Abstract 96: Thioredoxin-1 Is Essential for Hydrogen Sulfide-Mediated Cardioprotection in the Setting of Ischemic-Induced Heart Failure

2012 ◽  
Vol 111 (suppl_1) ◽  
Author(s):  
Chad K Nicholson ◽  
Bridgette F Moody ◽  
Rebecca L Hood ◽  
Junichi Sadoshima ◽  
John W Calvert
Keyword(s):  
Heart Failure ◽  
Hydrogen Sulfide ◽  
Left Ventricular ◽  
Dominant Negative ◽  
Left Ventricular Ejection ◽  
Protective Effects ◽  
Ventricular Ejection Fraction ◽  
Left Ventricular Dimensions ◽  
Thioredoxin 1 ◽  
And Function

Background: Numerous studies have reported the cytoprotective effects of hydrogen sulfide (H2S) in various models of myocardial injury. Here we examined the role that thioredoxin-1 (Trx1) plays in mediating the protective effects of H2S in a model of heart failure. Methods and Results: Mice were subjected to 60 min of left coronary artery ischemia followed by 4 wks of reperfusion (R) at which time left ventricular dimensions and function were assessed. Mice received saline (Veh) or H2S in the form of sodium sulfide (Na2S, 100 μ g/kg) at the time of R followed by daily i.v. injections for the first 7 days of R. Mice treated with Na2S experienced less left ventricular dilatation and hypertrophy, displayed improved left ventricular ejection fraction, and displayed improved contractility and relaxation when compared to Veh-treated mice. Studies aimed at evaluating the underlying cardioprotective mechanisms found that Na2S treatment increased the expression of Trx1. Further analysis revealed that this was accompanied by an increase in phosphorylation of apoptosis signaling kinase-1 (ASK1) at serine residue 966 (inhibitory site), as well as a decrease in the phosphorylation of JNK and p38 (downstream targets of ASK1). We also found that Na2S treatment did not improve cardiac dilatation, cardiac dysfunction, or cardiac hypertrophy in cardiac specific Trx1 dominant negative transgenic (Trx1 dnTg) mice when compared to Veh-treated mice. Conclusion: These findings provide important information that the upregulation of cardiac Trx1 by H2S in the setting of ischemic-induced heart failure sets into motion events, including ASK1 inhibition, which ultimately leads to cardioprotection.

Abstract 17994: Echocardiographic parameters of Left Ventricular Size and Function as Predictors of Symptomatic Heart Failure in Patients with Low Normal Ejection Fraction Treated with Anthracyclines

Circulation ◽  
2014 ◽  
Vol 130 (suppl_2) ◽  
Author(s):  
Negareh Mousavi ◽  
Timothy Tan ◽  
Mohammad Ali ◽  
Elkan F. Halpern ◽  
Lin Wang ◽  
...  
Keyword(s):  
Heart Failure ◽  
Ejection Fraction ◽  
Longitudinal Strain ◽  
Global Longitudinal Strain ◽  
Left Ventricular ◽  
Left Ventricular Ejection ◽  
Ventricular Ejection Fraction ◽  
Symptomatic Heart Failure ◽  
Echocardiographic Parameters ◽  
And Function

Objectives: The aim of this study was to assess whether baseline echocardiographic measures of left ventricular (LV) size and function predict the development of symptomatic heart failure or cardiac death (major adverse cardiac events, MACE) in patients treated with anthracyclines who have a pre-chemotherapy left ventricular ejection fraction (LVEF) in the low normal range (between 50-59%). Background: Anthracycline-induced symptomatic heart failure and impaired LVEF are late and often irreversible manifestations of anthracycline-induced cardiotoxicity. The value of echocardiographic parameters of myocardial size and function before chemotherapy to identify patients at high-risk for development of symptomatic heart failure in patients with low normal LVEF was studied. Methods: Patients with a LVEF between 50 and 59% before anthracyclines were selected. In these patients, LV volumes, LVEF and peak longitudinal strain (GLS) were measured. Individuals were followed for MACE and all-cause mortality over a median of 659 days (range; 3-3704 days). Results: Of 2234 patients undergoing echocardiography for pre-anthracycline assessment, 158 (7%) had a resting ejection fraction of 50-59%. Their average LV end-diastolic volume (LVEDV) was 101±22ml, LVEF was 54 ±3% and global longitudinal strain (GLS) was -17.7±2.6%. Twelve patients experienced a MACE (congestive heart failure) at a median of 173 days (range; 15-530). Age, diabetes, previous coronary artery disease, LVEDV, LVESV and GLS were all-predictive of MACE (P= 0.015, 0.0043 and 0.0065 for LVEDV, LVESV, and GLS respectively). LVEDV and GLS remained predictive of MACE when adjusted for age. Age and GLS were also predictive of overall mortality (p<0.0001 and 0.0105 respectively). Conclusions: In patients treated with anthracyclines with an LVEF of 50-59%, both baseline EDV and GLS predict the occurrence of MACE. These parameters may help target patients who could bene[[Unable to Display Character: &#64257;]]t from closer cardiac surveillance and earlier initiation of cardioprotective medical therapy.

