Heart Failure and Coexisting Morbidities

A special issue of Life (ISSN 2075-1729). This special issue belongs to the section "Physiology and Pathology".

Deadline for manuscript submissions: closed (31 October 2023) | Viewed by 23395

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Guest Editor
Department of Cardiology, University Hospital of Larissa, 41110 Larissa, Greece
Interests: heart failure; acute heart failure; chronic heart failure; LVAD; heart transplantation; amyloidosis; devices; pulmonary hypertension
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Special Issue Information

Dear Colleagues,

Heart failure (HF) is a clinical syndrome associated with increased morbidity, mortality, and healthcare costs. Several coexisting diseases and/or conditions are present in HF patients (both cardiovascular and non-cardiovascular), with diverse clinical relevance. For example, HF in the young is attributed to factors predominantly or exclusively affecting the heart (i.e., adult congenital heart disease, cardiomyopathies, myocarditis, or cardiotoxicity), while HF in the elderly is the result of risk factors (i.e., hypertension, obesity, type 2 diabetes mellitus, coronary artery disease, valvular heart disease) accelerating cardiovascular aging and influencing both the heart and the vasculature. Multiple mechanisms may underlie the coexistence of HF and morbidities, including direct causation, associated risk factors, heterogeneity, and independence. The complex inter-relationship of coexisting morbidities and their impact on the cardiovascular system contribute to the features of HF, both with reduced (HFrEF) and preserved ejection fraction (HFpEF). In other words, coexisting morbidities determine the phenotypes and outcomes of HF. An improved understanding of HF pathogenesis and its complex association with coexisting morbidities may lead to more effective HF prevention and treatment.

The Special Issue is now open for submissions (including original research articles, review papers, and opinion papers) from healthcare providers related to cardiology as well as researchers specializing in different areas (i.e. diabetology, hematology, intensive care medicine, rheumatology, endocrinology, nephrology etc.). We kindly ask that prospective authors send a short abstract or tentative title to the Editorial Office prior to submitting a full paper so that its suitability for the scope of this Special Issue can be evaluated.

Dr. Andrew Xanthopoulos
Guest Editor

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Keywords

  • aging
  • heart failure
  • morbidities
  • risk factors
  • treatment

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Published Papers (9 papers)

