scholarly journals Heart functional and structural compendium of cardiosplenic and cardiorenal networks in acute and chronic heart failure pathology

2018 ◽  
Vol 314 (2) ◽  
pp. H255-H267 ◽  
Author(s):  
Ganesh V. Halade ◽  
Vasundhara Kain ◽  
Kevin. A. Ingle
Keyword(s):  
Heart Failure ◽  
Chronic Heart Failure ◽  
Temporal Dynamics ◽  
Inflammatory Responses ◽  
Function Analysis ◽  
Left Ventricular ◽  
Integrative Approach ◽  
Lv Function ◽  
Renal Histology ◽  
Pathological Remodeling

Heart failure (HF) secondary to myocardial infarction (MI) is linked to kidney complications that comprise cellular, structural, functional, and survival indicators. However, HF research is focused on left ventricular (LV) pathology. Here, we determined comprehensive functional analysis of the LV using echocardiography in transition from acute heart failure (AHF) to progressive chronic heart failure (CHF) pathology and developed a histological compendium of the cardiosplenic and cardiorenal networks in pathological remodeling. In surgically induced MI using permanent coronary ligation, the LV dysfunction is pronounced, with myocardium necrosis, wall thinning, and 20–30% LV rupture events that indicated AHF and CHF pathological remodeling in C57BL/6 male mice (2–4 mo old, n = 50). Temporal LV function analysis indicated that fractional shortening and strain are reduced from day 1 to day 5 in AHF and sustained to advance to CHF from day 28 to day 56 compared with naïve control mice ( n = 6). During the transition of AHF ( day 1 to day 5) to advanced CHF ( day 28 to day 56), histological and cellular changes in the spleen were definite, with bimodal inflammatory responses in kidney inflammatory biomarkers. Likewise, there was a unidirectional, progressive, and irreversible deposition of compact collagen in the LV along with dynamic changes in the cardiosplenic and cardiorenal networks post-MI. The renal histology and injury markers suggested that cardiac injury triggers irreversible dysregulation that actively alters the cardiosplenic and cardiorenal networks. In summary, the novel strategies or pathways that modulate comprehensive cardiosplenic and cardiorenal networks in AHF and CHF would be effective approaches to study either cardiac repair or cardiac pathology. NEW & NOTEWORTHY The present compendium shows irreversible ventricular dysfunction as assessed by temporal echocardiography while histological and structural measurements of the spleen and kidney added a novel direction to study cardiosplenic and cardiorenal networks in heart failure pathology. Therefore, the consideration of systems biology and integrative approach is essential to develop novel treatments. Listen to this article's corresponding podcast at http://ajpheart.podbean.com/e/temporal-dynamics-of-acute-and-chronic-heart-failure/ .

scholarly journals Uric Acid, Oxidative Stress and Inflammation in Chronic Heart Failure with Reduced Ejection Fraction

2015 ◽  
Vol 23 (4) ◽  
pp. 397-406 ◽  
Author(s):  
Adriana Iliesiu ◽  
Alexandru Campeanu ◽  
Daciana Marta ◽  
Irina Parvu ◽  
Gabriela Gheorghe
Keyword(s):  
Oxidative Stress ◽  
Heart Failure ◽  
Uric Acid ◽  
Chronic Heart Failure ◽  
Ejection Fraction ◽  
Xanthine Oxidase ◽  
Left Ventricular ◽  
Paraoxonase 1 ◽  
Lv Function ◽  
The Relationship

