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Open AccessArticle

Serum Selenium and Ceruloplasmin in Nigerians with Peripartum Cardiomyopathy

by Kamilu M. Karaye, Isah A. Yahaya, Krister Lindmark and Michael Y. Henein

Int. J. Mol. Sci. 2015, 16(4), 7644-7654; https://doi.org/10.3390/ijms16047644 - 7 Apr 2015

Cited by 47 | Viewed by 6032

Abstract

The study aimed to determine if selenium deficiency, serum ceruloplasmin and traditional birth practices are risk factors for peripartum cardiomyopathy (PPCM), in Kano, Nigeria. This is a case-control study carried out in three hospitals, and PPCM patients were followed up for six months. [...] Read more.

The study aimed to determine if selenium deficiency, serum ceruloplasmin and traditional birth practices are risk factors for peripartum cardiomyopathy (PPCM), in Kano, Nigeria. This is a case-control study carried out in three hospitals, and PPCM patients were followed up for six months. Critically low serum selenium concentration was defined as <70 µg/L. A total of 39 PPCM patients and 50 controls were consecutively recruited after satisfying the inclusion criteria. Mean serum selenium in patients (61.7 ± 14.9 µg/L) was significantly lower than in controls (118.4 ± 45.6 µg/L) (p < 0.001). The prevalence of serum selenium <70 µg/L was significantly higher among patients (76.9%) than controls (22.0%) (p < 0.001). The mean ceruloplasmin and prevalence of socio-economic indices, multiparity, pregnancy-induced hypertension, obesity and twin pregnancy were not different between the groups (p > 0.05). Logistic regression showed that rural residency significantly increased the odds for serum selenium <70 µg/L by 2.773-fold (p = 0.037). Baseline serum levels of selenium and ceruloplasmin were not associated with six-month mortality. This study has shown that selenium deficiency is a risk factor for PPCM in Kano, Nigeria, and is related to rural residency. However, serum ceruloplasmin, customary birth practices and some other characteristics were not associated with PPCM in the study area. Full article

(This article belongs to the Special Issue Pathogenesis of Cardiac Arrhythmias and Heart Failure)

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Open AccessArticle

MiR-25 Protects Cardiomyocytes against Oxidative Damage by Targeting the Mitochondrial Calcium Uniporter

by Lei Pan, Bi-Jun Huang, Xiu-E Ma, Shi-Yi Wang, Jing Feng, Fei Lv, Yuan Liu, Yi Liu, Chang-Ming Li, Dan-Dan Liang, Jun Li, Liang Xu and Yi-Han Chen

Int. J. Mol. Sci. 2015, 16(3), 5420-5433; https://doi.org/10.3390/ijms16035420 - 10 Mar 2015

Cited by 78 | Viewed by 7635

Abstract

MicroRNAs (miRNAs) are a class of small non-coding RNAs, whose expression levels vary in different cell types and tissues. Emerging evidence indicates that tissue-specific and -enriched miRNAs are closely associated with cellular development and stress responses in their tissues. MiR-25 has been documented [...] Read more.

MicroRNAs (miRNAs) are a class of small non-coding RNAs, whose expression levels vary in different cell types and tissues. Emerging evidence indicates that tissue-specific and -enriched miRNAs are closely associated with cellular development and stress responses in their tissues. MiR-25 has been documented to be abundant in cardiomyocytes, but its function in the heart remains unknown. Here, we report that miR-25 can protect cardiomyocytes against oxidative damage by down-regulating mitochondrial calcium uniporter (MCU). MiR-25 was markedly elevated in response to oxidative stimulation in cardiomyocytes. Further overexpression of miR-25 protected cardiomyocytes against oxidative damage by inactivating the mitochondrial apoptosis pathway. MCU was identified as a potential target of miR-25 by bioinformatical analysis. MCU mRNA level was reversely correlated with miR-25 under the exposure of H₂O₂, and MCU protein level was largely decreased by miR-25 overexpression. The luciferase reporter assay confirmed that miR-25 bound directly to the 3' untranslated region (UTR) of MCU mRNA. MiR-25 significantly decreased H₂O₂-induced elevation of mitochondrial Ca²⁺ concentration, which is likely to be the result of decreased activity of MCU. We conclude that miR-25 targets MCU to protect cardiomyocytes against oxidative damages. This finding provides novel insights into the involvement of miRNAs in oxidative stress in cardiomyocytes. Full article

(This article belongs to the Special Issue Pathogenesis of Cardiac Arrhythmias and Heart Failure)

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9906 KiB

Open AccessArticle

Simvastatin Attenuates the Oxidative Stress, Endothelial Thrombogenicity and the Inducibility of Atrial Fibrillation in a Rat Model of Ischemic Heart Failure

by Kyoung-Im Cho, Sang-Ho Koo, Tae-Joon Cha, Jung-Ho Heo, Hyun-Su Kim, Gee-Bum Jo and Jae-Woo Lee

Int. J. Mol. Sci. 2014, 15(8), 14803-14818; https://doi.org/10.3390/ijms150814803 - 22 Aug 2014

Cited by 17 | Viewed by 7634

Abstract

Increased atrial oxidative stress has an important role in inducing and maintaining atrial fibrillation (AF), and the activation of the small GTPase Rac1 contributes to the oxidative stress. We investigated the relationship of Rac1, atrial endothelial thromboprotective markers and AF inducibility and if [...] Read more.

