scholarly journals Is hepatojugular reflux a good predictor of heart failure with preserved ejection fraction?

2019 ◽  
Vol 65 (5) ◽  
pp. 592-595
Author(s):  
Guilherme Cristianini Baldivia ◽  
João Vitor Moraes Pithon Napoli ◽  
Josiane Motta e Motta ◽  
Normando Gomes Vieira Filho ◽  
Heno Ferreira Lopes
Keyword(s):  
Heart Failure ◽  
Blood Pressure ◽  
Diastolic Dysfunction ◽  
Left Ventricular ◽  
Uncontrolled Blood Pressure ◽  
Volume Increase ◽  
Functional Changes ◽  
Left Atrium Volume ◽  
Lv Diastolic Dysfunction ◽  
Symptoms And Signs

SUMMARY Hypertension may occur with left ventricular (LV) diastolic dysfunction, and the consequence may be symptoms and signs of heart failure (HF). Hepatojugular reflux (HJR), described as a sign of regurgitation of the tricuspid valve, may reflect structural and functional changes of the LV in the hypertensive patient. The signal may be present in the presence of HF. Case: male, 49 years old with uncontrolled blood pressure. Physical examination showed jugular turgescence, HJR, and elevated blood pressure. Complementary exams showed signs of atrial and left ventricular overload in the electrocardiogram and, the echocardiogram showed left atrium volume increase, concentric LV hypertrophy and signs of grade I diastolic dysfunction. DISCUSSIO: The HJR present correlates with pulmonary artery pressure and probably reflect the increase in central blood volume.

Using A 21-Year Real-World Database from a Private Cardiologist's Practice to Test the Hypothesis that Combining Pharmacological Therapies (Carvedilol, Spironolactone and Statins) with Weight Loss May Benefit Patients with HFpEF

2020 ◽  
pp. 1-9
Keyword(s):  
Heart Failure ◽  
Atrial Fibrillation ◽  
Weight Loss ◽  
Clinical Trials ◽  
Endothelial Dysfunction ◽  
Combination Therapy ◽  
Ejection Fraction ◽  
Diastolic Dysfunction ◽  
Left Ventricular ◽  
Lv Diastolic Dysfunction

Heart Failure with preserved Ejection Fraction (HFpEF) is a clinical syndrome in which patients have symptoms of Heart Failure (HF), such as dyspnea and fatigue, a Left Ventricular Ejection Fraction (LVEF) ≥ 50% and evidence of cardiac dysfunction as a cause of symptoms, such as abnormal Left Ventricular (LV) diastolic dysfunction with elevated filling pressures. Besides LV diastolic dysfunction, recent investigations suggest a more complex and heterogeneous pathophysiology, including systolic reserve abnormalities, chronotropic incompetence, stiffening of ventricular tissue, atrial dysfunction, secondary Pulmonary Arterial Hypertension (PAH), impaired vasodilatation and endothelial dysfunction. Unlike Heart Failure with Reduced Ejection Fraction (HFrEF), clinical trials over the years have not yet identified effective treatments that reduce mortality in patients with HFpEF. A database on use of carvedilol in a private cardiologist's practice was begun in 1997 and concluded at the end of 2018. We used this database to test the hypothesis that combining pharmacological interventions to address diastolic dysfunction (carvedilol), volume overload (spironolactone/eplerenone) and endothelial dysfunction (statins) with weight loss may benefit patients with HFpEF. We report analysis of 335 patients with HFpEF comprised of 61% female (mean age 74 ± 8) and 39% males (mean age 72 ± 7). Initial EF ranged between 50 and 77% with mean EF of 57 ± 6%. Only 15 patients were changed to metoprolol succinate, verapamil or diltiazem because of adverse side effects. Two hundred and twenty of the patients were in normal sinus rhythm when started on carvedilol, spironolactone/eplerenone and statin therapy with weight loss counseling. After 5 years, 191 patients were still on combination therapy, and only 31 (17%) had developed Atrial Fibrillation (AF). Compared to previous HFpEF trials reporting a 32% risk of developing atrial fibrillation after 4 years, our combination therapy significantly (p < 0.05) reduced the risk of developing AF over 5 years. Thus, irrespective of age and sex with comorbidities of type 2 Diabetes Mellitus (DM) and Chronic Kidney Disease (CKD), patients with HFpEF can be managed successfully with carvedilol, spironolactone/eplerenone and statins with a clinical benefit being a reduced risk of developing AF. We consider these data hypothesis-generating and hope these results will be tested further in database analyses and clinical trials.