Abstract Background. Oxidative stress (OS) and inflammation are major mechanisms involved in the progression of chronic heart failure (CHF). Serum uric acid (sUA) is related to CHF severity and could represent a marker of xanthine-oxidase activation. The relationship between sUA, oxidative stress (OS) and inflammation markers was assessed in patients with moderate-severe CHF and reduced left ventricular (LV) ejection fraction (EF). Methods. In 57 patients with stable CHF, functional NYHA class III, with EF<40%, the LV function was assessed by N-terminal of the prohormone brain natriuretic peptide (NT-proBNP) levels and echocardiographically through the EF and E/e’ ratio, a marker of LV filling pressures. The relationship between LV function, sUA, malondialdehyde (MDA), myeloperoxidase (MPO), paraoxonase 1 (PON-1) as OS markers and high sensitivity C-reactive protein (hsCRP) and interleukin 6 (IL-6) as markers of systemic inflammation was evaluated. Results. The mean sUA level was 7.9 ± 2.2 mg/dl, and 61% of the CHF patients had hyperuricemia. CHF patients with elevated LV filling pressures (E/e’ ≥ 13) had higher sUA (8.6 ± 2.3 vs. 7.3 ± 1.4, p=0.08) and NT-proBNP levels (643±430 vs. 2531±709, p=0.003) and lower EF (29.8 ± 3.9 % vs. 36.3 ± 4.4 %, p=0.001). There was a significant correlation between sUA and IL-6 (r = 0.56, p<0.001), MDA (r= 0.49, p= 0.001), MPO (r=0.34, p=0.001) and PON-1 levels (r= −0.39, p= 0.003). Conclusion. In CHF, hyperuricemia is associated with disease severity. High sUA levels in CHF with normal renal function may reflect increased xanthine-oxidase activity linked with chronic inflammatory response.

Abstract 3791: Improved Ventricular-Arterial Coupling After 4 Weeks of Exercise Training in Patients with Chronic Heart Failure

Circulation ◽  
2007 ◽  
Vol 116 (suppl_16) ◽  
Author(s):  
Marcus Sandri ◽  
Stephan Gielen ◽  
Norman Mangner ◽  
Volker Adams ◽  
Sandra Erbs ◽  
...  
Keyword(s):  
Heart Failure ◽  
Chronic Heart Failure ◽  
Exercise Training ◽  
Endothelial Function ◽  
Training Group ◽  
Left Ventricular ◽  
Left Ventricular Ejection ◽  
Control Group ◽  
Lv Function ◽  
Ventricular Ejection Fraction

Background: The concept of ventricular-arterial coupling implies that LV-function is determined by the three factors left ventricular diastolic, left ventricular systolic and arterial elastance. We have previously documented an improvement in endothelial function and systolic LV-function in patients with chronic heart failure (CHF) after 6 months of exercise training (ET). It remains, however, unclear, how shorter ET periods may affect endothelial, systolic and diastolic ventricular function as echocardiographic parameters related to ventricular arterial coupling in patients with CHF. METHODS: In this ongoing study we randomised 43 patients with stable CHF (age 60.3 ± 2.9 years, EF 27.4 ± 1.7%, VO 2 max 14.7 ± 4.3ml/kg*min) to a training or a control group (C). Patients in the training group exercised 4 times daily at 70% of the individual heart rate reserve for 4 weeks under supervision. At baseline and after 4 weeks the E/A ratio and septal/lateral E’/A’ velocities were determined by echocardiography with tissue Doppler. Exercise capacity was measured by ergospirometry and flow-mediated dilatation (FMD) was assessed by high-resolution radial ultrasound. RESULTS: After only 4 weeks of ET oxygen uptake at peak exercise increased from 14.9 ± 3.3 to 18.1 ± 4.7 ml/min/kg, (p<0.01 vs. C) in training subjects. Left ventricular ejection fraction improved from 26.8 ± 4.6 to 33.1 ± 5.5% (p<0.05 vs. C) in patients of the training group while it remained unchanged in the control group. E/A-ratio mended from 0.63 ± 0.12 to 0.81 ± 0.22 (p<0.01 vs. C) in training patients. Septal E’ velocities increased from 5.5 ± 0.5 to 7.8 ± 1.4 cm/s in training patients (p<0.05 vs. C). FMD of the radial artery improved from 8.2 ± 2.1 to 15.2 ± 3.8% (p<0.01 vs. C) as a result of ET. CONCLUSIONS: Only 4 weeks of endurance training are highly effective with significantly improved FMD accompanied by an emended systolic and diastolic LV-function. We hypothesise that the improvement in LV-EF in training patients may be caused by a corrected ventricular-arterial coupling: ventricular diastolic relaxation and effective endothelial function are ameliorated resulting in an augmentation of stroke volume.

