scholarly journals Cardiorenal syndrome in COVID-19

2021 ◽  
Vol 14 (4) ◽  
pp. e241914
Author(s):  
Uzair Akbar Ali ◽  
Muhammad Sajjad Sadiq ◽  
Muhammad Jawad Yunus
Keyword(s):  
Heart Failure ◽  
Renal Failure ◽  
Cardiorenal Syndrome ◽  
Multiple Organ ◽  
Comorbid Illness ◽  
Reduced Ejection Fraction ◽  
Organ Systems ◽  
Underlying Mechanisms ◽  
Work Up ◽  
Intermittent Renal Replacement Therapy

SARS-CoV-2 preferentially targets the human’s lungs, but it can affect multiple organ systems. We report a case of cardiorenal syndrome in a 37-year-old man who had symptoms of fever, myalgia and cough. He tested positive for COVID-19 and presented 5 days later with acute heart failure. Work up was done including echocardiography showing reduced ejection fraction. Later in the hospital course he developed acute renal failure and was treated with intermittent renal replacement therapy. No other definite cause of cardiorenal complications was identified during the course of the disease. A possible link with COVID-19 was considered with underlying mechanisms still needed to be explored. This case highlights the potential of SARS-CoV-2 affecting heart and kidneys. The disease not only involves the organs directly but can exacerbate the underlying comorbid illness.

scholarly journals Drug Targets for Heart Failure with Preserved Ejection Fraction: A Mechanistic Approach and Review of Contemporary Clinical Trials

2019 ◽  
Vol 59 (1) ◽  
pp. 41-63 ◽  
Author(s):  
Ravi B. Patel ◽  
Sanjiv J. Shah
Keyword(s):  
Heart Failure ◽  
Ejection Fraction ◽  
Drug Targets ◽  
Multiple Organ ◽  
Preserved Ejection Fraction ◽  
Research Strategies ◽  
Reduced Ejection Fraction ◽  
Mechanistic Approach ◽  
Organ Systems ◽  
Heterogeneous Nature

Heart failure with preserved ejection fraction (HFpEF) accounts for over half of prevalent heart failure (HF) worldwide, and prognosis after hospitalization for HFpEF remains poor. Due, at least in part, to the heterogeneous nature of HFpEF, drug development has proved immensely challenging. Currently, there are no universally accepted therapies that alter the clinical course of HFpEF. Despite these challenges, important mechanistic understandings of the disease have revealed that the pathophysiology of HFpEF is distinct from that of HF with reduced ejection fraction and have also highlighted potential new therapeutic targets for HFpEF. Of note, HFpEF is a systemic syndrome affecting multiple organ systems. Depending on the organ systems involved, certain novel therapies offer promise in reducing the morbidity of the HFpEF syndrome. In this review, we aim to discuss novel pharmacotherapies for HFpEF based on its unique pathophysiology and identify key research strategies to further elucidate mechanistic pathways to develop novel therapeutics in the future.

scholarly journals Chamber-enriched gene expression profiles in failing human hearts with reduced ejection fraction

2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Xin Luo ◽  
Jun Yin ◽  
Denise Dwyer ◽  
Tracy Yamawaki ◽  
Hong Zhou ◽  
...  
Keyword(s):  
Heart Failure ◽  
Ejection Fraction ◽  
Human Genetics ◽  
Expression Profiles ◽  
Gene Expression Profiles ◽  
Left Heart ◽  
Reduced Ejection Fraction ◽  
Cell Type Composition ◽  
Type Composition ◽  
Underlying Mechanisms

AbstractHeart failure with reduced ejection fraction (HFrEF) constitutes 50% of HF hospitalizations and is characterized by high rates of mortality. To explore the underlying mechanisms of HFrEF etiology and progression, we studied the molecular and cellular differences in four chambers of non-failing (NF, n = 10) and HFrEF (n = 12) human hearts. We identified 333 genes enriched within NF heart subregions and often associated with cardiovascular disease GWAS variants. Expression analysis of HFrEF tissues revealed extensive disease-associated transcriptional and signaling alterations in left atrium (LA) and left ventricle (LV). Common left heart HFrEF pathologies included mitochondrial dysfunction, cardiac hypertrophy and fibrosis. Oxidative stress and cardiac necrosis pathways were prominent within LV, whereas TGF-beta signaling was evident within LA. Cell type composition was estimated by deconvolution and revealed that HFrEF samples had smaller percentage of cardiomyocytes within the left heart, higher representation of fibroblasts within LA and perivascular cells within the left heart relative to NF samples. We identified essential modules associated with HFrEF pathology and linked transcriptome discoveries with human genetics findings. This study contributes to a growing body of knowledge describing chamber-specific transcriptomics and revealed genes and pathways that are associated with heart failure pathophysiology, which may aid in therapeutic target discovery.