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Research

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13 pages, 1012 KiB  
Article
Association between Dapagliflozin, Cardiac Biomarkers and Cardiac Remodeling in Patients with Diabetes Mellitus and Heart Failure
by Andrew Xanthopoulos, Nikolaos Katsiadas, Spyridon Skoularigkis, Dimitrios E. Magouliotis, Niki Skopeliti, Sotirios Patsilinakos, Alexandros Briasoulis, Filippos Triposkiadis and John Skoularigis
Life 2023, 13(8), 1778; https://doi.org/10.3390/life13081778 - 20 Aug 2023
Cited by 2 | Viewed by 2016
Abstract
Sodium–glucose cotransporter-2 inhibitors (SGLT2is) are a relatively new class of antidiabetic drugs that have shown favorable effects in heart failure (HF) patients, irrespective of the left ventricular ejection fraction (LVEF). Recent studies have demonstrated the beneficial effects of empagliflozin on cardiac function and [...] Read more.
Sodium–glucose cotransporter-2 inhibitors (SGLT2is) are a relatively new class of antidiabetic drugs that have shown favorable effects in heart failure (HF) patients, irrespective of the left ventricular ejection fraction (LVEF). Recent studies have demonstrated the beneficial effects of empagliflozin on cardiac function and structure; however, less is known about dapagliflozin. The purpose of the current work was to investigate the association between the use of dapagliflozin and cardiac biomarkers as well as the cardiac structure in a cohort of patients with HF and diabetes mellitus (DM). The present work was an observational study that included 118 patients (dapagliflozin group n = 60; control group n = 58) with HF and DM. The inclusion criteria included: age > 18 years, a history of DM and HF, regardless of LVEF, and hospitalization for HF exacerbation within the previous 6 months. The exclusion criteria were previous treatment with SGLT2i or glucagon-like peptide-1 receptor agonists, a GFR< 30 and life expectancy < 1 year. The evaluation of patients (at baseline, 6 and 12 months) included a clinical assessment, laboratory blood tests and echocardiography. The Mann–Whitney test was used for the comparison of continuous variables between the two groups, while Friedman’s analysis of variance for repeated measures was used for the comparison of continuous variables. Troponin (p < 0.001) and brain natriuretic peptide (BNP) (p < 0.001) decreased significantly throughout the follow-up period in the dapagliflozin group, but not in the control group (p > 0.05 for both). The LV end-diastolic volume index (p < 0.001 for both groups) and LV end-systolic volume index (p < 0.001 for both groups) decreased significantly in the dapagliflozin and the control group, respectively. The LVEF increased significantly (p < 0.001) only in the dapagliflozin group, whereas the global longitudinal strain (GLS) improved in the dapagliflozin group (p < 0.001) and was impaired in the control group (p = 0.021). The left atrial volume index decreased in the dapagliflozin group (p < 0.001) but remained unchanged in the control group (p = 0.114). Lastly, the left ventricular mass index increased significantly both in the dapagliflozin (p = 0.003) and control group (p = 0.001). Dapagliflozin, an SGLT2i, was associated with a reduction in cardiac biomarkers and with reverse cardiac remodeling in patients with HF and DM. Full article
(This article belongs to the Special Issue Heart Failure and Coexisting Morbidities)
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11 pages, 505 KiB  
Article
Levosimendan in the Treatment of Patients with Severe Septic Cardiomyopathy
by Vasiliki Tsolaki, George E. Zakynthinos, John Papanikolaou, Vasileios Vazgiourakis, Kyriaki Parisi, George Fotakopoulos, Demosthenes Makris and Epaminondas Zakynthinos
Life 2023, 13(6), 1346; https://doi.org/10.3390/life13061346 - 8 Jun 2023
Cited by 3 | Viewed by 1867
Abstract
(1) Background: The optimal treatment of septic cardiomyopathy (SCM) remains questionable. The aim of the study was to compare the treatment of SCM based on levosimendan versus the best available therapy. (2) Methods: We conducted an observational study including patients with severe septic [...] Read more.
(1) Background: The optimal treatment of septic cardiomyopathy (SCM) remains questionable. The aim of the study was to compare the treatment of SCM based on levosimendan versus the best available therapy. (2) Methods: We conducted an observational study including patients with severe septic cardiomyopathy and circulatory failure. (3) Results: Fourteen patients (61%) received levosimendan, and nine received other treatments. The patients in the levosimendan group were more severely ill [APACHE II: 23.5 (14, 37) vs. 14 (13, 28), respectively, p = 0.012], and there was a trend for more decompensated LV function depicted by the LVEF [15% (10, 20) vs. 25% (5, 30), respectively, p = 0.061]. However, they presented a significantly higher increase in LVEF after seven days [15% (10, 20) to 50% (30, 68) (p < 0.0001) vs. 25% (5, 30) to 25% (15, 50) (p = 0.309), and a significantly higher decrease in lactate levels during the first 24 h [4.5 (2.5, 14.4) to 2.85 (1.2, 15), p = 0.036 vs. 2.9 (2, 18.9) to 2.8 (1, 15), p = 0.536]. Seven-day survival (64.3% vs. 33.3%, p = 0.424) and ICU survival (50% vs. 22.2%, p = 0.172) were higher in the first group, although differences did not reach statistical significance. The degree of left ventricular impairment and the magnitude of EF improvement by the seventh-day post-SCM onset were associated with mortality in regression analysis. (4) Conclusions: Our study presents main hemodynamic data supporting the possible efficacy of levosimendan treatment in patients with severe SCM. Full article
(This article belongs to the Special Issue Heart Failure and Coexisting Morbidities)
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Review

