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Current Cardiology Reviews

Editor-in-Chief

ISSN (Print): 1573-403X
ISSN (Online): 1875-6557

General Review Article

High-output Cardiac Failure: A Forgotten Phenotype in Clinical Practice

Author(s): Diane Xavier de Ávila*, Humberto Villacorta, Wolney de Andrade Martins and Evandro Tinoco Mesquita

Volume 18, Issue 1, 2022

Published on: 05 August, 2021

Article ID: e050821195319 Pages: 7

DOI: 10.2174/1573403X17666210805142010

Price: $65

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Abstract

Introduction: The knowledge on High-Output Cardiac Failure (HOCF) has greatly improved in the last two decades. One of the advances was the identification of a new phenotype of HOCF, characterized by the absence of ventricular dilation, already associated with liver disease, Arteriovenous Fistulas (AVF), lung disease, myelodysplastic syndromes, and obesity. However, it has been noted that any aetiology can present with one of the two phenotypes, depending on the evolution.

Objective: The study aims to describe, through an integrative review, the physiopathology and aetiologies of HOCF and to discuss phenotypes associated with this condition.

Methods: Revisions, guidelines, case-controls, cohort studies and clinical studies were searched in MEDLINE and LILACS, using the connectives in the “cardiac output, high” database (MeSH Terms) OR “high cardiac output” (All Fields).

Discussion: Two distinct phenotypes are currently described in the HOCF, regardless of the aetiology: 1) one with enlarged cardiac chambers; and 2) with normal heart chambers. The mechanisms related to HOCF are vasodilation, arteriovenous shunts that cause increased microvascular density, Reduced Systemic Vascular Resistance (RSVR), and high metabolism. These mechanisms lead to activation of the renin-angiotensin-aldosterone system, sodium and water retention, activation of neprilysin, of the sodium-glucose-2 transporter, which promote interstitial fibrosis, ventricular remodeling and a consequent increase in cardiac output >8L/min.

Conclusion: Many aetiologies of HOCF have been described, and some of them are potentially curable. Prompt recognition of this condition and proper treatment may lead to better outcomes.

Keywords: High output cardiac failure, reduced systemic vascular resistance, heart failure, ventricular dilation, arteriovenous fistulas, metabolism.

