natriuretic peptide (BNP) is used as a marker of HF with reduced EF (HFrEF). However, the role of BNP in HFpEF is not well known. The purpose of the present study was to compare the levels of BNP together with the echocardiographic findings between HFpEF and HFrEF. Methods: The study subjects consisted of 1574 patients with HF and early diastolic flow velocity (E)/velocity of early diastolic mitral annular motion (e′) or E/e′≥15 (as a measure of elevated left atrial pressure) (574 men and 1000 women, mean age 78.8±10.7) admitted at our hospital. They were divided into 1238 patients with HFpEF (373 men and 865 women, mean age 79.7±10.2) [left ventricular (LV) EF≥50% and E/e′≥15] and 336 patients with HFrEF (201 men and 135 women, mean age 75.4±11.8) (LVEF<50%). Echocardiographic parameters, age, gender, and BNP were examined. Results: The levels of BNP were lower [107(47, 225) pg/ml vs. 296(121, 626) pg/ml, P<0.001] in the HFpEF group than in the HFrEF group. The frequencies of female gender, age, EF, LV posterior wall thickness were higher (all P<0.001, respectively) and LV mass, LV end-diastolic diameter (LVDd), LV end-systolic diameter (LVDs) and left atrial diameter (LAD) were lower (all P<0.001, respectively) in the HFpEF group than in the HFrEF group. A multiple regression analysis revealed EF (t=-17.0), age (t=11.2), E/e′ (t=10.5), LAD (t=9.0), LV mass (t=7.9), and LVDd (t=-5.3) were independent predictors (all P<0.001, respectively) for the BNP level (P<0.001, R2=0.40) in this order. Conclusions: HFpEF was associated with lower levels of BNP and smaller heart and was more prevalent in the elders and women as compared with HFrEF. Predictors for the levels of BNP were EF, age, and E/e′ in this order. These findings imply that the plasma levels of BNP reflect LVEF more than LV diastolic function (E/e′) and thus are lower in the HFpEF group than in the HFrEF group. These findings suggest that the role of BNP in HF may be different between HFpEF and HFrEF.

scholarly journals Role of estrogen in diastolic dysfunction

2014 ◽  
Vol 306 (5) ◽  
pp. H628-H640 ◽  
Author(s):  
Zhuo Zhao ◽  
Hao Wang ◽  
Jewell A. Jessup ◽  
Sarah H. Lindsey ◽  
Mark C. Chappell ◽  
...  
Keyword(s):  
Heart Failure ◽  
Diastolic Dysfunction ◽  
G Protein ◽  
Intracellular Signaling ◽  
Diastolic Heart Failure ◽  
Left Ventricular ◽  
Female Rat ◽  
Cardiac Phenotype ◽  
G Protein Coupled

The prevalence of left ventricular diastolic dysfunction (LVDD) sharply increases in women after menopause and may lead to heart failure. While evidence suggests that estrogens protect the premenopausal heart from hypertension and ventricular remodeling, the specific mechanisms involved remain elusive. Moreover, whether there is a protective role of estrogens against cardiovascular disease, and specifically LVDD, continues to be controversial. Clinical and basic science have implicated activation of the renin-angiotensin-aldosterone system (RAAS), linked to the loss of ovarian estrogens, in the pathogenesis of postmenopausal diastolic dysfunction. As a consequence of increased tissue ANG II and low estrogen, a maladaptive nitric oxide synthase (NOS) system produces ROS that contribute to female sex-specific hypertensive heart disease. Recent insights from rodent models that mimic the cardiac phenotype of an estrogen-insufficient or -deficient woman (e.g., premature ovarian failure or postmenopausal), including the ovariectomized congenic mRen2.Lewis female rat, provide evidence showing that estrogen modulates the tissue RAAS and NOS system and related intracellular signaling pathways, in part via the membrane G protein-coupled receptor 30 (GPR30; also called G protein-coupled estrogen receptor 1). Complementing the cardiovascular research in this field, the echocardiographic correlates of LVDD as well as inherent limitations to its use in preclinical rodent studies will be briefly presented. Understanding the roles of estrogen and GPR30, their interactions with the local RAAS and NOS system, and the relationship of each of these to LVDD is necessary to identify new therapeutic targets and alternative treatments for diastolic heart failure that achieve the cardiovascular benefits of estrogen replacement without its side effects and contraindications.

scholarly journals Does the volume overload exaggerate the severity of mitral regurgitation in patients with decompensated heart failure?