Abstract 16485: The Nitroxyl Donor 1-Nitrosocyclohexyl Acetate Limits Cardiac Superoxide Upregulation and Diastolic Dysfunction in a Mouse Model of Diabetic Cardiomyopathy

Circulation ◽  
2014 ◽  
Vol 130 (suppl_2) ◽  
Author(s):  
Rebecca H Ritchie ◽  
Nga Cao ◽  
Yung George Wong ◽  
Sarah Rosli ◽  
Helen Kiriazis ◽  
...  
Keyword(s):  
Heart Failure ◽  
Mouse Model ◽  
Diastolic Dysfunction ◽  
Diabetic Cardiomyopathy ◽  
Ex Vivo ◽  
Systolic Function ◽  
Left Ventricular ◽  
Cardiomyocyte Hypertrophy ◽  
Lv Diastolic Dysfunction ◽  
The Impact

Nitroxyl (HNO), a redox congener of NO•, is a novel regulator of cardiovascular function combining vasodilator and positive inotropic properties. Our previous studies have demonstrated these properties occur concomitantly in the intact heart; HNO moreover also exhibits antihypertrophic and superoxide-suppressing actions. HNO donors may thus offer favorable actions in heart failure. The impact of chronic HNO donor administration has however yet to be reported in this context. We tested the hypothesis that the HNO donor 1-nitrosocyclohexyl acetate (1-NCA) limits cardiomyocyte hypertrophy and left ventricular (LV) diastolic dysfunction in a mouse model of diabetic cardiomyopathy in vivo. Male 6 week-old FVB/N mice received either streptozotocin (55 mg/kg/day i.p. for 5 days, n=17), to induce type 1 diabetes, or citrate vehicle (n=16). After 4 weeks of hyperglycemia, mice were allocated to 1-NCA therapy (83mg/kg/day i.p.) or vehicle, and followed for a further 4 weeks. As shown in the table, blood glucose was unaffected by 1-NCA. LV diastolic dysfunction was evident in diabetic mice, measured as echocardiography-derived A wave velocity, deceleration time and E:A ratio; LV systolic function was preserved. Diabetes-induced diastolic dysfunction was accompanied by increased LV cardiomyocyte size, hypertrophic and pro-fibrotic gene expression, and upregulation of LV superoxide. These characteristics of diabetic cardiomyopathy were largely prevented by 1-NCA treatment. Selectivity of 1-NCA as a donor of HNO versus NO• was demonstrated by the sensitivity of the coronary vasodilation response of 1-NCA to the HNO scavenger L-cysteine (4mM), but not to the NO• scavenger hydroxocobalamin (50μM), in the normal rat heart ex vivo (n=3-7). Collectively, our studies provide the first evidence that HNO donors may represent a promising new strategy for the treatment of diabetic cardiomyopathy, and implies their therapeutic efficacy in settings of chronic heart failure.