Increased atrial oxidative stress has an important role in inducing and maintaining atrial fibrillation (AF), and the activation of the small GTPase Rac1 contributes to the oxidative stress. We investigated the relationship of Rac1, atrial endothelial thromboprotective markers and AF inducibility and if simvastatin has a potential beneficial effect on a myocardial infarction (MI)-induced heart failure (HF) rat model. Rats were randomized into three groups (shams, MI group and simvastatin treatment group) and underwent echocardiography, AF induction studies and left atrial (LA) fibrosis analysis. Atrial Rac 1, sodium calcium exchanger (I_NCX), sarcoplasmic reticulum calcium ATPase (SERCA), endothelial nitric oxide synthase (eNOS) and induced nitric oxide synthase (iNOS) were measured. AF inducibility, AF duration and LA fibrosis were significantly higher in the MI group (p < 0.001 vs. sham), which were significantly reduced by simvastatin (p < 0.05 vs. MI). The reduced expressions of atrial eNOS, SERCA, thrombomodulin, tissue factor pathway inhibitor and tissue plasminogen activator in the MI group were significantly improved by simvastatin. Furthermore, the increased expression of atrial iNOS, I_NCX and Rac1 activity were significantly decreased by the simvastatin. Oxidative stress, endothelial dysfunction and thrombogenicity are associated with the promotion of AF in a rat model of ischemic HF. These were associated with increased Rac1 activity, and simvastatin treatment prevents these changes. Full article

(This article belongs to the Special Issue Pathogenesis of Cardiac Arrhythmias and Heart Failure)

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Review

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Open AccessReview

Is Correction of Iron Deficiency a New Addition to the Treatment of the Heart Failure?

by Donald S. Silverberg, Dov Wexler and Doron Schwartz

Int. J. Mol. Sci. 2015, 16(6), 14056-14074; https://doi.org/10.3390/ijms160614056 - 18 Jun 2015

Cited by 23 | Viewed by 6690

Abstract

Anemia is present in about 40% of heart failure (HF) patients. Iron deficiency (ID) is present in about 60% of the patients with anemia (about 24% of all HF patients) and in about 40% of patients without anemia (about 24% of all HF [...] Read more.

Anemia is present in about 40% of heart failure (HF) patients. Iron deficiency (ID) is present in about 60% of the patients with anemia (about 24% of all HF patients) and in about 40% of patients without anemia (about 24% of all HF patients). Thus ID is present in about half the patients with HF. The ID in HF is associated with reduced iron stores in the bone marrow and the heart. ID is an independent risk factor for severity and worsening of the HF. Correction of ID with intravenous (IV) iron usually corrects both the anemia and the ID. Currently used IV iron preparations are very safe and effective in treating the ID in HF whereas little information is available on the effectiveness of oral iron. In HF IV iron correction of ID is associated with improvement in functional status, exercise capacity, quality of life and, in some studies, improvement in rate of hospitalization for HF, cardiac structure and function, and renal function. Large long-term adequately-controlled intervention studies are needed to clarify the effect of IV iron in HF. Several heart associations suggest that ID should be routinely sought for in all HF patients and corrected if present. In this paper we present our approach to diagnosis and treatment of iron deficiency in heart failure. Full article

(This article belongs to the Special Issue Pathogenesis of Cardiac Arrhythmias and Heart Failure)

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Open AccessReview

Potential Role of Dipeptidyl Peptidase IV in the Pathophysiology of Heart Failure

by Thiago A. Salles, Leonardo Dos Santos, Valério G. Barauna and Adriana C. C. Girardi

Int. J. Mol. Sci. 2015, 16(2), 4226-4249; https://doi.org/10.3390/ijms16024226 - 16 Feb 2015

Cited by 19 | Viewed by 9441

Abstract

Dipeptidyl peptidase IV (DPPIV) is a widely expressed multifunctional serine peptidase that exists as a membrane-anchored cell surface protein or in a soluble form in the plasma and other body fluids. Numerous substrates are cleaved at the penultimate amino acid by DPPIV, including [...] Read more.