2020 ◽  
Vol 50 (6) ◽  
pp. 1552-1558
Author(s):  
Göktuğ SAVAŞ ◽  
Ömer ŞAHİN ◽  
Mustafa YAŞAN ◽  
Uğur KARABIYIK ◽  
Nihat KALAY ◽  
...  
Keyword(s):  
Heart Failure ◽  
Mitral Regurgitation ◽  
Volume Overload ◽  
Integrated Approach ◽  
Left Ventricular ◽  
Functional Mitral Regurgitation ◽  
Systolic Pulmonary Artery Pressure ◽  
Vena Contracta ◽  
Echocardiographic Parameters ◽  
Echocardiographic Assessment

Background/aim: Diagnosing and managing functional mitral regurgitation (MR) is often challenging and requires an integrated approach including a comprehensive echocardiographic examination. However, the effects of volume overload on the echocardiographic assessment of MR severity are uncertain. The purpose of this study was to weigh the effects of volume overload in the echocardiographic assessment of MR severity among patients with heart failure (HF).Materials and methods: Twenty-nine patients with decompensated HF, who had moderate or severe MR, were included in the present study. The volume status and the N-terminal pro-B-type natriuretic peptide (proBNP) levels were recorded and the echocardiographic parameters were assessed. After the conventional treatment for HF, the proBNP levels and the echocardiographic parameters were assessed again.Results: The mean age of the patients was 72 ± 9 years and the average hospitalization time was 10.9 ± 5.9 days. Between the beginning and the end of the treatment, there were significant reductions in the effective regurgitant orifice area (EROA) (0.36 ± 0.09 cm2 to 0.29 ± 0.09 cm2, P < 0.001), vena contracta (VC) (P < 0.001), the regurgitant volume (RV) (P < 0.001), and systolic pulmonary artery pressure (sPAP) (P < 0.001). Conclusion: This is the first study to investigate the relationship of changes in severity of MR with volume-load by monitoring the proBNP levels among patients with HF. The present results demonstrated that volume reduction, as evidenced by a decline in the proBNP levels, was accompanied by a marked reduction in the EROA, VC, and the RV among patients with left ventricular dysfunction.

scholarly journals Sickle cell disease: at the crossroads of pulmonary hypertension and diastolic heart failure

Heart ◽  
2019 ◽  
Vol 106 (8) ◽  
pp. 562-568 ◽  
Author(s):  
Katherine C Wood ◽  
Mark T Gladwin ◽  
Adam C Straub
Keyword(s):  
Heart Failure ◽  
Pulmonary Hypertension ◽  
Sickle Cell Disease ◽  
Ejection Fraction ◽  
Diastolic Dysfunction ◽  
Sickle Cell ◽  
Diastolic Heart Failure ◽  
Left Ventricular ◽  
Cell Disease ◽  
Lv Diastolic Dysfunction