Abstract 608: Uric Acid Potentially Interacts With Parathyroid Hormone To Promote Left Ventricular Diastolic Dysfunction In Mice Fed A Western Diet

Hypertension ◽  
2014 ◽  
Vol 64 (suppl_1) ◽  
Author(s):  
Guanghong Jia ◽  
Brian P Bostick ◽  
Javad Habibi ◽  
Annayya R. Aroor ◽  
Vincent G. DeMarco ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Body Weight ◽  
Uric Acid ◽  
Parathyroid Hormone ◽  
Diastolic Dysfunction ◽  
Cardiac Mri ◽  
Left Ventricular ◽  
Western Diet ◽  
P Value ◽  
Lv Diastolic Dysfunction

Hyperuricemia is frequently observed in obese people and rising obesity rates parallel increased consumption of a high-fat/high-fructose western diet (WD). Epidemiologic and clinical data suggest that serum uric acid (UA) is positively associated with serum parathyroid hormone (PTH) and may be linked with left ventricular (LV) hypertrophy and LV diastolic dysfunction. Accordingly, we hypothesized that allopurinol, a potent xanthine oxidase (XO) inhibitor, would prevent development of LV diastolic dysfunction, independent of blood pressure, by reducing the levels of UA and PTH. Four week-old C57BL6/J male mice were fed a WD and water with 125mg/L allopurinol. After 16 weeks, we assessed levels of UA, XO activity, PTH, as well as diastolic function by cardiac MRI and cardiac ultrastructure by transmission electron microscopy (TEM). Body weight and fat composition were obtained along with HOMA -IR testing for insulin resistance. Allopurinol has been show to exert no effect on blood pressure. High resolution cardiac MRI revealed diastolic dysfunction with WD feeding that was prevented by allopurinol (LV diastolic relaxation time 35.3 ms for WD, 25.4 ms for CD and 27.7 ms for WD+ allopurinol, p value <0.01; Initial filling rate 0. 28 μl/ms for WD, 0.43 μl/ms for CD and 0.42 μl/ms for WD+ allopurinol, p value <0.05). Body weight, fat mass, and HOMA-IR were increased by WD feeding but not significantly improved by allopurinol. However, allopurinol markedly decreased the WD-induced increase in heart weight associated with activation of translational S6 kinase. TEM examination of myocardial ultrastructure revealed that WD induced remodeling changes with large mitochondria with disordered cristae and increased lysosomes. The ultrastructural changes were improved with treatment by allopurinol. Furthermore, allopurinol significantly inhibited both of plasma and urine UA levels and cardiac XO activity caused by WD. Interestingly , WD increased PTH levels which were decreased in parallel with reductions in uric acid with allopurinol. These findings support the notion that increased plasma levels of UA, in concert with elevated PTH, may play a key role in LV hypertrophy and associated LV diastolic dysfunction that result from consuming a WD high in fructose and fat.

scholarly journals Left Ventricular Diastolic Dysfunction in the Intensive Care Unit: Trends and Perspectives

2012 ◽  
Vol 2012 ◽  
pp. 1-5 ◽  
Author(s):  
Lewis Ari Eisen ◽  
Pericles Davlouros ◽  
Dimitrios Karakitsos
Keyword(s):  
Heart Failure ◽  
Intensive Care Unit ◽  
Intensive Care ◽  
Diastolic Dysfunction ◽  
Left Ventricular Diastolic Dysfunction ◽  
Left Ventricular ◽  
Lack Of Information ◽  
Normal Left Ventricular ◽  
Ventricular Diastolic Dysfunction ◽  
Lv Diastolic Dysfunction

Heart failure with a normal or nearly normal left ventricular (LV) ejection fraction (HFNEF) may represent more than 50% of heart failure cases. Although HFNEF is being increasingly recognized, there is a relative lack of information regarding its incidence and prognostic implications in intensive care unit (ICU) patients. In the ICU, many factors related to patient’s history, or applied therapies, may induce or aggravate LV diastolic dysfunction. This may impact on patients’ morbidity and mortality. This paper discusses methods for assessing LV diastolic function and the feasibility of their implementation for diagnosing HFNEF in the ICU.

scholarly journals Peripartum Cardiomyopathy Presenting with Predominant Left Ventricular Diastolic Dysfunction: Efficacy of Bromocriptine