Abstract 3295: De-induction of the Maladaptive Fetal Gene Program During Chronic Monotherapy with Metoprolol Succinate is Retained Following Withdrawal of Therapy in Dogs with Chronic Heart Failure

Circulation ◽  
2007 ◽  
Vol 116 (suppl_16) ◽  
Author(s):  
Rasha Bazari ◽  
Sharad Rastogi ◽  
Valerio Zaca ◽  
Sidney Goldstein ◽  
Hani N Sabbah
Keyword(s):  
Heart Failure ◽  
Chronic Heart Failure ◽  
Mrna Expression ◽  
Natriuretic Peptide ◽  
Left Ventricular ◽  
Lv Function ◽  
Metoprolol Succinate ◽  
Myosin Heavy Chain Isoform ◽  
Chronic Therapy ◽  
Lv Remodeling

Background: Chronic therapy with extended release metoprolol succinate (MET), a selective β1 adrenergic receptor blocker, improves left ventricular (LV) function and attenuates global LV remodeling in dogs with chronic heart failure (HF). We previously showed that chronic therapy with β-blockade results in de-induction of the fetal gene program (FGP) in LV myocardium of dogs with HF. In this study, we tested the hypothesis that in dogs with HF withdrawal of chronic MET does not lead to re-induction of FGP. Methods: Studies were performed in 17 intracoronary microembolization-induced HF dogs randomized to 3 months oral therapy with MET (100 mg, once daily, n=11) or no therapy at all (Controls, n=6). In dogs randomized to MET, 6 were sacrificed after 3 months of therapy and in the remaining 5, MET was withdrawn after 3 months of therapy and dogs were observed for 6 weeks after withdrawal of MET (MET-W) and then sacrificed. LV tissue was also obtained from 6 normal (NL) dogs for comparison. mRNA expression of the FGP genes namely, atrial natriuretic peptide (ANP), brain natriuretic peptide (BNP), sarcoplasmic reticulum calcium ATPase (CAA), cardiac β-1 adren-ergic receptor (AR) and α-myosin heavy chain isoform (α-MHC) was measured using reverse transcriptase polymerase chain reaction (RT-PCR) and bands were quantified in densitometric units (du). Results: In Controls, mRNA expression of ANP and BNP increased and expression of CAA, β 1-AR and α-MHC decreased. Treatment with MET decreased expression of ANP and BNP and increased expression of CAA, β 1-AR and α-MHC. Except for α-MHC, the improvement in FGP seen during MET treatment was preserved in MET-W dogs. Conclusions: Withdrawal of MET is associated with sustained de-induction of the FGP in LV myocardium of dogs with HF. This observation supports the concept that chronic β-blockade therapy in HF confers lasting reversal of LV remodeling and molecular recovery of the failing myocardium.

scholarly journals Clinical efficacy of various forms of continuing education of patients with chronic heart failure

2013 ◽  
Vol 4 (1) ◽  
pp. 55-62
Author(s):  
G. P Arutyunov ◽  
A. V Evzerikhina ◽  
A. K Rylova ◽  
V. I Lobzeva
Keyword(s):  
Heart Failure ◽  
Chronic Heart Failure ◽  
Performance Test ◽  
Hospital Admissions ◽  
Clinical Status ◽  
Developed Countries ◽  
Left Ventricular ◽  
Structured Learning ◽  
Lv Function ◽  
Minute Walk

Data from numerous epidemiological studies indicate that in many developed countries, heart failure is one of the most common, progressive and predictive of adverse complications of diseases of the cardiovascular system. At the moment, that is a rather acute problem of cardiac rehabilitation of such patients. The purpose of our study was to investigate the effect of various forms of structured learning in special schools for CHF patients on the clinical course and prognosis. Materials and Methods: This study consisted of two phases, including 158 patients with chronic heart failure II–III FC. Evaluated the survival of the knowledge, clinical status, distance of a 6-minute walk, Minnesota QoL questionnaire, adherence to therapy, the frequency of hospital admissions for heart failure decompensation, referral to the clinic, the frequency of deaths, the level of CRP, LV function the results of echocardiography. The results: the use of interactive learning will significantly improve patient compliance to treatment (D=5%), which in turn significantly improved the clinical condition of patients, quality of life, performance test, 6-minute walk, and left ventricular function, as well as reduced the number of hospitalizations with circulatory decompensation (1,6-times), and uptake to the clinic (up to 0,5 times a month). Thus, the use of interactive patient education is an integral part of the cardiorehabilitation events in patients with CHF.