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12 pages, 246 KiB  
Review
Light-Chain Amyloidosis: The Great Impostor
by Georgia Stefani, Evangelia Kouvata and George Vassilopoulos
Life 2024, 14(1), 42; https://doi.org/10.3390/life14010042 - 26 Dec 2023
Cited by 1 | Viewed by 1642
Abstract
Light-chain amyloidosis (AL) is a disease of protean manifestations due to a wide spectrum of organs that can be affected. The disorder is caused by the deposition of an extracellular amorphous material, the amyloid, which is produced by malignant plasma cells. The latter [...] Read more.
Light-chain amyloidosis (AL) is a disease of protean manifestations due to a wide spectrum of organs that can be affected. The disorder is caused by the deposition of an extracellular amorphous material, the amyloid, which is produced by malignant plasma cells. The latter usually reside in the bone marrow; plasma cell infiltration is often low, in sharp contrast to what we observe in multiple myeloma. The disease may run below the physician’s radar for a while before clinical suspicion is raised and targeted tests are performed. In this short review, we try to answer most of the questions that a practicing physician may ask in a relative clinical setting. The text is formed as a series of reader-friendly questions that cover the subject of AL amyloidosis from history to current therapy. Full article
(This article belongs to the Special Issue Heart Failure and Coexisting Morbidities)
13 pages, 1194 KiB  
Review
Sodium–Glucose Transporter 2 (SGLT2) Inhibitors and Iron Deficiency in Heart Failure and Chronic Kidney Disease: A Literature Review
by Maria Tziastoudi, Georgios Pissas, Spyridon Golfinopoulos, Georgios Filippidis, Periklis Dousdampanis, Theodoros Eleftheriadis and Ioannis Stefanidis
Life 2023, 13(12), 2338; https://doi.org/10.3390/life13122338 - 13 Dec 2023
Cited by 3 | Viewed by 3120
Abstract
Heart failure (HF) and chronic kidney disease (CKD) are associated with high mortality. In both disorders, impaired iron homeostasis, mostly in the form of a functional iron deficiency, is a frequent co-morbidity. In HF, functional iron deficiency and management by i.v. iron supplementation [...] Read more.
Heart failure (HF) and chronic kidney disease (CKD) are associated with high mortality. In both disorders, impaired iron homeostasis, mostly in the form of a functional iron deficiency, is a frequent co-morbidity. In HF, functional iron deficiency and management by i.v. iron supplementation have been proven to affect both prognosis and functional capacity. In the same context, iron supplementation is routine for the adequate management of renal anemia in CKD. In numerous recent studies in HF and in CKD, sodium–glucose transporter 2 (SGLT2) inhibitor treatment has been proven to significantly reduce mortality. Furthermore, the same trials showed that these drugs alleviate iron deficiency and anemia. These effects of SGLT2 inhibitors may be due to an amelioration of inflammation with reduced interleukin-6 (IL-6) and to an enhancement of autophagy with increased sirtuin 1 (SIRT1), both associated with modified production of hepcidin and enhanced ferritinophagy. However, the exact pathogenic basis of the beneficial SGLT2 inhibitor action is not fully elucidated. Nevertheless, effects on iron homeostasis might be a potential explanatory mechanism for the powerful SGLT2 inhibitors’ cardiovascular and renal outcome benefits. In addition, the interaction between iron supplementation and SGLT2 inhibitors and its potential impact on prognosis remains to be clarified by future studies. This review represents a significant effort to explore the complex relationships involved, seeking to elucidate the intricate mechanisms by which SGLT2 inhibitors influence iron homeostasis. Full article
(This article belongs to the Special Issue Heart Failure and Coexisting Morbidities)
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13 pages, 1059 KiB  
Review
The Importance of the Nephrologist in the Treatment of the Diuretic-Resistant Heart Failure
by Ákos Géza Pethő, Mihály Tapolyai, Maria Browne, Tibor Fülöp, Petronella Orosz and Réka P. Szabó
Life 2023, 13(6), 1328; https://doi.org/10.3390/life13061328 - 6 Jun 2023
Viewed by 2075
Abstract
Heart failure is not only a global problem but also significantly limits the life prospects of these patients. The epidemiology and presentation of heart failure are intensively researched topics in cardiology. The risk factors leading to heart failure are well known; however, the [...] Read more.
Heart failure is not only a global problem but also significantly limits the life prospects of these patients. The epidemiology and presentation of heart failure are intensively researched topics in cardiology. The risk factors leading to heart failure are well known; however, the real challenge is to provide effective treatments. A vicious cycle develops in heart failure of all etiologies, sooner or later compromising both cardiac and kidney functions simultaneously. This can explain the repeated hospital admissions due to decompensation and the significantly reduced quality of life. Moreover, diuretic-refractory heart failure represents a distinct challenge due to repeated hospital admissions and increased mortality. In our narrative review, we wanted to draw attention to nephrology treatment options for severe diuretic-resistant heart failure. The incremental value of peritoneal dialysis in severe heart failure and the feasibility of percutaneous peritoneal dialysis catheter insertion have been well known for many years. In contrast, the science and narrative of acute peritoneal dialysis in diuretic-resistant heart failure remains underrepresented. We believe that nephrologists are uniquely positioned to help these patients by providing acute peritoneal dialysis to reduce hospitalization dependency and increase their quality of life. Full article
(This article belongs to the Special Issue Heart Failure and Coexisting Morbidities)
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13 pages, 640 KiB  
Review
Sodium-Glucose Co-Transporter 2 Inhibitors in Heart Failure—Current Evidence in Special Populations
by Gassan Moady, Tuvia Ben Gal and Shaul Atar
Life 2023, 13(6), 1256; https://doi.org/10.3390/life13061256 - 25 May 2023
