Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0018801 (heart failure)
72,216 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The use of colloids in hypo-oncotic individuals to increase plasma volume has been shown to have distinct and consistent advantages compared with the use of crystalloid fluids. Colloids increase plasma colloid oncotic pressure, whereas crystalloids decrease it, an effect that can be extremely detrimental in individuals with low basal plasma colloid oncotic pressure. Increasing plasma volume in hypo-oncotic individuals without inducing large increases in interstitial water content is difficult when crystalloid fluids are used. However, colloids have much better plasma volume expansion ability without the induction of concurrent increases in interstitial water content, even in hypooncotic individuals. Review of the literature indicates that hetastarch is an extremely safe colloid for acute and long-term use in humans and dogs. Its excellent safety record probably is attributable to its structural analogy to the natural compound glycogen. The lack of availability of a substance analogous to human 5% serum albumin and the scarcity of plasma in veterinary medicine leaves hetastarch as the safest option of available colloids. Its ability to increase plasma volume and colloid oncotic pressure is equal to or better than dextran 70 and 5% albumin and is clearly better than plasma or whole blood. Increases in plasma volume and colloid oncotic pressure usually last approximately 48 hours after a single injection, but the duration of increases significantly after multiple infusions. Contraindications to its use include heart failure and oliguric renal failure, because of its excellent ability to increase plasma volume, and the presence of von Willebrand's disease, because of its ability to significantly lower all components of Factor VIII-related complex in humans.
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PMID:The use of hetastarch for plasma expansion. 128 53

Many acquired risk factors may be identified to avoid the scholarly nature of these interminable lists, they may be reclassified with respect to their originality or their mechanism of action and those of current interest, whose data is still often hypothetical but recent, can be underlined. The following order may be proposed: risk factors which cannot be changed: age (which remains the principal factor) and gender (women being at higher risk than men); true acquired risk factors such as cancer, dysimmune conditions (more specifically, the antiphospholipid syndrome) and hormone replacement therapy (oestroprogestative contraception which has been updated by the debate about "third generation pills" and the risk related to progesterone-like substances themselves; hormone replacement therapy of the menopause which still has no clinical trials to assess "our" forms with natural hormones administered transdermally or transmucosally). Smoking has also been accused of being a risk factor for venous thrombosis in the latest clinical trials. Metabolic factors increase the risk of thrombosis: this is established for obesity, still suspected for hyperhomocystonaemia, the abnormalities being the result of complex gene-environment interactions. Other dysmetabolic conditions (diabetes, hypercholesterolaemia, hypertriglyceridaemia), responsible for arterial complications, are not clearly related to increased venous thromboembolic risk although a preventive effect of statins (yet another I) has just been reported. Similarly to these metabolic factors, the origin of which, genetic or environmental, is difficult to establish, interest has recently been shown in quantitative and functional changes in blood clotting factors. This has been established for arterial disease for fibrinogen but, in addition to this factor which slightly increases the risk of venous thrombosis, increases of factor VIII independent of inflammatory conditions, of blood group and Von Willebrand factor, which all influence the level of factor VIII, an increase by 150% of the normal increases the risk of venous thromboembolic disease by 3 or 4 times. As for factor VIII, increases in factor IX, factor XI, and resistance to activated C protein (independently of the Leiden mutation on the gene for factor V), are also associated in increased venous thromboembolic risk. Without knowing into which category to classify them, previous personal and family history of thromboembolic disease, in the absence of the already mentioned hereditary risk factors, must be noted. Finally, amongst the acquired risk factors, the authors also list conditions of blood stasis and vascular lesions with or without hypercoagulability (surgery, prolonged hospital stays, cardiac failure, paralysis, pregnancy...). Of these acquired conditions which increase the risk of thrombotic complications, particular attention has been given over the last few years to forced immobilisation in uncomfortable positions as in certain forms of transport. Although clinical reports have discordant results, it would seem that the risk is increased and the benefits of supportive elastic stockings have been confirmed. If the acquired risk is identified and quantified for a patient, it allows evaluation of global risk and the installation of appropriate therapeutic measures.
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PMID:[Venous thromboembolic pathology. New acquired risk factors or new data on acquired risk factors]. 1179 76