Abstract 12563: Retrospective Analysis of Cardiovascular Events With the Use of Immune Checkpoint Inhibitors

Circulation ◽  
2020 ◽  
Vol 142 (Suppl_3) ◽  
Author(s):  
Tushar Tarun ◽  
Brian P Bostick ◽  
Deepa Baswaraj ◽  
Nishchayjit Basra ◽  
Meeshal Khan ◽  
...  
Keyword(s):  
Heart Failure ◽  
Atrial Fibrillation ◽  
Retrospective Analysis ◽  
Immune Checkpoint ◽  
Immune Checkpoint Inhibitors ◽  
Checkpoint Inhibitors ◽  
Multiple Organ ◽  
Fulminant Myocarditis ◽  
Organ Systems ◽  
History Of

Introduction: Immune checkpoint inhibitors have emerged as a promising, novel therapy for multiple malignancies. Immune-related adverse reactions pose a serious concern with use of these agents and reportedly involve multiple organ systems, notably cardiotoxicity. Early identification and management of these adverse events is essential in the prevention of morbidity and mortality. Hypothesis: Immune checkpoint inhibitors cause multiple cardiotoxic effects, and patients with prior cardiac history have a higher likelihood of cardiotoxicity. Methods: 1. A retrospective analysis of 150 patients was performed who had received immunotherapy with either the cytotoxic T lymphocyte associated antigen 4 inhibitors (CTLA4) or with the programmed cell death inhibitors (PD1) or programmed death-ligand 1 (PD-L1) inhibitors for a period of two years at a Tertiary health Care from 7/1/2016-6/30/2018. 2. Patients' cardiac diagnoses prior to the initiation of therapy were noted and included, including history of heart failure, coronary artery disease, atrial fibrillation, and sudden cardiac arrest. 3. Patients’ clinic visits and hospitalizations with admitting and discharge diagnosis, electrocardiogram, echocardiogram, troponin T, and NT-proBNP were reviewed. Results: 6% of patients had new onset heart failure (both preserved and reduced), 1.3% had evidence of myocardial infarction, 2% had new atrial fibrillation with rapid ventricular rate, and 0.6% had fulminant myocarditis. Of patients with new cardiac events, 60% had a history of cardiac disease, which was significantly higher than in patients without (p< 0.05). There were no age or sex differences between the groups with and without cardiotoxicity. Conclusion: Immunotherapy with immune checkpoint inhibitors have broadened the horizon for treatment of multiple solid and hematological malignancies. Nonetheless, new adverse effects on multiple organ systems, specifically cardiac involvement, occur with these therapies, which are important and potentially detrimental toxicities. Patients with a history of prior cardiovascular disease have higher likelihood to develop cardiotoxicity.

scholarly journals Altered Hemodynamics and End-Organ Damage in Heart Failure

Circulation ◽  
2020 ◽  
Vol 142 (10) ◽  
pp. 998-1012 ◽  
Author(s):  
Frederik H. Verbrugge ◽  
Marco Guazzi ◽  
Jeffrey M. Testani ◽  
Barry A. Borlaug
Keyword(s):  
Heart Failure ◽  
Cardiac Myocyte ◽  
Organ Damage ◽  
Multiple Organ ◽  
Pulmonary Vascular Disease ◽  
Downstream Effects ◽  
Capillary Stress ◽  
Organ Systems ◽  
Patients With Heart Failure ◽  
Cardiac Filling