Cited by 5 | Viewed by 3974
Abstract
Sodium-glucose co-transporter 2 (SGLT2) inhibitors, originally used for diabetes mellitus, are gaining more popularity for other indications, owing to their positive cardiovascular and renal effects. SGLT2 inhibitors reduce heart failure (HF) hospitalization and improve cardiovascular outcomes in patients with type 2 diabetes. Later, [...] Read more.
Sodium-glucose co-transporter 2 (SGLT2) inhibitors, originally used for diabetes mellitus, are gaining more popularity for other indications, owing to their positive cardiovascular and renal effects. SGLT2 inhibitors reduce heart failure (HF) hospitalization and improve cardiovascular outcomes in patients with type 2 diabetes. Later, SGLT2 inhibitors were evaluated in patients with HF with reduced ejection fraction (HFREF) and had beneficial effects independent of the presence of diabetes. Recently, reductions in cardiovascular outcomes were also observed in patients with HF with preserved ejection fraction (HFPEF). SGLT2 inhibitors also reduced renal outcomes in patients with chronic kidney disease. Overall, these drugs have an excellent safety profile with a negligible risk of genitourinary tract infections and ketoacidosis. In this review, we discuss the current data on SGLT2 inhibitors in special populations, including patients with acute myocardial infarction, acute HF, right ventricular (RV) failure, left ventricular assist device (LVAD), and type 1 diabetes. We also discuss the potential mechanisms behind the cardiovascular benefits of these medications. Full article
(This article belongs to the Special Issue Heart Failure and Coexisting Morbidities)
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10 pages, 466 KiB  
Review
Should We Change the Target of Therapy in Pulmonary Hypertension?
by Panagiotis Karyofyllis, Eftychia Demerouti, Pavlos Habibis, Styliani Apostolopoulou, Eleftheria-Garyfallia Tsetika and Dimitrios Tsiapras
Life 2023, 13(5), 1202; https://doi.org/10.3390/life13051202 - 17 May 2023
Viewed by 3058
Abstract
Despite the evolution of drug therapy in pulmonary arterial hypertension and the more aggressive treatment approach according to the guidelines, patients continue to have unacceptable mortality rates. Furthermore, specific drug therapy alone in chronic thromboembolic pulmonary hypertension also does not seem to have [...] Read more.
Despite the evolution of drug therapy in pulmonary arterial hypertension and the more aggressive treatment approach according to the guidelines, patients continue to have unacceptable mortality rates. Furthermore, specific drug therapy alone in chronic thromboembolic pulmonary hypertension also does not seem to have any beneficial impact on survival. As the function of the right ventricle (RV) determines the prognosis of patients with pulmonary hypertension, the treatment strategy should focus on modifying factors involved in RV dysfunction. Although some previous reports demonstrated that the survival of patients with pulmonary hypertension was associated with mPAP, nevertheless, mPAP is still not considered as a target of therapy. There are many examples of effective mPAP lowering with early and aggressive drug therapy in pulmonary arterial hypertension, or with interventions in chronic thromboembolic pulmonary hypertension. This effective mPAP reduction can lead to reverse RV remodeling, and thus, improvement in survival. In this article, the importance of mPAP lowering is stated, as well as why the change of our current strategy and considering mPAP reduction as the target of therapy could make pulmonary hypertension a chronic but not fatal disease. Full article
(This article belongs to the Special Issue Heart Failure and Coexisting Morbidities)
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11 pages, 1433 KiB  
Review
Demystifying the Value of Minimal Clinically Important Difference in the Cardiothoracic Surgery Context
by Dimitrios E. Magouliotis, Metaxia Bareka, Arian Arjomandi Rad, Grigorios Christodoulidis and Thanos Athanasiou
Life 2023, 13(3), 716; https://doi.org/10.3390/life13030716 - 6 Mar 2023
Cited by 2 | Viewed by 1675
Abstract
The aim of this review is to describe the different statistical methods used in estimating the minimal clinically important difference (MCID) for the assessment of quality of life (QOL)-related and clinical improvement interventions, along with their implementation in cardiothoracic surgery. A thorough literature [...] Read more.
The aim of this review is to describe the different statistical methods used in estimating the minimal clinically important difference (MCID) for the assessment of quality of life (QOL)-related and clinical improvement interventions, along with their implementation in cardiothoracic surgery. A thorough literature search was performed in three databases (PubMed/Medline, Scopus, Google Scholar) for relevant articles from 1980 to 2022. We included articles that implemented and assessed statistical methods used to estimate the concept of MCID in cardiothoracic surgery. MCID has been successfully implemented in several medical specialties. Anchor-based and distribution-based methods are the most common approaches when evaluating the MCID. Nonetheless, we found only five studies investigating the MCID in the context of cardiothoracic surgery. Four of them used anchor-based approaches, and one used both anchor-based and distribution-based methods. MCID values were very variable depending on the methods applied, as was the clinical context of the study. The variables of interest were certain QOL measuring questionnaires, used as anchors. Multiple anchors and methods were applied, leading to different estimations of MCID. Since cardiothoracic surgery is related to important perioperative morbidity, MCID might represent an important and efficient adjunct tool to interpret clinical outcomes. The need for MCID methodology implementation is even higher in patients with heart failure undergoing cardiac surgery. More studies are needed to validate different MCID methods in this context. Full article
(This article belongs to the Special Issue Heart Failure and Coexisting Morbidities)
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Other