Abstract 23: Immunosuppression with FTY720 Reverses Cardiac Dysfunction to Prevent Chronic Heart Failure in Mice that Survive Diet-induced Myocardial Infarction

2015 ◽  
Vol 35 (suppl_1) ◽  
Author(s):  
Fu Sang Luk ◽  
Roy Y Kim ◽  
Kang Li ◽  
Daniel Ching ◽  
Sunil Joshi ◽  
...  
Keyword(s):  
Myocardial Infarction ◽  
Heart Failure ◽  
Chronic Heart Failure ◽  
Cardiac Dysfunction ◽  
Coronary Atherosclerosis ◽  
Left Ventricular ◽  
Lv Function ◽  
Chow Diet ◽  
Type I ◽  
Gene Repair

We recently reported that immunosuppression with FTY720 improves cardiac function and extends longevity in the HypoE/SR-BI-/- mouse model of diet-induced coronary atherosclerosis and myocardial infarction (MI). In this study we tested whether FTY720 could also reverse cardiac dysfunction in mice that survive MI and subsequently develop chronic heart failure (CHF). HypoE/SR-BI-/- mice were bred to Mx1-Cre mice and offspring were fed a high fat diet (HFD) for 21 days to provoke hyperlipidemia, coronary atherosclerosis and recurrent MIs. HypoE/SR-BI-/-Mx1-Cre mice were subsequently given oral FTY720 in drinking water or not. Hyperlipidemia was permanently reversed by inducible Cre-mediated gene repair of the HypoE allele (also known as the Apoeh/h allele) that rapidly restores normal apoE expression in all tissues and by switching mice to a normal chow diet. In cohorts of mice that survived this period of HFD, left ventricular (LV) function was monitored using serial echocardiography for up to 15 weeks. In untreated mice, LV performance progressively deteriorated. Although FTY720 treatment did not initially prevent a decline of heart function among HypoE/SR-BI-/-Mx1-Cre mice six weeks after Cre-mediated gene repair, it almost completely restored normal LV function in these mice by 15 weeks after cessation of HFD. Reversal of heart failure did not result from reduced atherosclerosis as the burden of both aortic and coronary atherosclerosis increased to similar levels in both groups of mice. Rather, FTY720 caused systemic immunosuppression as assessed by reduced numbers of circulating T and B lymphocytes. In the heart, FTY720 led to reduced expression of MMP-2 along with the expression of genes involved in Type I innate inflammation that we have recently demonstrated as major contributors to heart failure. Our data demonstrate the benefit of immunosuppression with FTY720 post MI to prevent progressive pathological remodeling of the heart, which leads to CHF.

Abstract 17383: Total Left Ventricular Unloading with Impella® during Ischemia Reperfusion Minimizes Infarct Size, Preserves Left Ventricular Function and Prevents Chronic Heart Failure

Circulation ◽  
2014 ◽  
Vol 130 (suppl_2) ◽  
Author(s):  
Takamoro Kakaino ◽  
Keita Saku ◽  
Takahiro Arimura ◽  
Takuya Akashi ◽  
Akiko Nishizaki ◽  
...  
Keyword(s):  
Heart Failure ◽  
Chronic Heart Failure ◽  
Ischemia Reperfusion ◽  
Oxygen Demand ◽  
Chronic Phase ◽  
Left Ventricular ◽  
Lv Function ◽  
Ventricular Assist ◽  
Left Ventricular Assist ◽  
Acute Mi

