scholarly journals Systemic Consequences of Pulmonary Hypertension and Right-Sided Heart Failure

Circulation ◽  
2020 ◽  
Vol 141 (8) ◽  
pp. 678-693 ◽  
Author(s):  
Stephan Rosenkranz ◽  
Luke S. Howard ◽  
Mardi Gomberg-Maitland ◽  
Marius M. Hoeper
Keyword(s):  
Heart Failure ◽  
Pulmonary Hypertension ◽  
Structural Changes ◽  
Immune Cell ◽  
Organ Damage ◽  
Multiple Organ ◽  
Clinical Syndrome ◽  
Morbidity And Mortality ◽  
High Morbidity ◽  
Organ Systems

Pulmonary hypertension (PH) is a feature of a variety of diseases and continues to harbor high morbidity and mortality. The main consequence of PH is right-sided heart failure which causes a complex clinical syndrome affecting multiple organ systems including left heart, brain, kidneys, liver, gastrointestinal tract, skeletal muscle, as well as the endocrine, immune, and autonomic systems. Interorgan crosstalk and interdependent mechanisms include hemodynamic consequences such as reduced organ perfusion and congestion as well as maladaptive neurohormonal activation, oxidative stress, hormonal imbalance, and abnormal immune cell signaling. These mechanisms, which may occur in acute, chronic, or acute-on-chronic settings, are common and precipitate adverse functional and structural changes in multiple organs which contribute to increased morbidity and mortality. While the systemic character of PH and right-sided heart failure is often neglected or underestimated, such consequences place additional burden on patients and may represent treatable traits in addition to targeted therapy of PH and underlying causes. Here, we highlight the current state-of-the-art understanding of the systemic consequences of PH and right-sided heart failure on multiple organ systems, focusing on self-perpetuating pathophysiological mechanisms, aspects of increased susceptibility of organ damage, and their reciprocal impact on the course of the disease.

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 Levosimendan in pulmonary hypertension and right heart failure

2018 ◽  
Vol 8 (3) ◽  
pp. 204589401879090 ◽  
Author(s):  
Mona Sahlholdt Hansen ◽  
Asger Andersen ◽  
Jens Erik Nielsen-Kudsk
Keyword(s):  
Heart Failure ◽  
Pulmonary Hypertension ◽  
Right Ventricular ◽  
Current Knowledge ◽  
Right Heart Failure ◽  
Morbidity And Mortality ◽  
High Morbidity ◽  
Ventricular Failure ◽  
Right Heart ◽  
Pharmacodynamic Profile

Pulmonary hypertension is a multifactorial disease with a high morbidity and mortality. Right ventricular function is the most important predictor of morbidity and mortality in patients suffering from pulmonary hypertension, but currently there are no approved treatments directly supporting the failing right ventricle. Levosimendan is a calcium sensitizing agent with inotropic, pulmonary vasodilatory, and cardioprotective properties. Given its pharmacodynamic profile, levosimendan could be a potential novel agent for the treatment of right ventricular failure caused by pulmonary hypertension. The aim of this review is to provide an overview of the current knowledge on the effects of levosimendan in pulmonary hypertension and right heart failure.

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 The Diagnostic and Therapeutic Value of Multimarker Analysis in Heart Failure. An Approach to Biomarker-Targeted Therapy

2020 ◽  
Vol 7 ◽  
Author(s):  
Albert Topf ◽  
Moritz Mirna ◽  
Bernhard Ohnewein ◽  
Peter Jirak ◽  
Kristen Kopp ◽  
...  
Keyword(s):  
Heart Failure ◽  
Morbidity And Mortality ◽  
Therapeutic Interventions ◽  
Stress Axis ◽  
High Morbidity ◽  
Matrix Remodeling ◽  
Therapeutic Approaches ◽  
Therapeutic Setting ◽  
Therapeutic Value