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7 pages, 902 KiB  
Opinion
The Neurohormonal Overactivity Syndrome in Heart Failure
by Andrew Xanthopoulos, John Skoularigis and Filippos Triposkiadis
Life 2023, 13(1), 250; https://doi.org/10.3390/life13010250 - 16 Jan 2023
Cited by 4 | Viewed by 2448
Abstract
Heart failure (HF) is categorized arbitrarily based on the left ventricular ejection fraction (LVEF) in HF with reduced (HFrEF; LVEF < 40%), mildly reduced (HFmrEF; LVEF 40–49%), or preserved ejection fraction (HFpEF; LVEF ≥ 50%). In this opinion paper, based on (patho)physiological considerations, [...] Read more.
Heart failure (HF) is categorized arbitrarily based on the left ventricular ejection fraction (LVEF) in HF with reduced (HFrEF; LVEF < 40%), mildly reduced (HFmrEF; LVEF 40–49%), or preserved ejection fraction (HFpEF; LVEF ≥ 50%). In this opinion paper, based on (patho)physiological considerations, we contend that the neurohormonal overactivity syndrome (NOHS), which is present in all symptomatic HF patients irrespective of their LVEF, not only contributes to the development of signs and symptoms but it is also a major determinant of patients’ outcomes. In this regard, NHOS is the only currently available treatment target in HF and should be combatted in most patients with the combined use of diuretics and neurohormonal inhibitors (β-blockers, angiotensin receptor-neprilysin inhibitor/angiotensin-converting enzyme inhibitors/angiotensin receptor blockers, mineralocorticoid antagonists, and sodium-glucose co-transporter 2 inhibitors). Unfortunately, despite the advances in therapeutics, HF mortality remains high. Probably machine learning approaches could better assess the multiple and higher-dimension interactions leading to the HF syndrome and define clusters of HF treatment efficacy. Full article
(This article belongs to the Special Issue Heart Failure and Coexisting Morbidities)
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