scholarly journals Positive Effects of Perindopril on Microvascular Vessels in Patients With Chronic Heart Failure

Kardiologiia ◽  
2020 ◽  
Vol 60 (8) ◽  
pp. 65-70
Author(s):  
J. I. Safonova ◽  
M. V. Kozhevnikova ◽  
Yu. A. Danilogorskaya ◽  
E. A. Zheleznykh ◽  
V. Y. Zektser ◽  
...  
Keyword(s):  
Heart Failure ◽  
Chronic Heart Failure ◽  
Endothelial Function ◽  
Reactive Hyperemia ◽  
Left Ventricular ◽  
Structure And Function ◽  
Left Ventricular Ejection ◽  
Ventricular Ejection Fraction ◽  
Positive Effects ◽  
And Function

Aim      To evaluate the effect of 12-month perindopril treatment on structure and function of microvasculature (MV) in patients with chronic heart failure with preserved (HFpEF) and intermediate (HFiEF) left ventricular ejection fraction.Material and methods  30 patients with HFpEF and HFiEF were evaluated. Perindopril at a maximum tolerated dose was administered to all patients for 12 months. Changes in MV structure and function were assessed with photoplethysmography and capillaroscopy prior to the treatment onset and at 12 months, i.e., after completion of the perindopril treatment.Results The 12-month perindopril treatment was associated with improvement of the endothelial function evident as increases in the occlusion index (OI) and the phase shift (PS). OI increased from 1.45 [1.3; 1.6] to 1.8 [1.6; 2.2] (p=0.00004). PS increased from 7.1 ms [4.8; 10.2] to 9.2 ms [6.7; 13.2] (p=0.0003). Stiffness of muscular large blood vessels was decreased. Arterial stiffness index (aSI) decreased from 8.8 [6.6; 11.0] to 7.45 [6.5; 9.4] m /s (р=0.01). The perindopril treatment was associated with increased density of the capillary network at rest (р=0.008) and in tests with venous occlusion (р=0.003) and reactive hyperemia (р=0.0003).Conclusion      The study showed an improvement of endothelial function associated with the 12-month perindopril therapy in patients with HFpEF and HFiEF.  

scholarly journals Determinants of exercise intolerance symptoms considered non-specific for heart failure in patients with stage A and B: role of the left atrium in the transition phase to overt heart failure

2021 ◽  
Author(s):  
Caterina Maffeis ◽  
Riccardo M. Inciardi ◽  
Muhammad Shahzeb Khan ◽  
Elvin Tafciu ◽  
Corinna Bergamini ◽  
...  
Keyword(s):  
Heart Failure ◽  
Roc Curves ◽  
Left Ventricular ◽  
Structure And Function ◽  
Exercise Intolerance ◽  
Left Ventricular Ejection ◽  
Ventricular Ejection Fraction ◽  
Incremental Value ◽  
Adjusted Logistic Regression ◽  
And Function

AbstractTo assess to what extent left atrial (LA) structure and function are associated with non-specific heart failure symptoms, so that patients were classified as HF stage A and B. Mechanisms underlying the transition to overt HF in patients with stage A and B HF are unclear. Consecutive outpatients undergoing echocardiography and clinical evaluation and classified as HF stage A and B with preserved left ventricular ejection fraction (LVEF) were included. The association between LA measures [volume (LAVi), peak longitudinal-(PALS), contraction-(PACS) and conduit-strain] and non-specific HF symptoms was assessed using adjusted logistic regression analyses. The incremental value of atrial myopathy in symptoms prediction on top of clinical or echocardiographic confounders was assessed through ROC curves analyses. The cohort comprehended 185 patients (63 ± 16 years, 47% women) of whom 133 (72%) were asymptomatic, and 52 (28%) reported non-specific HF symptoms. After adjustment for clinical and echocardiographic confounders for HF symptoms, LAVi, PALS and PACS were associated with symptoms (p < 0.05). Among echocardiographic variables, only LA parameters were significantly associated with symptoms on top of clinical confounders (for LAVi OR [95% CI] 1.56 [1.21–2.00], p < 0.0001; for PALS 1.45 (1.10–1.91), p = 0.0009; for PACS 2.10 [1.33–3.30], p = 0.002). After adjustment for age, hypertension and COPD or E/E′, LV mass-i and mitral ERO, atrial myopathy added predictive value for symptoms presence compared to the clinical variables or echocardiographic parameters described (AUC increase 0.80 to 0.88, p = 0.004, and 0.79 to 0.84, p = 0.06, respectively). In patients with HF stages A–B and preserved LVEF, measures of LA structure and function were associated with non-specific HF symptoms. A comprehensive LA remodeling evaluation may help clinicians in the appropriate identification of overt HF.