Background: Despite marked advances of revascularization, acute myocardial infarction (MI) remains a major cause of chronic heart failure (CHF). Since excessive oxygen demand relative to supply is the fundamental mechanism of ischemia, we previously demonstrated, using a conventional left ventricular assist device (VAD), that total left ventricular (LV) unloading markedly reduced the MI size in ischemia reperfusion (IR) model through minimizing the myocardial oxygen consumption in acute experiment. The purpose of this investigation was to examine if the transvascular VAD, Impella®, could totally unload LV during IR and preserve LV function in chronic phase. Methods: We allocated 15 dogs into 3 groups, Sham (n=4), IR (n=6) and IR+Impella® (n=5). In IR and IR+Impella®, we ligated the left anterior descending artery for 180min through a left thoracotomy and then reperfused. In IR+Impella®, we introduced Impella® through the left subclavian artery from 60 min after the beginning of ischemia to 90 min after reperfusion. We then assessed LV function and MI size 4 weeks after IR injury. Results: Under Impella® support, LV pressure was much lower than arterial pressure indicating total LV unloading. In comparison with IR, Impella® significantly improved LV ejection fraction (2D-echo, Fig) (Sham 64±2.8, IR 48±3.1, IR+Impella® 64±1.2%, p=0.0007), lowered LVEDP (Sham 5.9±1.1, IR 16±3.7, IR+Impella® 4.3±0.87mmHg, p<0.05) and increased end-systolic elastance (sonomicrometric volumetry) (Sham 11±3.1, IR 5.7±1.5, IR+Impella® 12±1.6 mmHg/ml, p<0.05). Furthermore, Impella markedly reduced MI size (%LV circumferential area, IR 18±9.2, IR+Impella® 2.1±0.76%, p=0.0044, Fig) and decreased NT-proBNP (Sham 1004±462, IR 3385±677, IR+Impella® 1463±217pg/ml). Conclusions: Total LV unloading during IR with Impella® strikingly reduces MI size and preserves LV function in chronic phase. Impella® is a powerful tool in the management of acute MI in preventing CHF.

Beneficial effects of delayed ivabradine treatment on cardiac anatomical and electrical remodeling in rat severe chronic heart failure

2009 ◽  
Vol 296 (2) ◽  
pp. H435-H441 ◽  
Author(s):  
Paul Milliez ◽  
Smail Messaoudi ◽  
Johnny Nehme ◽  
Camille Rodriguez ◽  
Jane-Lise Samuel ◽  
...  
Keyword(s):  
Heart Failure ◽  
Chronic Heart Failure ◽  
Ejection Fraction ◽  
Diastolic Pressure ◽  
Interstitial Fibrosis ◽  
Left Ventricular ◽  
Lv Function ◽  
Electrical Remodeling ◽  
Beneficial Effects ◽  
Protein Expressions

We tested the hypothesis that heart rate (HR) reduction, induced by the selective hyperpolarization-activated current inhibitor ivabradine (Iva), might improve left ventricular (LV) function, structure, and electrical remodeling in severe post-myocardial infarction (MI) chronic heart failure (HF). MI was produced in adult male Wistar rats. After 2 mo, echocardiography was performed before the randomization into MI and MI + Iva (10 mg·kg−1·day−1) groups. After 3 mo of treatment, echocardiography and 24-h telemetry were recorded. Cardiac collagen, mRNA, and protein expressions of angiotensin-converting enzyme (ACE) and ANG II type 1 (AT1) receptor were quantified. As a result, at 2 mo post-MI, all rats displayed severe congestive HF signs (ejection fraction < 30%). At 5 mo post-MI, body and heart weights were similar in the MI and MI + Iva groups. LV ejection fraction and LV end-diastolic pressure were worsened in the MI group, whereas both were improved with Iva. Iva reduced HR by 10.4% ( P < 0.03 vs. MI) and ventricular premature complexes by 89% ( P < 0.03) and improved HR variability (standard deviation of the RR interval) by 22% ( P < 0.05). There were no effects of Iva on PR, QRS, and QT durations. Interstitial fibrosis in the MI-remote LV was markedly reduced by Iva (4.0 ± 0.1 vs. 1.8 ± 0.1%, P < 0.005). Increases in ventricular gene and protein expressions of ACE and AT1 receptor in MI were completely blunted by Iva. In conclusion, these data indicated that HR reduction by Iva prevents the worsening of LV dysfunction and remodeling that may be related to a downregulation of cardiac renin-angiotensin-aldosterone system transcripts. Such beneficial effects of Iva on cardiac remodeling open new clinical perspectives for the treatment of severe HF.

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