2012 ◽  
Vol 2012 ◽  
pp. 1-6 ◽  
Author(s):  
Piercarlo Ballo ◽  
Irene Betti ◽  
Giuseppe Mangialavori ◽  
Leandro Chiodi ◽  
Gherardo Rapisardi ◽  
...  
Keyword(s):  
Heart Failure ◽  
Diastolic Dysfunction ◽  
Diastolic Function ◽  
Systolic Function ◽  
Systolic Dysfunction ◽  
Left Ventricular ◽  
Peripartum Cardiomyopathy ◽  
Lv Function ◽  
Lv Diastolic Dysfunction ◽  
Lv Diastolic Function

Management of patients with peripartum cardiomyopathy (PPCM) is still a major clinical problem, as only half of them or slightly more show complete recovery of left ventricular (LV) function despite conventional evidence-based treatment for heart failure. Recent observations suggested that bromocriptine might favor recovery of LV systolic function in patients with PPCM. However, no evidence exists regarding its effect on LV diastolic dysfunction, which is commonly observed in these patients. Tissue Doppler (TD) is an echocardiographic technique that provides unique information on LV diastolic performance. We report the case of a 37-year-old white woman with heart failure (NYHA class II), moderate LV systolic dysfunction (ejection fraction 35%), and severe LV diastolic dysfunction secondary to PPCM, who showed no improvement after 2 weeks of treatment with ramipril, bisoprolol, and furosemide. At 6-week followup after addition of bromocriptine, despite persistence of LV systolic dysfunction, normalization of LV diastolic function was shown by TD, together with improvement in functional status (NYHA I). At 18-month followup, the improvement in LV diastolic function was maintained, and normalization of systolic function was observed. This paper might support the clinical utility of bromocriptine in patients with PPCM by suggesting a potential benefit on LV diastolic dysfunction.

Significance of Brain Natriuretic Peptide Measurement as a Diagnostic Indicator of Cardiac Function

2000 ◽  
Vol 39 (03) ◽  
pp. 249-253 ◽  
Author(s):  
N. Iida ◽  
T. Ishihara ◽  
S. Waku
Keyword(s):  
Heart Failure ◽  
Blood Pressure ◽  
Brain Natriuretic Peptide ◽  
Natriuretic Peptide ◽  
Diagnostic Value ◽  
Left Ventricular ◽  
Control Group ◽  
Healthy Control ◽  
Group 5 ◽  
Lv Diastolic Dysfunction

AbstractBrain natriuretic peptide (BNP) is increased in patients with heart failure due to myocardial infarction and cardiac hypertrophy, in proportion to the severity of left ventricular dysfunction. The aims of this study were to clarify the clinical features of BNP and to determine the diagnostic value of BNP for mass screening.The subjects were 818 office workers (565 males and 253 females; mean age 47 ± 12 years) who participated in a 1996 routine health check at Kansai University All individuals were examined for blood pressure, serological findings, ECG and plasma BNP level. Thirty-three males underwent 2-D echocardiography. Plasma BNP levels were measured using IRMA (immunoradiometric assay).The results were as follows: (1) BNP levels in females were higher than those in males for healthy subjects (N = 551), in each age group from 20 to 60 years. (2) BNP levels increased with age. (3) There were significant correlations between BNP level and systolic blood pressure and creatinine level. (4) There were significant differences in BNP level between the hypertensive groups with and without hypertensive ECG changes and the age-matched healthy control group. (5) Marked correlations were observed between BNP level and left ventricular wall thickness, fractional shortening, deceleration time and peak early filling velocity. (6) A BNP cut-off-point of 25 pg/ml was best for detecting LV diastolic dysfunction and LV hypertrophy. Measurement of BNP is useful for detecting asymptomatic heart failure in the general population, and is a clinical marker useful in preventing symptomatic heart failure.

scholarly journals Moderate Loss of the Extracellular Matrix Proteoglycan Lumican Attenuates Cardiac Fibrosis in Mice Subjected to Pressure Overload

