Heart failure with multiple comorbidities

Moe, Gordon W.

doi:10.1097/hco.0000000000000257

Cited by 20 publications

(20 citation statements)

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“…Chronic heart failure (CHF) is a common and complex clinical syndrome that results from impaired cardiac relaxation or contraction. It is a complex end stage of various cardiovascular diseases with a high rate of mortality . Ventricular remodeling is the major mechanism contributing to heart failure.…”

Section: Introductionmentioning

confidence: 99%

Induction of LOX by TGF‐β1/Smad/AP‐1 signaling aggravates rat myocardial fibrosis and heart failure

Qin

Yao

et al. 2019

IUBMB Life

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This study aims to evaluate the efficacy of lysyl oxidase (LOX) inhibition in regulating rat myocardial fibrosis and chronic heart failure (CHF) and to validate the regulation of LOX by TGF-β1/Smad2/3 signaling in this process. A rat model of CHF was established by abdominal aortic coarctation. The renin-angiotensinaldosterone system (RAAS) indexes (PRA, ACE2, Ang II, and ALD), cardiac function indicators (LVEF, LVFS, SAP, DAP, and LVEDP), ventricular remodeling-and fibrosis-related indicators (hydroxyproline, collagen deposition, and MMP-2/9), and morphological changes of myocardial tissues were examined. Rat cardiac fibroblasts (RCFs) were used in vitro assays. CHF patients showed increased LOX activity, accompanied by activated RAAS and TGF-β1. Furthermore, inhibition of LOX by β-aminopropionitrile (BAPN) mitigated the RAAS activation and attenuated cardiac dysfunction, ventricular remodeling, myocardial fibrosis, and collagen deposition in CHF rats. Moreover, TGF-β1 signaling diminished the LOX inhibition-mediated antiheart failure effect. Further assays showed that TGF-β1/ Smad2/3 signaling increased expression of c-jun (AP-1 transcription factor subunit), which transcriptionally induced LOX expression. Additionally, BAPN abrogated the TGF-β1-mediated increase in cell proliferation and levels of MMP-2/9 and collagen I/III in RCFs. In conclusion, LOX can be induced by TGF-β1/Smad/AP-1 signaling and LOX inhibition attenuates rat myocardial fibrosis and CHF. K E Y W O R D S chronic heart failure, c-Jun, LOXSmadTGF-β1

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Section: Introductionmentioning

confidence: 99%

Induction of LOX by TGF‐β1/Smad/AP‐1 signaling aggravates rat myocardial fibrosis and heart failure

Qin

Yao

et al. 2019

IUBMB Life

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“…Given the poor prognosis and the difficultly of treating heart failure, even in Europe and North America, attention has been focused on understanding which comorbidities in the setting of heart failure are associated with poor outcome and how they may be treated and managed to ameliorate outcomes (Moe, 2016) It has recently been recognised that anaemia is not only a frequent and important co-factor in refractory heart failure (Mahfoud et al, 2009), but also is potentially amenable to intervention (Lund & Mancini, 2004).…”

Section: Anaemia As An Important Comorbidity In Heart Failurementioning

confidence: 99%

Investigation and treatment for iron deficiency in heart failure: the unmet need in Lower and Middle Income Countries

Makubi

Roberts

2017

Br J Haematol

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Summary Frank iron deficiency has been associated with a wide range of cardiac and pulmonary abnormalities including non‐ischaemic cardiomyopathy. Iron deficiency anaemia and isolated iron deficiency are well‐defined adverse prognostic factors in non‐ischaemic cardiac failure. Furthermore, iron‐deficient patients in chronic heart failure with a serum ferritin of <100 μg/l or <300 μg/l with reduced transferrin saturation of <20%, who were given intravenous iron showed improved clinical outcomes. Iron deficiency with or without anaemia affects over a quarter of the world's population, but the impact of iron deficiency in heart failure and the effective management of iron deficiency in heart failure in Lower and Middle Income Countries (LMICs) is not well described. Heart failure in African cohorts occurs at a younger age than in North America and Europe and is more likely to be due to hypertension. Recent studies suggest that iron deficiency anaemia, which is very common in heart failure patients in Africa, and iron deficiency are independently associated with a poor prognosis in heart failure. Preliminary data suggest that iron deficiency in patients with heart failure can be treated with oral iron, with significant beneficial effects on haematological and physiological variables. Cost may prohibit the use of intravenous iron on a large scale in LMICs and optimal regimes to treat iron deficiency in heart failure patients with oral iron therapy remain to be defined.