Heart failure is characterized by pathologic hemodynamic derangements, including elevated cardiac filling pressures (“backward” failure), which may or may not coexist with reduced cardiac output (“forward” failure). Even when normal during unstressed conditions such as rest, hemodynamics classically become abnormal during stressors such as exercise in patients with heart failure. This has important upstream and downstream effects on multiple organ systems, particularly with respect to the lungs and kidneys. Hemodynamic abnormalities in heart failure are affected by processes that extend well beyond the cardiac myocyte, including important roles for pericardial constraint, ventricular interaction, and altered venous capacity. Hemodynamic perturbations have widespread effects across multiple heart failure phenotypes, ranging from reduced to preserved ejection fraction, acute to chronic disease, and cardiogenic shock to preserved perfusion states. In the lung, hemodynamic derangements lead to the development of abnormalities in ventilatory control and efficiency, pulmonary congestion, capillary stress failure, and eventually pulmonary vascular disease. In the kidney, hemodynamic perturbations lead to sodium and water retention and worsening renal function. Improved understanding of the mechanisms by which altered hemodynamics in heart failure affect the lungs and kidneys is needed in order to design novel strategies to improve clinical outcomes.

scholarly journals The Cardioprotective Actions of Hydrogen Sulfide in Acute Myocardial Infarction and Heart Failure

Scientifica ◽  
2014 ◽  
Vol 2014 ◽  
pp. 1-8 ◽  
Author(s):  
David J. Polhemus ◽  
John W. Calvert ◽  
Javed Butler ◽  
David J. Lefer
Keyword(s):  
Myocardial Infarction ◽  
Heart Failure ◽  
Acute Myocardial Infarction ◽  
Hydrogen Sulfide ◽  
Ischemia Reperfusion Injury ◽  
Ischemia Reperfusion ◽  
Multiple Organ ◽  
Organ Systems ◽  
Myocardial Ischemia Reperfusion Injury ◽  
Myocardial Ischemia Reperfusion

It has now become universally accepted that hydrogen sulfide (H2S), previously considered only as a lethal toxin, has robust cytoprotective actions in multiple organ systems. The diverse signaling profile of H2S impacts multiple pathways to exert cytoprotective actions in a number of pathological states. This paper will review the recently described cardioprotective actions of hydrogen sulfide in both myocardial ischemia/reperfusion injury and congestive heart failure.

scholarly journals Suppression of Tumourigenicity 2 in Heart Failure With Preserved Ejection Fraction

2020 ◽  
Vol 6 ◽  
Author(s):  
Veronika Zach ◽  
Felix Lucas Bähr ◽  
Frank Edelmann
Keyword(s):  
Heart Failure ◽  
Ejection Fraction ◽  
Incidence Rates ◽  
Current Evidence ◽  
Ageing Population ◽  
Preserved Ejection Fraction ◽  
Reduced Ejection Fraction ◽  
Novel Biomarkers ◽  
Underlying Mechanisms ◽  
Receptor Family

Heart failure (HF), with steadily increasing incidence rates and mortality in an ageing population, represents a major challenge. Evidence suggests that more than half of all patients with a diagnosis of HF suffer from HF with preserved ejection fraction (HFpEF). Emerging novel biomarkers to improve and potentially guide the treatment of HFpEF are the subject of discussion. One of these biomarkers is suppression of tumourigenicity 2 (ST2), a member of the interleukin (IL)-1 receptor family, binding to IL-33. Its two main isoforms – soluble ST2 (sST2) and transmembrane ST2 (ST2L) – show opposite effects in cardiovascular diseases. While the ST2L/IL-33 interaction is considered as being cardioprotective, sST2 antagonises this beneficial effect by competing for binding to IL-33. Recent studies show that elevated levels of sST2 are associated with increased mortality in HF with reduced ejection fraction. Nevertheless, the significance of sST2 in HFpEF remains uncertain. This article aims to give an overview of the current evidence on sST2 in HFpEF with an emphasis on prognostic value, clinical association and interaction with HF treatment. The authors conclude that sST2 is a promising biomarker in HFpEF. However, further research is needed to fully understand underlying mechanisms and ultimately assess its full value.

scholarly journals Cardiorenal Syndrome Caused by Heart Failure with Preserved Ejection Fraction

2011 ◽  
Vol 2011 ◽  
pp. 1-7 ◽  
Author(s):  
Chiara Lazzeri ◽  
Serafina Valente ◽  
Roberto Tarquini ◽  
Gian Franco Gensini
Keyword(s):  
Heart Failure ◽  
Ejection Fraction ◽  
Venous Pressure ◽  
Renin Angiotensin System ◽  
Cardiorenal Syndrome ◽  
Preserved Ejection Fraction ◽  
Reduced Ejection Fraction ◽  
Patients With Heart Failure ◽  
Optimal Therapeutic Strategy