Efficacy of Vitamin D on Chronic Heart Failure Among Adults

2020 ◽  
Vol 90 (1-2) ◽  
pp. 49-58 ◽  
Author(s):  
Wang Chunbin ◽  
Wang Han ◽  
Cai Lin
Keyword(s):  
Heart Failure ◽  
Vitamin D ◽  
Chronic Heart Failure ◽  
Left Ventricular Ejection Fraction ◽  
Confidence Interval ◽  
Left Ventricular ◽  
Left Ventricular Ejection ◽  
Controlled Trials ◽  
Ventricular Ejection Fraction ◽  
Randomized Controlled

Abstract. Vitamin D deficiency commonly occurs in chronic heart failure. Whether additional vitamin D supplementation can be beneficial to adults with chronic heart failure remains unclear. We conducted a meta-analysis to derive a more precise estimation. PubMed, Embase, and Cochrane databases were searched on September 8, 2016. Seven randomized controlled trials that investigated the effects of vitamin D on cardiovascular outcomes in adults with chronic heart failure, and comprised 592 patients, were included in the analysis. Compared to placebo, vitamin D, at doses ranging from 2,000 IU/day to 50,000 IU/week, could not improve left ventricular ejection fraction (Weighted mean difference, WMD = 3.31, 95% confidence interval, CL = −0.93 to 7.55, P < 0.001, I2 = 92.1%); it also exerts no beneficial effects on the 6 minute walk distance (WMD = 18.84, 95% CL = −24.85 to 62.52, P = 0.276, I2 = 22.4%) and natriuretic peptide (Standardized mean difference, SMD = −0.39, 95% confidence interval CL = −0.48 to 0.69, P < 0.001, I2 = 92.4%). However, a dose-response analysis from two studies demonstrated an improved left ventricular ejection fraction with vitamin D at a dose of 4,000 IU/day (WMD = 6.58, 95% confidence interval CL = −4.04 to 9.13, P = 0.134, I2 = 55.4%). The results showed that high dose vitamin D treatment could potentially benefit adults with chronic heart failure, but more randomized controlled trials are required to confirm this result.

Emerging Cardiac Resynchronisation Therapy Indications

2011 ◽  
Vol 7 (1) ◽  
pp. 29
Author(s):  
Charlotte Eitel ◽  
Gerhard Hindricks ◽  
Christopher Piorkowski ◽  
◽  
◽  
...  
Keyword(s):  
Heart Failure ◽  
Systolic Heart Failure ◽  
Cardiac Resynchronisation Therapy ◽  
Left Ventricular ◽  
Left Ventricular Ejection ◽  
Current Evidence ◽  
Class Iii ◽  
Ventricular Ejection Fraction ◽  
Cardiac Resynchronisation ◽  
Resynchronisation Therapy

Cardiac resynchronisation therapy (CRT) is an efficacious and cost-effective therapy in patients with highly symptomatic systolic heart failure and delayed ventricular conduction. Current guidelines recommend CRT as a class I indication for patients with sinus rhythm, New York Heart Association (NYHA) functional class III or ambulatory class IV, a QRS duration ≥120ms, and left ventricular ejection fraction (LVEF) ≤35%, despite optimal pharmacological therapy. Recent trials resulted in an extension of current recommendations to patients with mild heart failure, patients with atrial fibrillation, and patients with an indication for permanent right ventricular pacing with the aim of morbidity reduction. The effectiveness of CRT in patients with narrow QRS, patients with end-stage heart failure and cardiogenic shock, and patients with an LVEF >35% still needs to be proved. This article reviews current evidence and clinical applications of CRT in heart failure and provides an outlook on future developments.

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.