Dipeptidyl peptidase IV (DPPIV) is a widely expressed multifunctional serine peptidase that exists as a membrane-anchored cell surface protein or in a soluble form in the plasma and other body fluids. Numerous substrates are cleaved at the penultimate amino acid by DPPIV, including glucagon-like peptide-1 (GLP-1), brain natriuretic peptide (BNP) and stromal cell-derived factor-1 (SDF-α), all of which play important roles in the cardiovascular system. In this regard, recent reports have documented that circulating DPPIV activity correlates with poorer cardiovascular outcomes in human and experimental heart failure (HF). Moreover, emerging evidence indicates that DPPIV inhibitors exert cardioprotective and renoprotective actions in a variety of experimental models of cardiac dysfunction. On the other hand, conflicting results have been found when translating these promising findings from preclinical animal models to clinical therapy. In this review, we discuss how DPPIV might be involved in the cardio-renal axis in HF. In addition, the potential role for DPPIV inhibitors in ameliorating heart disease is revised, focusing on the effects of the main DPPIV substrates on cardiac remodeling and renal handling of salt and water. Full article

(This article belongs to the Special Issue Pathogenesis of Cardiac Arrhythmias and Heart Failure)

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Open AccessReview

Heart Failure and Atrial Fibrillation: From Basic Science to Clinical Practice

by João Pedro Ferreira and Mário Santos

Int. J. Mol. Sci. 2015, 16(2), 3133-3147; https://doi.org/10.3390/ijms16023133 - 30 Jan 2015

Cited by 42 | Viewed by 12774

Abstract

Heart failure (HF) and atrial fibrillation (AF) are two growing epidemics associated with significant morbidity and mortality. They often coexist due to common risk factors and shared pathophysiological mechanisms. Patients presenting with both HF and AF have a worse prognosis and present a [...] Read more.

Heart failure (HF) and atrial fibrillation (AF) are two growing epidemics associated with significant morbidity and mortality. They often coexist due to common risk factors and shared pathophysiological mechanisms. Patients presenting with both HF and AF have a worse prognosis and present a particular therapeutic challenge to clinicians. This review aims to appraise the common pathophysiological background, as well as the prognostic and therapeutic implications of coexistent HF and AF. Full article

(This article belongs to the Special Issue Pathogenesis of Cardiac Arrhythmias and Heart Failure)

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3070 KiB

Open AccessReview

Cardiac Arrhythmias and Sleep-Disordered Breathing in Patients with Heart Failure

by Wolfram Grimm and Ulrich Koehler

Int. J. Mol. Sci. 2014, 15(10), 18693-18705; https://doi.org/10.3390/ijms151018693 - 16 Oct 2014

Cited by 19 | Viewed by 8811

Abstract

The relationship between heart failure (HF), sleep-disordered breathing and cardiac arrhythmias is complex and poorly understood. Whereas the frequency of predominantly obstructive sleep apnea in HF patients is low and similar or moderately higher to that observed in the general population, central sleep [...] Read more.

The relationship between heart failure (HF), sleep-disordered breathing and cardiac arrhythmias is complex and poorly understood. Whereas the frequency of predominantly obstructive sleep apnea in HF patients is low and similar or moderately higher to that observed in the general population, central sleep apnea (CSA) has been observed in approximately 50% of HF patients, depending on the methods used to detect CSA and patient selection. Despite this high prevalence, it is still unclear whether CSA is merely a marker or an independent risk factor for an adverse prognosis in HF patients and whether CSA is associated with an increased risk for supraventricular as well as ventricular arrhythmias in HF patients. The current review focuses on the relationship between CSA and atrial fibrillation as the most common atrial arrhythmia in HF patients, and on the relationship between CSA and ventricular tachycardia and ventricular fibrillation as the most frequent cause of sudden cardiac death in HF patients. Full article

(This article belongs to the Special Issue Pathogenesis of Cardiac Arrhythmias and Heart Failure)

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Open AccessReview

The Three Integrated Phases of Left Atrial Macrophysiology and Their Interactions

by Raman Mehrzad, Mohammad Rajab and David H. Spodick

Int. J. Mol. Sci. 2014, 15(9), 15146-15160; https://doi.org/10.3390/ijms150915146 - 27 Aug 2014

Cited by 33 | Viewed by 8271

Abstract

Our understanding of the left atrium is growing, although there are many aspects that are still poorly understood. The left atrium size as an imaging biomarker has been consistently shown to be a powerful predictor of outcomes and of different cardiovascular disorders, such [...] Read more.

Our understanding of the left atrium is growing, although there are many aspects that are still poorly understood. The left atrium size as an imaging biomarker has been consistently shown to be a powerful predictor of outcomes and of different cardiovascular disorders, such as, but not limited to, atrial fibrillation, congestive heart failure, mitral regurgitation and stroke. Left atrial function has been conventionally divided into three integrated phases: reservoir, conduit and booster-pump. The highly dynamic left atrium and its response to the stretch and secretion of atrial neuropeptides leaves the left atrium far from being a simple transport chamber. The aim of this review is to provide an understanding of the left atrial physiology and its relation to disorders within the heart. Full article

(This article belongs to the Special Issue Pathogenesis of Cardiac Arrhythmias and Heart Failure)

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