Background: Heart failure is a pathophysiological state, which is still associated with high morbidity and mortality despite established therapies. Diverse well-known biomarkers fail to assess the variety of individual pathophysiology in the context of heart failure.Methods: An analysis of prospective, multimarker-specific therapeutic approaches to heart failure based on studies in current literature was performed. A total of 159 screened publications in the field of biomarkers in heart failure were hand-selected and found to be eligible for this study by a team of experts.Results: Established biomarkers of the inflammatory axis, matrix remodeling, fibrosis and oxidative stress axis, as well as potential therapeutic interventions were investigated. Interaction with end organs, such as cardio-hepatic, cardio-renal and cardio-gastrointestinal interactions show the complexity of the syndrome and could be of further therapeutic value. MicroRNAs are involved in a wide variety of physiologic and pathophysiologic processes in heart failure and could be useful in diagnostic as well as therapeutic setting.Conclusion: Based on our analysis by a biomarker-driven approach in heart failure therapy, patients could be treated more specifically in long term with a consideration of different aspects of heart failure. New studies evaluating a multimarker – based therapeutic approach could lead in a decrease in the morbidity and mortality of heart failure patients.

scholarly journals Neurological, neuropsychiatric and neurodevelopmental complications of COVID-19

2020 ◽  
pp. 000486742096147
Author(s):  
Christos Pantelis ◽  
Mahesh Jayaram ◽  
Anthony J Hannan ◽  
Robb Wesselingh ◽  
Jess Nithianantharajah ◽  
...  
Keyword(s):  
Organ Damage ◽  
Multiple Organ ◽  
Global Pandemic ◽  
Organ Systems ◽  
Future Challenges ◽  
The Central Nervous System ◽  
The Impact ◽  
Collaborative Efforts ◽  
The Brain

Although COVID-19 is predominantly a respiratory disease, it is known to affect multiple organ systems. In this article, we highlight the impact of SARS-CoV-2 (the coronavirus causing COVID-19) on the central nervous system as there is an urgent need to understand the longitudinal impacts of COVID-19 on brain function, behaviour and cognition. Furthermore, we address the possibility of intergenerational impacts of COVID-19 on the brain, potentially via both maternal and paternal routes. Evidence from preclinical models of earlier coronaviruses has shown direct viral infiltration across the blood–brain barrier and indirect secondary effects due to other organ pathology and inflammation. In the most severely ill patients with pneumonia requiring intensive care, there appears to be additional severe inflammatory response and associated thrombophilia with widespread organ damage, including the brain. Maternal viral (and other) infections during pregnancy can affect the offspring, with greater incidence of neurodevelopmental disorders, such as autism, schizophrenia and epilepsy. Available reports suggest possible vertical transmission of SARS-CoV-2, although longitudinal cohort studies of such offspring are needed. The impact of paternal infection on the offspring and intergenerational effects should also be considered. Research targeted at mechanistic insights into all aspects of pathogenesis, including neurological, neuropsychiatric and haematological systems alongside pulmonary pathology, will be critical in informing future therapeutic approaches. With these future challenges in mind, we highlight the importance of national and international collaborative efforts to gather the required clinical and preclinical data to effectively address the possible long-term sequelae of this global pandemic, particularly with respect to the brain and mental health.

scholarly journals Severe Acute Respiratory Syndrome Coronavirus 2, COVID-19, and the Renin-Angiotensin System

Hypertension ◽  
2020 ◽  
Vol 76 (5) ◽  
pp. 1350-1367 ◽  
Author(s):  
Matthew A. Sparks ◽  
Andrew M. South ◽  
Andrew D. Badley ◽  
Carissa M. Baker-Smith ◽  
Daniel Batlle ◽  
...  
Keyword(s):  
Severe Acute Respiratory Syndrome ◽  
Renin Angiotensin System ◽  
Organ Damage ◽  
Experimental Models ◽  
Multiple Organ ◽  
Host Cells ◽  
Ang Ii ◽  
Angiotensin System ◽  
Renin Angiotensin ◽  
Organ Systems

The coronavirus disease 2019 (COVID-19) pandemic is associated with significant morbidity and mortality throughout the world, predominantly due to lung and cardiovascular injury. The virus responsible for COVID-19—severe acute respiratory syndrome coronavirus 2—gains entry into host cells via ACE2 (angiotensin-converting enzyme 2). ACE2 is a primary enzyme within the key counter-regulatory pathway of the renin-angiotensin system (RAS), which acts to oppose the actions of Ang (angiotensin) II by generating Ang-(1–7) to reduce inflammation and fibrosis and mitigate end organ damage. As COVID-19 spans multiple organ systems linked to the cardiovascular system, it is imperative to understand clearly how severe acute respiratory syndrome coronavirus 2 may affect the multifaceted RAS. In addition, recognition of the role of ACE2 and the RAS in COVID-19 has renewed interest in its role in the pathophysiology of cardiovascular disease in general. We provide researchers with a framework of best practices in basic and clinical research to interrogate the RAS using appropriate methodology, especially those who are relatively new to the field. This is crucial, as there are many limitations inherent in investigating the RAS in experimental models and in humans. We discuss sound methodological approaches to quantifying enzyme content and activity (ACE, ACE2), peptides (Ang II, Ang-[1–7]), and receptors (types 1 and 2 Ang II receptors, Mas receptor). Our goal is to ensure appropriate research methodology for investigations of the RAS in patients with severe acute respiratory syndrome coronavirus 2 and COVID-19 to ensure optimal rigor and reproducibility and appropriate interpretation of results from these investigations.