Cardiology ◽  
2020 ◽  
Vol 145 (3) ◽  
pp. 187-198 ◽  
Author(s):  
Naiyereh Mohammadzadeh ◽  
Arne Olav Melleby ◽  
Sheryl Palmero ◽  
Ivar Sjaastad ◽  
Shukti Chakravarti ◽  
...  
Keyword(s):  
Heart Failure ◽  
Extracellular Matrix ◽  
Diastolic Dysfunction ◽  
Cardiac Fibrosis ◽  
Pressure Overload ◽  
Left Ventricular ◽  
Cross Linking ◽  
Myocardial Remodeling ◽  
Functional Changes ◽  
Collagen Cross Linking

Introduction: The heart undergoes myocardial remodeling during progression to heart failure following pressure overload. Myocardial remodeling is associated with structural and functional changes in cardiac myocytes, fibroblasts, and the extracellular matrix (ECM) and is accompanied by inflammation. Cardiac fibrosis, the accumulation of ECM molecules including collagens and collagen cross-linking, contributes both to impaired systolic and diastolic function. Insufficient mechanistic insight into what regulates cardiac fibrosis during pathological conditions has hampered therapeutic so­lutions. Lumican (LUM) is an ECM-secreted proteoglycan known to regulate collagen fibrillogenesis. Its expression in the heart is increased in clinical and experimental heart failure. Furthermore, LUM is important for survival and cardiac remodeling following pressure overload. We have recently reported that total lack of LUM increased mortality and left ventricular dilatation, and reduced collagen expression and cross-linking in LUM knockout mice after aortic banding (AB). Here, we examined the effect of LUM on myocardial remodeling and function following pressure overload in a less extreme mouse model, where cardiac LUM level was reduced to 50% (i.e., moderate loss of LUM). Methods and Results: mRNA and protein levels of LUM were reduced to 50% in heterozygous LUM (LUM+/–) hearts compared to wild-type (WT) controls. LUM+/– mice were subjected to AB. There was no difference in survival between LUM+/– and WT mice post-AB. Echocardiography revealed no striking differences in cardiac geometry between LUM+/– and WT mice 2, 4, and 6 weeks post-AB, although markers of diastolic dysfunction indicated better function in LUM+/– mice. LUM+/– hearts revealed reduced cardiac fibrosis assessed by histology. In accordance, the expression of collagen I and III, the main fibrillar collagens in the heart, and other ECM molecules central to fibrosis, i.e. including periostin and fibronectin, was reduced in the hearts of LUM+/– compared to WT 6 weeks post-AB. We found no differences in collagen cross-linking between LUM+/– and WT mice post-AB, as assessed by histology and qPCR. Conclusions: Moderate lack of LUM attenuated cardiac fibrosis and improved diastolic dysfunction following pressure overload in mice, adding to the growing body of evidence suggesting that LUM is a central profibrotic molecule in the heart that could serve as a potential therapeutic target.

Abstract 14069: Subclinical Impairment of Left Ventricular Function in Stage A Subjects in a Community-based Population

Circulation ◽  
2015 ◽  
Vol 132 (suppl_3) ◽  
Author(s):  
Takuya Hasegawa ◽  
Masanori Asakura ◽  
Hideaki Kanzaki ◽  
Hiroshi Asanuma ◽  
Seiji Takashio ◽  
...  
Keyword(s):  
Risk Factors ◽  
Blood Pressure ◽  
Systolic Blood Pressure ◽  
Diastolic Dysfunction ◽  
Left Ventricular ◽  
Community Dwelling ◽  
Lv Function ◽  
Mitral Annular Velocity ◽  
Lv Mass ◽  
Lv Diastolic Dysfunction

