Abstract

Simple SummaryMultiple myeloma is a plasma cell disorder that accounts for around 10% of all haematological malignancies. This neoplasia is often associated with a significant prevalence of cardiovascular complications resulting from several factors, unrelated and/or related to the disease. Among cardiovascular complications, the high output heart failure is of great importance as it is related to a worse prognosis for patients. It is important to point out that, despite the availability of more and more numerous and effective drugs, myeloma remains an incurable disease, with frequent relapses and several treatment lines, with the need, therefore, for a careful evaluation of patients, especially from a cardiological point of view. For this reason, we are proposing a comprehensive overview of different pathogenetic mechanisms responsible for high output heart failure in multiple myeloma, including artero-venous shunts, enhanced angiogenesis, glutamminolysis, hyperammonemia and hemorheological alterations, with the belief that a multidisciplinary approach, in clinical evaluation is critical for the optimal management of the patient.The high output heart failure is a clinical condition in which the systemic congestion is associated to a high output state, and it can be observed in a non-negligible percentage of hematological diseases, particularly in multiple myeloma, a condition in which the risk of adverse cardiovascular events may increase, with a worse prognosis for patients. For this reason, though an accurate literature search, we provided in this review a complete overview of different pathogenetic mechanisms responsible for high output heart failure in multiple myeloma. Indeed, this clinical finding is present in the 8% of multiple myeloma patients, and it may be caused by artero-venous shunts, enhanced angiogenesis, glutamminolysis, hyperammonemia and hemorheological alterations with increase in plasma viscosity. The high output heart failure in multiple myeloma is associated with significant morbidity and mortality, emphasizing the need for a multidisciplinary approach.

Highlights

  • High output heart failure (HOHF) is a clinical condition in which the systemic congestion is associated with a high output state, and it is characterized, at rest, by a cardiac output greater than 8 L/min or a cardiac index > 3.9 L/min/m2 [1,2,3]

  • HOHF is a clinical condition characterized by a systemic congestion with a high output state

  • HOHF can be observed in different hematological diseases, including m. yeloma (MM), a plasma cell dyscrasia characterized by an increased risk of cardiovascular events, determined by both the disease itself and some specific drugs using treatment protocol

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Summary

Introduction

High output heart failure (HOHF) is a clinical condition in which the systemic congestion is associated with a high output state, and it is characterized, at rest, by a cardiac output greater than 8 L/min or a cardiac index > 3.9 L/min/m2 [1,2,3]. Congestive heart failure is a complex syndrome with several symptoms and signs, including dyspnea, increased fatigability, tachypnea, tachycardia, pulmonary rales, and peripheral edema This syndrome is associated with low cardiac output, but it may occur in several so-called. In patients with MM the incidence of venous thromboembolism varies from 3% to 10%, the possibility of congestive heart failure is around an average of 8% and those who have received steroid treatment and at least three different anti-MM therapies have arterial hypertension in 36% of cases Another noticeable complication during the treatment of these patients appears to be the presence of elongated QT on the ECG evaluation [5]. MMeetthhooddss uufassiiilnnuggWrWeaaeealnlcciisodosttnnmososufufullsslttptepeidedpecclMMeiiffiimEEccDDysseeLeLalaIIorNNrmcchEEha(”t(tPePe. ruruPmmbbaMsMps,,eeesrsddusu))ccwheheleleearacecssttrar““oolhhsnnioigiigccshhdcdroaoaeututeaatntbpbpeaauudsstteeicsscnaafftrorohddrreiiEaEarcncnegfgffealaliriiissellhuhunrcrlleaeea”n”nlgigaasuuntnadaodggf“e“ercceppaalaearrpdvpdeaieiaranrcscst fraeivluierwe sa/nadrtmiculelsti.pOlerimgiynealloamrtaic”l.ePs,arpeevrisewwse,rceaaslesorespcorretesn, ceadseinstehrieesreafnerdelnectetelrissttoofthreeleevdaitnotr from all years of publication have been reviewed

Artero-Venous Shunts
Enhanced Angiogenesis
Glutamminolysis and Hyperammonemia
Hemorheological Alterations
Findings
Conclusions
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