Since cardiorenal dysfunction is usually secondary to multiple factors acting in concert (and not only reduced cardiac output) in the present paper we are going to focus on the interrelationship between heart failure with normal ejection fraction and the development of cardiorenal syndrome. The coexistence of renal impairment in heart failure with preserved ejection fraction (CRS type 2 and 4) is common especially in older females with hypertension and/or diabetes. It can be hypothesized that the incidence of this disease association is growing, while clinical trials enrolling these patients are still lacking. The main mechanisms thought to be involved in the pathophysiology of this condition are represented by the increase of intra-abdominal and central venous pressure and the activation of the renin-angiotensin system. Differently from CRS in heart failure with reduced ejection fraction, the involvement of the kidney may be under-diagnosed in patients with heart failure and preserved ejection fraction and the optimal therapeutic strategy in this condition, though challenging, is far to be completely elucidated. Further studies are needed to assess the best therapeutic regimen in patients with renal dysfunction (and worsening) and heart failure and preserved ejection fraction.

scholarly journals MANAGING HEART FAILURE WITH REDUCED EJECTION FRACTION: WHAT TO KNOW?

2021 ◽  
Vol 54 (3) ◽  
pp. 205-206
Author(s):  
Tariq Ashraf ◽  
Muhammad Ishaq
Keyword(s):  
Heart Failure ◽  
Heart Disease ◽  
Ejection Fraction ◽  
American Heart Association ◽  
American Heart ◽  
Young Patients ◽  
Heart Association ◽  
Sglt2 Inhibitors ◽  
Reduced Ejection Fraction ◽  
Work Up

The estimated population of congestive heart failure (CHF) patients in Pakistan is 28 millions.1 Besides epidemics of type 2 diabetes mellitus and coronary heart disease, South Asian countries are also be at an increased risk of heart failure at earlier ages than other racial/ethnic groups.2 Heart failure sub classified into three categories: With preserved ejection fraction (LVEF>50%), Mid-range ejection fraction (LVEF41-49%), Reduced ejection fraction (LVEF<40%).3 According to studies in United States of American (USA) and United Kingdom (UK)4,5 heart failure with reduced ejection fraction (HFrEF) prevalence has increased due to ageing population, improved survival from myocardial infarction and high prevalence of co-morbid conditions like diabetes and obesity. With increasing number of young patients (<40 years) with acute myocardial infarction (AMI) 12%6 in our population, prevalence of heart failure with predisposing factors need to be explored. Other than diagnosing and work up of these patients, the most challenging part is the pharmacological treatment by therapeutic agents proven to reduce morbidity and mortality in HRrEF. Registries have shown under-usage of angiotensin-converting enzyme (ACE) inhibitors, angiotensin II receptor blockers (ARBs), angiotensin receptor-neprilysin inhibitor (ARNI), Beta-blockers and mineralocorticoid receptor antagonists (MRA) in such patients.7 Reason of not acheving the outcomes were due to not attaining the target levels of drugs dosages.8 With recommendations from new guidelines new novel drug therapies i.e. sodium-glucose cotransporter-2 (SGLT2) inhibitors, most debatable questions from the physicians are keeping in view the hemodynamic status and kidney function. Questions coming to the Physicians minds include;9 Should all guideline directed medical therapies be started together or stage wise? Which drugs should be titrated first? How quick can one up-titrate B-blockers and ARNI? At what level of kidney impairment should one stop ACE/ARB/ARNI/SGLT2 inhibitors? When should one refer these patients for cardiac resynchronization therapy device (CRTD) or Heart Transplantation? When should one repeat transesophageal echocardiography (TEE)? Physicians need to have clear answers and stance on the above queries. HFrEF is a major public health concern in our population especially with early onset of ischemic heart disease (IHD). Awareness, education and up to date knowledge regarding early diagnosis, work up and adjustments of drugs in such patients with proper follow up is important to reduce the ever rising morbidity and mortality in our population.   References Sheikh SA. Heart failure in Pakistan: A demographic survey. J Card Fail. 2006;12(8):S157. Martinez-Amezcua P, Haque W, Khera R, Kanaya AM, Sattar N, Lam CS, et al. The upcoming epidemic of heart failure in South Asia. Circ Heart Fail. 2020;13(10):e007218. Yancy CW, Jessup M, Bozkurt B, Butler J, Casey Jr DE, Colvin MM, et al. 2017 ACC/AHA/HFSA focused update of the 2013 ACCF/AHA guideline for the management of heart failure: a report of the American College of Cardiology/American Heart Association Task Force on Clinical Practice Guidelines and the Heart Failure Society of America. J Am Coll Cardiol. 2017;70(6):776-803. Virani SS, Alonso A, Benjamin EJ, Bittencourt MS, Callaway CW, Carson AP, et al. Heart disease and stroke statistics—2020 update: a report from the American Heart Association. Circulation. 2020;141(9):e139-596. Mozaffarian D, Benjamin EJ, Go AS, Arnett DK, Blaha MJ, Cushman M, et al. Heart disease and stroke statistics—2015 update: a report from the American Heart Association. Ccirculation. 2015;131(4):e29-322. Batra MK, Rizvi NH, Sial JA, Saghir T, Karim M. Angiographic Characteristics and in Hospital Outcome of Young Patients, Age Up to 40 Versus More Than 40 Years Undergoing Primary Percutaneous Coronary Intervention. J Pak Med Assoc. 2019;69(9):1308-12. Greene SJ, Butler J, Albert NM, DeVore AD, Sharma PP, Duffy CI, et al. Medical therapy for heart failure with reduced ejection fraction: the CHAMP-HF registry. J Am Coll Cardiol. 2018;72(4):351-66. Konstam MA, Neaton JD, Dickstein K, Drexler H, Komajda M, Martinez FA, et al. Effects of high-dose versus low-dose losartan on clinical outcomes in patients with heart failure (HEAAL study): a randomised, double-blind trial. Lancet. 2009;374(9704):1840-8. Murphy SP, Ibrahim NE, Januzzi JL. Heart failure with reduced ejection fraction: a review. JAMA. 2020;324(5):488-504.