scholarly journals Correlation of lateral placental location with development of preeclampsia

2020 ◽  
Vol 9 (3) ◽  
pp. 1017
Author(s):  
Anjali Gupta ◽  
Priyanka Bansal ◽  
Jyotsna Sen ◽  
Savita Rani Singhal
Keyword(s):  
Prospective Observational Study ◽  
Previous History ◽  
Antenatal Clinic ◽  
Severe Anaemia ◽  
Multiple Organ ◽  
Clinical Syndrome ◽  
Chronic Hypertension ◽  
Singleton Pregnancy ◽  
Organ Systems ◽  
History Of

Background: Preeclampsia is a complex clinical syndrome which involves multiple organ systems and remains the principle cause of maternal and perinatal morbidity and mortality. Preeclampsia is a disease of trophoblastic tissue. Placental abnormality is one of the initial events in patients who are destined to develop pregnancy induced hypertension subsequently. Objective of this study was to evaluate the association of laterally located placenta on ultrasound with development of preeclampsia.Methods: This prospective observational study was conducted on 200 antenatal women with singleton pregnancy at 18-24 weeks of gestation who attended antenatal clinic of obstetrics and gynaecology, PGIMS Rohtak from October 2017 to October 2018. Detailed antenatal transabdominal ultrasound along with placental location was done between 18-24 weeks of gestation in women who fitted into inclusion criteria. All the antenatal women belonged to 18-24 weeks of gestation were included in the study except those women with chronic hypertension, diabetes mellitus, renal disease, severe anaemia, thyrotoxicosis, low lying placenta, previous history of preeclampsia or eclampsia.Results: Out of 200 antenatal women, 84 had lateral placenta while 116 had central placenta. Out of these 84 women who had lateral placenta, 55 women (65.5%) developed preeclampsia and out of 116 (58%) women who had central placenta, 28 women (24.1%) developed preeclampsia.Conclusions: From the above study, we concluded that women with laterally located placenta by ultrasound at 18-24 weeks of gestation have greater risk of developing preeclampsia.

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.

The place of beta-adrenoreceptor-blocking drugs in the treatment of congestive heart failure in elderly people: review of current opinion

1998 ◽  
Vol 8 (1) ◽  
pp. 89-92
Author(s):  
L Woosnam ◽  
M Hasan
Keyword(s):  
Heart Failure ◽  
Congestive Heart Failure ◽  
Angiotensin Converting Enzyme ◽  
Elderly People ◽  
Ace Inhibitors ◽  
Survival Benefit ◽  
Clinical Syndrome ◽  
Morbidity And Mortality ◽  
Converting Enzyme ◽  
Current Opinion

The clinical syndrome of heart failure affects more than 1% of the population, and its prevalence increases steeply with advancing age, especially after 75, where it reaches approximately 10%. It is one of the commonest reasons for the admission of elderly people to hospital.Despite recent advances in treatment of heart failure with angiotensin-converting enzyme (ACE) inhibitors, which were proven to provide survival benefit, the rates of morbidity and mortality from heart failure remain high, and new therapeutic strategie s are needed.

[PP.27.14] PHEOCHROMOCYTOMA PRESENTED WITH ACUTE HEART FAILURE AND MULTIPLE ORGAN DAMAGE

2017 ◽  
Vol 35 ◽  
pp. e315
Author(s):  
I. Papadakis ◽  
M. Velegraki ◽  
P. Ioannou ◽  
V. Theodorakopoulou
Keyword(s):  
Heart Failure ◽  
Acute Heart Failure ◽  
Organ Damage ◽  
Multiple Organ
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