Sickle cell disease (SCD) is caused by a single point mutation in the gene that codes for beta globin synthesis, causing haemoglobin polymerisation, red blood cell stiffening and haemolysis under low oxygen and pH conditions. Downstream effects include widespread vasculopathy due to recurring vaso-occlusive events and haemolytic anaemia, affecting all organ systems. Cardiopulmonary complications are the leading cause of death in patients with SCD, primarily resulting from diastolic heart failure (HF) and/or pulmonary hypertension (PH). HF in SCD often features biventricular cardiac hypertrophy and left ventricular (LV) diastolic dysfunction. Among HF cases in the general population, approximately half occur with preserved ejection fraction (HFpEF). The insidious evolution of HFpEF differs from the relatively acute evolution of HF with reduced ejection fraction. The PH of SCD has diverse origins, which can be pulmonary arterial (precapillary), pulmonary venous (postcapillary) or pulmonary thromboembolic. It is also appreciated that patients with SCD can develop both precapillary and postcapillary PH, with elevations in LV diastolic pressures, as well as elevations in transpulmonary pressure gradient and pulmonary vascular resistance. Regardless of the cause of PH in SCD, its presence significantly reduces functional capacity and increases mortality. PH that occurs in the presence of HFpEF is usually of postcapillary origin. This review aims to assemble what has been learnt from clinical and animal studies about the manifestation of PH-HFpEF in SCD, specifically the contributions of LV diastolic dysfunction and myocardial fibrosis, in an attempt to gain an understanding of its evolution.

Constrictive pericarditis: diagnosis, management and clinical outcomes

Heart ◽  
2017 ◽  
Vol 104 (9) ◽  
pp. 725-731 ◽  
Author(s):  
Terrence D Welch
Keyword(s):  
Risk Factors ◽  
Heart Failure ◽  
Constrictive Pericarditis ◽  
Diastolic Heart Failure ◽  
Left Ventricular ◽  
Left Ventricular Ejection ◽  
Cross Sectional ◽  
Ventricular Ejection Fraction ◽  
Echocardiographic Assessment ◽  
Cardiac Filling

Constrictive pericarditis (CP) is a form of diastolic heart failure that arises because an inelastic pericardium inhibits cardiac filling. This disorder must be considered in the differential diagnosis for unexplained heart failure, particularly when the left ventricular ejection fraction is preserved. Risk factors for the development of CP include prior cardiac surgery and radiation therapy, but most cases are still deemed to be idiopathic. Making the diagnosis may be challenging and requires meticulous echocardiographic assessment, often supplemented by cross-sectional cardiac imaging and haemodynamic catheterisation. The key pathophysiological concepts, which serve as the basis for many of the diagnostic criteria, remain: (1) dissociation of intrathoracic and intracardiac pressures and (2) enhanced ventricular interaction. Complete surgical pericardiectomy is the only effective treatment for chronic CP. A subset of patients with subacute inflammatory CP, often identified by cardiac MRI, may respond to anti-inflammatory treatments.

Heart Failure with Preserved Ejection Fraction – A Review

2012 ◽  
Vol 9 (1) ◽  
pp. 90-95 ◽  
Author(s):  
Otto A Smiseth ◽  
Anders Opdahl ◽  
Espen Boe ◽  
Helge Skulstad
Keyword(s):  
Heart Failure ◽  
Ejection Fraction ◽  
Diastolic Heart Failure ◽  
The Elderly ◽  
Left Ventricular ◽  
Filling Pressure ◽  
Left Ventricular Ejection ◽  
Ventricular Ejection Fraction ◽  
Reduced Ejection Fraction ◽  
Objective Evidence

Heart failure with preserved left ventricular ejection fraction (HF-PEF), sometimes named diastolic heart failure, is a common condition most frequently seen in the elderly and is associated with arterial hypertension and left ventricular (LV) hypertrophy. Symptoms are attributed to a stiff left ventricle with compensatory elevation of filling pressure and reduced ability to increase stroke volume by the Frank-Starling mechanism. LV interaction with stiff arteries aggravates these problems. Prognosis is almost as severe as for heart failure with reduced ejection fraction (HF-REF), in part reflecting co-morbidities. Before the diagnosis of HF-PEF is made, non-cardiac etiologies must be excluded. Due to the non-specific nature of heart failure symptoms, it is essential to search for objective evidence of diastolic dysfunction which, in the absence of invasive data, is done by echocardiography and demonstration of signs of elevated LV filling pressure, impaired LV relaxation, or increased LV diastolic stiffness. Antihypertensive treatment can effectively prevent HF-PEF. Treatment of HF-PEF is symptomatic, with similar drugs as in HF-REF.

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