A translational model of chronic heart failure in rats

2018 ◽  
pp. 136-148
Author(s):  
С.А. Крыжановский ◽  
И.Б. Цорин ◽  
Е.О. Ионова ◽  
В.Н. Столярук ◽  
М.Б. Вититнова ◽  
...  
Keyword(s):  
Myocardial Infarction ◽  
Heart Failure ◽  
Chronic Heart Failure ◽  
Left Ventricular ◽  
Compensatory Hypertrophy ◽  
Experimental Myocardial Infarction ◽  
Left Ventricular Ejection ◽  
Translational Model ◽  
Innovative Drug ◽  
Ventricular Ejection Fraction

Цель исследования - разработка трансляционной модели хронической сердечной недостаточности (ХСН) у крыс, позволяющей, с одной стороны, изучить тонкие механизмы, лежащие в основе данной патологии, а с другой стороны, выявить новые биомишени для поиска и изучения механизма действия инновационных лекарственных средств. Методика. Использован комплекс эхокардиографических, морфологических, биохимических и молекулярно-биологических исследований, позволяющий оценивать и дифференцировать этапы формирования ХСН. Результаты. Динамические эхокардиографические исследования показали, что ХСН формируется через 90 дней после воспроизведения переднего трансмурального инфаркта миокарда. К этому времени у животных основной группы отмечается статистически значимое по сравнению со 2-ми сут. после воспроизведения экспериментального инфаркта миокарда снижение ФВ левого желудочка сердца (соответственно 55,9 ± 1,4 и 63,9 ± 1,6%, р = 0,0008). Снижение насосной функции сердца (на 13% по сравнению со 2-ми сут. после операции и на ~40% по сравнению с интактными животными) сопровождается увеличением КСР и КДР (соответственно с 2,49 ± 0,08 до 3,91 ± 0,17 мм, р = 0,0002, и с 3,56 ± 0,11 до 5,20 ± 0,19 мм, р = 0,0001), то есть к этому сроку развивается сердечная недостаточность. Результаты эхокардиографических исследований подтверждены данными морфометрии миокарда, продемонстрировавшими дилатацию правого и левого желудочков сердца. Параллельно проведенные гистологические исследования свидетельствуют о наличии патогномоничных для данной патологии изменений миокарда (постинфарктный кардиосклероз, компенсаторная гипертрофия кардиомиоцитов, очаги исчезновения поперечной исчерченности мышечных волокон и т.д.) и признаков венозного застоя в легких и печени. Биохимические исследования выявили значимое увеличение концентрации в плазме крови биохимического маркера ХСН - мозгового натрийуретического пептида. Данные молекулярно-биологических исследований позволяют говорить о наличии гиперактивности ренин-ангиотензин-альдостероновой и симпатоадреналовой систем, играющих ключевую роль в патогенезе ХСН. Заключение. Разработана трансляционная модель ХСН у крыс, воспроизводящая основные клинико-диагностические критерии этого заболевания. Показано наличие корреляции между морфометрическими, гистологическими, биохимическими и молекулярными маркерами прогрессирующей ХСН и эхокардиографическими диагностическими признаками, что позволяет использовать неинвазивный метод эхокардиографии, характеризующий состояние внутрисердечной гемодинамики, в качестве основного критерия оценки наличия/отсутствия данной патологии. Aim. Development of a translational model for chronic heart failure (CHF) in rats to identify new biotargets for finding and studying mechanisms of innovative drug effect in this disease. Methods. A set of echocardiographic, morphological, biochemical, and molecular methods was used to evaluate and differentiate stages of CHF development. Results. Dynamic echocardiographic studies showed that CHF developed in 90 days after anterior transmural myocardial infarction. By that time, left ventricular ejection fraction was significantly decreased in animals of the main group compared with rats studied on day 2 after experimental myocardial infarction (55.9 ± 1.4% vs . 63.9 ± 1.6%, respectively, p<0.0008). The decrease in heart’s pumping function (by 13% compared with day 2 after infarction and by approximately 40% compared to intact animals) was associated with increased ESD and EDD (from 2.49 ± 0.08 to 3.91 ± 0.17 mm, p = 0.0002, and from 3.56 ± 0.11 to 5.20 ± 0.19 mm, respectively, p = 0.0001); therefore, heart failure developed by that time. The results of echocardiographic studies were confirmed by myocardial morphometry, which demonstrated dilatation of both right and left ventricles. Paralleled histological studies indicated presence of the changes pathognomonic for this myocardial pathology (postinfarction cardiosclerosis, compensatory hypertrophy of cardiomyocytes, foci of disappeared transverse striation of muscle fibers, etc.) and signs of venous congestion in lungs and liver. Biochemical studies demonstrated a significant increase in plasma concentration of brain natriuretic peptide, a biochemical marker of CHF. Results of molecular studies suggested hyperactivity of the renin-angiotensin-aldosterone and sympathoadrenal systems, which play a key role in the pathogenesis of CHF. Conclusions. A translational model of CHF in rats was developed, which reproduced major clinical and diagnostic criteria for this disease. Morphometric, histological, biochemical, and molecular markers for progressive CHF were correlated with echocardiographic diagnostic signs, which allows using this echocardiographic, noninvasive method characterizing the intracardiac hemodynamics as a major criterion for the presence / absence of this pathology.

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