Arginine vasopressin (AVP), also known as vasopressin or anti-diuretic hormone, is a neuropeptide produced in the hypothalamus. It is primarily responsible for osmoregulation and thus maintains body fluid homeostasis. It is also a potent vasoconstrictor, may have a role in higher cognitive functions and affects metabolism. All the biological and cellular effects of vasopressin are mediated by the interaction of this hormone with three G-protein-coupled receptors - V(1a), V(1b) and V(2).Urological applications are based on the rationale that V(2) receptors mediate water conservation and increase urine osmolality. Due to their anti-diuretic properties mediated by the V(2) receptors, synthetic vasopressin agonists, such as desmopressin, are now commonly used for the treatment of nocturnal polyuria, central diabetes insipidus and nocturnal enuresis and potentially in urinary incontinence. Desmopressin has been licenced worldwide for haematological indications of haemophilia and von Willebrand disease. Vasopressin receptor antagonists correct hyponatremia by blocking the activation of the V(2) receptor and induce a free water diuresis without an accompanying natriuresis or kaliuresis; an effect termed 'aquaresis'. Interfering with vasopressin signalling by administering vasopressin antagonists may have clinical benefits in acute and chronic heart failure.
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PMID:Vasopressin receptors in voiding dysfunction. 2129 Feb 39

Axial-flow LVADs have become an integral tool in the management of end-stage heart failure. Consequently, nonsurgical bleeding has emerged as a major source of morbidity and mortality in this fragile population. The mechanisms responsible for these adverse events include acquired von Willebrand disease, GI tract angiodysplasia formation, impaired platelet aggregation, and overuse of anticoagulation therapy. Because of ongoing concerns for pump thrombosis and thromboembolic events, the thrombotic/bleeding paradigm has led to a difficult clinical dilemma for those managing patients treated with axial flow LVADs. As the field progresses, advances in the understanding of the pathological mechanisms underlying bleeding/thrombosis risk, careful risk stratification, and potential use of novel anticoagulants will all play a role in the management of the LVAD patient.
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PMID:Mechanisms of bleeding and approach to patients with axial-flow left ventricular assist devices. 2317 24

Continuous-flow left ventricular assist device (CF-LVAD) insertion is a life-saving procedure that is being increasingly used in patients with advanced heart failure. However, patients with CF-LVADs are at an increased risk of gastrointestinal bleeding (GIB). Bleeding can occur anywhere in the GI tract with lesions being more prevalent in the upper GI tract than in the lower GI tract. The pathophysiology of GIB in patients with CF-LVADs is unique and likely involves three synergistic mechanisms-coagulopathy, acquired von Willebrand disease and continuous non-pulsatile blood flow. Management strategies vary depending on the presentation and site of bleeding. Prevention strategies to prevent GIB in these patients include low pump speed, close hemodynamic monitoring and a low threshold for endoscopy. We aim to review in detail the pathophysiology, management, complications and preventive strategies in patients with CF-LVAD who present with GIB.
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PMID:Gastrointestinal bleeding with continuous-flow left ventricular assist devices. 2561 35

Continuous-flow left ventricular assist devices (CF-LVADs) have become an integral component of the management in patients with advanced heart failure, serving as destination therapy or as a bridge to heart transplantation. Despite significant advances in the design and longevity of the device, the ongoing risk for bleeding remains a significant concern. The genesis of gastrointestinal bleeding (GIB) in patients with CF-LVADs is likely multifactorial and may include components of acquired von Willebrand disease, angiodysplasia, and gastrointestinal arteriovenous malformations, as well as additional risk factors such as history of GIB and increased age. Several pharmacotherapy options have been used, but the data surrounding their overall efficacy remain sparse. The necessity for larger prospective studies is essential to further advance the management of this devastating complication. Within this review, we discuss the known pathophysiologic process of CF-LVAD-related GIB and highlight the therapeutic options discussed within the literature. In addition, we discuss potential therapeutic options based on mechanisms of action as they correlate to known pathophysiologic processes of CF-LVAD-related GIB. Finally, we provide recommendations for constructing drug therapy regimens in patients with CF-LVADs who develop GIB.
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PMID:Pharmacotherapeutic Management of Gastrointestinal Bleeding in Patients with Continuous-Flow Left Ventricular Assist Devices. 2883 32

Heart failure affects over 5 million Americans, with numbers expected to rise. While heart transplantation is the most effective long-term strategy for end-stage heart failure, there is a limited cardiac donor pool, and these organs are often unavailable at the time of need. Left ventricular assist devices, therefore, continue to be used to bridge this gap. Originally implanted as a bridge to transplant, these devices are now additionally utilized as destination therapy for patients ineligible for transplant. With the widespread applicability of these devices for not just temporary measures, but also for prolonged use, the short- and long-term impact on other organ systems has become more evident. For example, gastrointestinal (GI) bleeding, with an incidence approaching 30%, is one such complication post-continuous-flow left ventricular assist device implantation. This high incidence of GI bleeding is thought to stem from a combination of factors, including the need for concomitant anticoagulant and antiplatelet therapy, and intrinsic device-related properties resulting in acquired Von Willebrand disease and arteriovenous malformations. Due to the significant morbidity associated with these GI bleeding events, a standardized protocol optimizing medical and endoscopic management, alongside close coordination between the gastroenterology and cardiology services, should be advocated for and ultimately employed.
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PMID:The Predicament of Gastrointestinal Bleeding in Patients With a Continuous-Flow Left Ventricular Assist Device: Pathophysiology, Evaluation, and Management. 3036 5