Abstract 16393: In Hospital Outcomes and Prevalence of Comorbidities in Patients With Amyloidosis With and Without Atrial Fibrillation - Insight From National Inpatient Sample (nis) Database (2013-14)

Circulation ◽  
2020 ◽  
Vol 142 (Suppl_3) ◽  
Author(s):  
Asim Kichloo ◽  
Shakeel Jamal ◽  
Beth Bailey ◽  
muhammad shah zaib ◽  
HUH Virk ◽  
...  
Keyword(s):  
Heart Failure ◽  
Atrial Fibrillation ◽  
Cardiogenic Shock ◽  
Restrictive Cardiomyopathy ◽  
Multiple Organ ◽  
Bleeding Complications ◽  
National Inpatient Sample ◽  
Risk Of Mortality ◽  
Organ Systems ◽  
Increased Risk

Introduction: Amyloidosis is a systemic illness that affects multiple organ systems including cardiovascular, renal, gastrointestinal and pulmonary systems manifesting as restrictive cardiomyopathy, atrial and ventricular arrhythmias, nephrotic syndrome and gastrointestinal hemorrhage. Unknown is whether co-occurrence atrial fibrillation (AF), further worsens the outcomes in systemic amyloidosis. Hypothesis: Atrial Fibrillation worsen clinical outcomes in Amyloidosis. Methods: Patients with diagnosis of amyloidosis with and without concurrent AF were identified by querying the Healthcare Cost and Utilization (HCUP), specifically, National Inpatient Sample for year 2016 based on ICD10 codes. Results: During 2016, a total of 2997 patients were admitted with diagnosis of Amyloidosis, out of which 918 had concurrent AF. There was an increased risk of mortality (7.4% vs 5.6%), heart block (6.8% vs 2.8%), cardiogenic shock (5% vs 1.6%), placement of an ICD/CRT/PPM (14.5% vs 4.5%), renal failure (29% vs 21%), heart failure (66% vs 30%) and bleeding complications (5.7% vs 2.8%) in patients with diagnosis of Amyloidosis and concurrent AF when compared to patients with only diagnosis of Amyloidosis. It’s interesting to note that patients with amyloidosis without comorbid AF had increased risk of stroke when compared to concurrent AF (7.9% vs 3.4%). Conclusions: Concurrent AF increases the risk of heart failure, cardiogenic shock, supraventricular tachycardia, bleeding complications and an overall increase in mortality in patients with amyloidosis.

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