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“…Доля пациентов, у которых ХСН сочетается с другими коморбидными состояниями, достигает 80% [1]. Значительная часть их приходится на хроническую болезнь почек (ХБП).…”

Section: Remodeling Of the Heart And Vessels In Atrial Fibrillation Punclassified

Remodeling of the Heart and Vessels in Atrial Fibrillation Patients With Chronic Heart Failure According to Cystatin C-Related Glomerular Filtration Rate

Mironova¹,

Полянская²,

Суровцева³

2018

Russ J Cardiol

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Цель. Изучить структурно-функциональные особенности левых отделов сердца и артерий у больных с постоянной формой фибрилляции предсердий (ФП) в сочетании с хроническая сердечная недостаточность (ХСН) ишемической этиологии в зависимости от цистатин С-обусловленной скоростью клубочковой фильтрации (СКФ). Материал и методы. 60 пациентов в возрасте от 35 до 60 лет с постоянной формой ФП ишемической этиологии. Всем пациентам были выполнены эхокардиография с верификацией дисфункции: систолическая функция оценивалась по фракции выброса левого желудочка по методу Simpson, для оценки диастолической дисфункции производилось определение скоростных характеристик трансмитрального кровотока и тканевой визуализации движения фиброзного кольца митрального клапана; суточное монито-рирование ЭКГ, объемная сфигмоплетизмография периферических артерий, оценка почечной функции с использованием формулы Chronic Kidney Disease Epidemiology Collaboration (CKD-EPI) по креатинину и цистатину С, оценка статуса коллагенообразования по уровню тканевого ингибитора матриксных металлопротеиназ 1 типа (TIMP-1) определение N-терминального фрагмента мозгового натрийуретического гормона (NT-proBNP). В первой части исследования пациенты были разделены на три группы -по уровню СКФ <30 мл/мин/1,73 м 2 , 30-60 мл/мин/1,73 м 2 и >60 мл/мин/1,73 м 2 . Во второй -по уровню цистатина С ниже и выше референсного значения. Результаты. У больных постоянной формой ФП и ХСН ишемической этиологии концентрация цистатина С в крови имеет прямые сильной степени зависимости взаимосвязи с NT-proBNP (r=0,60; р=0,003), индекс массы миокарда левого желудочка (r=0,68; р=0,005), E/e' среднее (r=0,73; p<0,001), время изоволюмического расслабления (r=0,53; р=0,012), cреднесуточной частоты сердечных сокращений (r=0,51; р=0,016), низкой степени зависимости -с TIMP-1 (r=0,26, p=0,002), обратные сильной степени зависимости -с SDNN (r=-0,59; р<0,001). СКФ (CKD-EPIcys) имеет обратные сильной степени зависимости взаимосвязи с septal e' (r=-0,51 р=0,041), c R-AI (r=-0,74; p<0,001), c CAVI1 (r=-0,53; р=0,008), и прямые средней степени зависимости -с SDNN (r=0,42; р<0,001). Заключение. Определение концентрация цистатина С в крови и цистатин С-зависимой СКФ у больных постоянной формой ФП и ХСН ишемической этиологии являются не только ранними маркерами ХБП, но и факторами риска развития и прогрессирования поражения органов-мишеней (сердца, сосудов). REMODELING OF THE HEART AND VESSELS IN ATRIAL FIBRILLATION PATIENTS WITH CHRONIC HEART FAILURE ACCORDING TO CYSTATIN C-RELATED GLOMERULAR FILTRATION RATEMironova S. V., Polyanskaya E. A., Surovtseva M. V.Aim. To investigate on structural and functional specifics of the left cardiac chambers and arteries in patients with permanent atrial fibrillation (AF) comorbid with chronic heart failure (CHF) of ischemic origin, with relation to cystatin C-dependent glomerular filtration rate (GFR). Material and methods. Sixty patients, age 35-60 y. o., with permanent AF of ischemic origin. All patients underwent echocardiography for the dysfunction verifica...

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Heart failure with multiple comorbidities

Abstract: As patients with comorbid conditions are frequently excluded from clinical trials, future clinical trials should recruit these patients and include endpoints that will be reflective of these conditions.

Cited by 20 publications

References 80 publications

Induction of LOX by TGF‐β1/Smad/AP‐1 signaling aggravates rat myocardial fibrosis and heart failure

Induction of LOX by TGF‐β1/Smad/AP‐1 signaling aggravates rat myocardial fibrosis and heart failure

Investigation and treatment for iron deficiency in heart failure: the unmet need in Lower and Middle Income Countries

Remodeling of the Heart and Vessels in Atrial Fibrillation Patients With Chronic Heart Failure According to Cystatin C-Related Glomerular Filtration Rate

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