Introduction: The revised Ghent nosology presents the classical features of Marfan syndrome. However, behind its familiar face, Marfan syndrome hides less well-known features.Areas covered: The German Marfan Organization listed unusual symptoms and clinical experts reviewed the literature on clinical features of Marfan syndrome not listed in the Ghent nosology. Thereby we identified the following features: (1) bicuspid aortic valve, mitral valve prolapse, pulmonary valve prolapse, tricuspid valve prolapse, (2) heart failure and cardiomyopathy, (3) supraventricular arrhythmia, ventricular arrhythmia, and abnormal repolarization, (4) spontaneous coronary artery dissection, anomalous coronary arteries, and atherosclerotic coronary artery disease, tortuosity-, aneurysm-, and dissection of large and medium-sized arteries, (5) restrictive lung disease, parenchymal lung disease, and airway disorders, (6) obstructive- and central sleep apnea, (7) liver and kidney cysts, biliary tract disease, diaphragmatic hernia, and adiposity, (8) premature labor, and urinary incontinence, (9) myopathy, reduced bone mineral density, and craniofacial manifestations, (10) atrophic scars, (11) caries, and craniomandibular dysfunction, (12) headache from migraine and spontaneous cerebrospinal fluid leakage, (13) cognitive dysfunction, schizophrenia, depression, fatigue, and pain, (14) and activated fibrinolysis, thrombin, platelets, acquired von Willebrand disease, and platelet dysfunction.Expert commentary: Future research, nosologies, and guidelines may consider less well-known features of Marfan syndrome.
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PMID:Features of Marfan syndrome not listed in the Ghent nosology - the dark side of the disease. 3182 51

Heart failure affects more than 30 million people worldwide and its prevalence is constantly rising. In 2020, heart transplantation is the only curative treatment, but left ventricular assistance devices (LVADs) are fully integrated into the decision algorithm for management of patients with advanced heart failure, with more than 20,000 devices implanted worldwide in the last decade. Intended to support cardiac output, LVADs remove the blood from the left ventricle and eject it into the proximal aorta. Whereas first-generation LVADs were pulsatile, second- and third-generation LVADs are more reliable, but create a laminar flow, with reduced (or absent) blood flow pulsatility. Concomitantly, several new adverse events, some of them lethal, appeared when continuous-flow LVADs started to be implanted, including acquired von Willebrand disease, gastrointestinal bleeding and aortic valve fusion or regurgitation. This review aims to apply models describing pulsatility (such as the Windkessel effect applied by Frank, Guyton's continuity model of venous return and Sunagawa's left ventricular-arterial coupling) to LVADs, to better understand the physiopathology in patients using continuous-flow devices. This review also covers the means of exploring pulsatility and adverse events associated with a reduction in pulsatility, as well as the possible ways for restoring pulsatility in patients implanted with an LVAD.
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PMID:Pulsatility in ventricular assistance devices: A translational review focused on applied haemodynamics. 3265 40

Advancements in the design and functionality of continuous flow left ventricular assist devices (CF-LVADs), as well as a limited number of donor hearts, have resulted in an increased utilization of this therapy among advanced heart failure (HF) patients. Despite these advancements, gastrointestinal bleeding (GIB) remains a common complication after CF-LVAD implantation. The mechanism of GIB in these patients is complex and includes a combination of angiodysplasia, platelet dysfunction, acquired von Willebrand disease, and a variety of patient-specific factors including advanced age and history of GIB. Several pharmacotherapy options have been reported in the literature, though studies supporting the use of these agents are often small, retrospective reports. Within this review, we discuss the various pharmacologic agents, their proposed mechanisms of action, and the available literature pertaining to their effectiveness and tolerability. Additionally, we propose an evidence-based treatment algorithm, encompassing the updated literature, cost of therapy, medication side effects, and ease of administration.
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PMID:A reappraisal of the pharmacologic management of gastrointestinal bleeding in patients with continuous flow left ventricular assist devices. 3287 Apr 36


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