Introduction: Stage A heart failure (HF) is defined as an asymptomatic state with HF risk factors of hypertension, diabetes, obesity, metabolic syndrome, and atherosclerotic disease in the absence of obvious left ventricular (LV) structural changes including LV hypertrophy (LVH). ACC/AHA guidelines recommend us to treat these risk factors of Stage A HF patients to prevent the progression of HF, hinting us to investigate the prevalence of subclinical impairment of LV function in Stage A subjects in general populations. Methods: We studied 1162 community-dwelling subjects without obvious heart diseases (mean age, 63±11 years; 448 men, 714 women, 63% with hypertension and 11% with diabetes) in the annual health checkup in a rural community, Arita-cho, Saga, Japan. The population was divided into 3 groups; the subjects without either LVH or the HF risk factors ("Stage 0"), the subjects with the HF risk factors in the absence of LVH (Stage A) , and the subjects in the presence of LVH (Stage B). LV systolic and diastolic function were estimated by mitral annular velocity in systole (s'), and the waves of transmitral flow (E) and mitral annular velocity (e'), respectively. LVH was defined as the top quintile of LV mass index. Results: The subjects in Stage A had the lower and higher values of s' and E/e', respectively, and the higher prevalence of LV diastolic dysfunction than those in Stage 0, while 45% of Stages A subjects showed LV diastolic dysfunction (Table). In multivariate logistic analyses, age, systolic blood pressure and LV mass were independent determinants of s', whereas either overlapped or different risk factors, such as age, sex, systolic blood pressure, and body mass index emerged as the determinants for E/e'. Conclusions: Even without obvious LV remodeling, subclinical LV systolic and diastolic impairment was observed in Stage A subjects. The disparity of the risk factors between LV systolic and diastolic dysfunction may indicate their pathophysiological differences.

scholarly journals Sleep Apnea and Diabetes Predict Progression of Cardiac Diastolic Dysfunction in Pre-heart Failure Patients: a Prospective Cohort HSCAA Study

2020 ◽  
Author(s):  
Yonekazu Kidawara ◽  
Manabu Kadoya ◽  
Akiko Morimoto ◽  
Takashi Daimon ◽  
Miki Kakutani-Hatayama ◽  
...  
Keyword(s):  
Heart Failure ◽  
Heart Disease ◽  
Sleep Apnea ◽  
Diastolic Dysfunction ◽  
Prospective Cohort ◽  
Regression Line ◽  
Left Ventricular ◽  
Apnea Hypopnea Index ◽  
Annual Change ◽  
Lv Diastolic Dysfunction

Abstract [Background] Sleep apnea, a common co-morbid condition of diabetes, has been shown to be associated with established heart failure. However, its role in association of the presence of diabetes in the progression of cardiac diastolic function in pre-heart failure phase is not known. This prospective study is to longitudinally examine the predictive value of sleep apnea and diabetes on progression of left ventricular (LV) diastolic dysfunction in patients without heart disease.[Methods] Among 976 patients registered in HSCAA prospective cohort study, 517 without heart disease (175 type 2 diabetes, 342 non-diabetes) were followed with repeated echocardiography in every 1-3 years for a mean 34.7 months. LV diastolic dysfunction was determined by transmitral early inflow velocity/early diastolic tissue velocity (E/e´) >14. Annual change in E/e’ was calculated by using the slope of the linear regression line calculated from at least 3 echocardiographic measurements. Sleep apnea was determined by an apnomonitor device in conjunction with percutaneous oxygen saturation, and apnea hypopnea index (AHI) was calculated.[Results] Kaplan-Meier analyses revealed that subjects with diabetes or sleep apnea had a significantly (p<0.01) greater risk for LV diastolic dysfunction, with hazards ratio of 2.21 (1.41-3.47) and 2.23 (1.40-3.55), respectively. Subjects with sleep apnea exhibited significantly higher risk for LV diastolic dysfunction in non-diabetic subjects (p<0.01), while showed tendency of higher risk in diabetic subjects (p=0.10). The annual change of E/e’ was significantly and independently associated with both diabetes (β=0.278, p<0.01) and AHI (β=0.138, p<0.01). Finally, ROC analyses revealed that addition of AHI and diabetes to classical risk factors best predicted individuals with fast progression of diastolic dysfunction (annual change of E/e’ >1.0) with an AUC of 0.81.[Conclusions] In patients without heart disease, sleep apnea is an important predictor for progression of LV diastolic dysfunction. Its association is partly confounded, but still independent of the presence of diabetes.

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