Graphical Abstract
[1]
Jain CC, Borlaug BA. Hemodynamic assessment in heart failure. Catheter Cardiovasc Interv 2020; 95(3): 420-8.
[http://dx.doi.org/10.1002/ccd.28490] [PMID: 31507065]
[2]
Reddy YNV, Melenovsky V, Redfield MM, Nishimura RA, Borlaug BA. High-output heart failure: A 15-Year Experience. J Am Coll Cardiol 2016; 68(5): 473-82.
[http://dx.doi.org/10.1016/j.jacc.2016.05.043] [PMID: 27470455]
[3]
Mehta PA, Dubrey SW. High output heart failure. QJM 2009; 102(4): 235-41.
[http://dx.doi.org/10.1093/qjmed/hcn147] [PMID: 18990720]
[4]
Anand IS, Florea VG. High output cardiac failure. Curr treat options cardio med 2001; 151-9.
[5]
Anand IS. High-output heart failure revisited. J Am Coll Cardiol 2016; 68(5): 483-6.
[http://dx.doi.org/10.1016/j.jacc.2016.05.036] [PMID: 27470456]
[6]
Reutershan J, Kapp T, Unertl K, Fretschner R. [Noninvasive determination of cardiac output in ventilated patients. Clinical evaluation of a simplified quick method]. Anaesthesist 2003; 52(9): 778-86.
[http://dx.doi.org/10.1007/s00101-003-0547-2] [PMID: 14504803]
[7]
Moxon D, Pinder M, van Heerden PV, Parsons RW. Clinical evaluation of the hemosonic monitor in cardiac surgical patients in the ICU. Anaesth Intensive Care 2003; 31(4): 408-11.
[http://dx.doi.org/10.1177/0310057X0303100410] [PMID: 12973965]
[8]
Werawatganon T, Punyatavorn S, Chatkaew P, Bunburaphong P. Validity and reliability of cardiac output by arterial thermodilution and arterial pulse contour analysis compared with pulmonary artery thermodilution in intensive care unit. J Med Assoc Thai 2003; 86(Suppl. 2): S323-30.
[PMID: 12930006]
[9]
Gonzalez J, Delafosse C, Fartoukh M, et al. Comparison of bedside measurement of cardiac output with the thermodilution method and the fick method in mechanically ventilated patients. Crit Care 2003; 7(2): 171-8.
[http://dx.doi.org/10.1186/cc1848] [PMID: 12720564]
[10]
Fattori A, Oliveira DC, Castilho RF, Coelho OR. Sickle-cell anemia and latent diastolic dysfunction: Echocardiographic alterations. Arq Bras Cardiol 2015; 104(4): e30-3.
[http://dx.doi.org/10.5935/abc.20150027] [PMID: 25993599]
[11]
Mehari A, Alam S, Tian X, et al. Hemodynamic predictors of mortality in adults with sickle cell disease. Am J Respir Crit Care Med 2013; 187(8): 840-7.
[http://dx.doi.org/10.1164/rccm.201207-1222OC] [PMID: 23348978]
[12]
Detterich JA, Sangkatumvong S, Kato R, et al. Patients with sickle cell anemia on simple chronic transfusion protocol show sex differences for hemodynamic and hematologic responses to transfusion. Transfusion 2013; 53(5): 1059-68.
[http://dx.doi.org/10.1111/j.1537-2995.2012.03961.x] [PMID: 23176402]
[13]
Martins WdeA, Lopes HF, Consolim-Colombo FM, Gualandro SdeF, Arteaga-Fernández E, Mady C. Cardiovascular autonomic dysfunction in sickle cell anemia. Auton Neurosci 2012; 166(1-2): 54-9.
[http://dx.doi.org/10.1016/j.autneu.2011.07.011] [PMID: 21868290]
[14]
Martins WA, Mesquita ET, Cunha DM, Pinheiro LAF, Pareto RC Junior, Romeo JLM. Estudo ecodopplercardiográfico em adolescentes e adultos jovens portadores de anemia falciforme. Arq Bras Cardiol 1999; 73(6): 463-8.
[PMID: 10904267]
[15]
Gabrielli A, Caruso L, Stacpoole PW. Early recognition of acute cardiovascular beriberi by interpretation of hemodynamics. J Clin Anesth 2001; 13(3): 230-8.
[http://dx.doi.org/10.1016/S0952-8180(01)00246-X] [PMID: 11377164]
[16]
Akpan T, Peschard S, Brinkane AH, Bergheul S, Leroy-Terquem E, Levy R. Right heart failure caused by thiamine deficiency (cardiac beriberi). Presse Med 2000; 29(5): 240-1.
[PMID: 10701400]
[17]
Lozano HF, Sharma CN. Reversible pulmonary hypertension, tricuspid regurgitation and right-sided heart failure associated with hyperthyroidism: case report and review of the literature. Cardiol Rev 2004; 12(6): 299-305.
[http://dx.doi.org/10.1097/01.crd.0000137259.83169.e3] [PMID: 15476566]
[18]
Fazio S, Palmieri EA, Lombardi G, Biondi B. Effects of thyroid hormone on the cardiovascular system. Recent Prog Horm Res 2004; 59: 31-50.
[http://dx.doi.org/10.1210/rp.59.1.31] [PMID: 14749496]
[19]
Riaz K, Forker AD, Isley WL, Hamburg MS, McCullough PA. Hyperthyroidism: a “curable” cause of congestive heart failure-three case reports and a review of the literature. Congest Heart Fail 2003; 9(1): 40-6.
[http://dx.doi.org/10.1111/j.1527-5299.2003.01124.x] [PMID: 12556677]
[20]
Zhai AB, Haddad H. The impact of obesity on heart failure. Curr Opin Cardiol 2017; 32(2): 196-202.
[http://dx.doi.org/10.1097/HCO.0000000000000370] [PMID: 28092289]
[21]
Alpert MA, Karthikeyan K, Abdullah O, Ghadban R. Obesity and cardiac remodeling in adults: Mechanisms and clinical implications. Prog Cardiovasc Dis 2018; 61(2): 114-23.
[http://dx.doi.org/10.1016/j.pcad.2018.07.012] [PMID: 29990533]
[22]
Singer GM, Setaro JF. Secondary hypertension: Obesity and the metabolic syndrome. J Clin Hypertens (Greenwich) 2008; 10(7): 567-74.
[http://dx.doi.org/10.1111/j.1751-7176.2008.08178.x] [PMID: 18607142]
[23]
Upadhya B, Amjad A, Stacey RB. Optimizing the management of obese hfpef phenotype: Can we mind both the heart and the kidney? J Card Fail 2020; 26(2): 108-11.
[http://dx.doi.org/10.1016/j.cardfail.2019.11.018] [PMID: 31759161]
[24]
Packer M, Kitzman DW. Obesity-related heart failure with a preserved ejection fraction: The mechanistic rationale for combining inhibitors of aldosterone, neprilysin, and sodium-glucose cotransporter-2. JACC Heart Fail 2018; 6(8): 633-9.
[http://dx.doi.org/10.1016/j.jchf.2018.01.009] [PMID: 29525327]
[25]
Packer M. Leptin-aldosterone-neprilysin axis: Identification of its distinctive role in the pathogenesis of the three phenotypes of heart failure in people with obesity. Circulation 2018; 137(15): 1614-31.
[http://dx.doi.org/10.1161/CIRCULATIONAHA.117.032474] [PMID: 29632154]
[26]
Trivedi T, Liu J, Probst J, Merchant A, Jhones S, Martin AB. Obesity and obesity-related behaviors among rural and urban adults in the USA. Rural Remote Health 2015; 15(4): 3267.
[PMID: 26458564]
[27]
Madamanchi C, Alhosaini H, Sumida A, Runge MS. Obesity and natriuretic peptides, BNP and NT-proBNP: mechanisms and diagnostic implications for heart failure. Int J Cardiol 2014; 176(3): 611-7.
[http://dx.doi.org/10.1016/j.ijcard.2014.08.007] [PMID: 25156856]
[28]
Oatmen KE, Cull E, Spinale FG. Heart failure as interstitial cancer: Emergence of a malignant fibroblast phenotype. Nat Rev Cardiol 2019.
[http://dx.doi.org/10.1038/s41569-019-0286-y] [PMID: 31686012]
[29]
Brandt MM, Nguyen ITN, Krebber MM, et al. Limited synergy of obesity and hypertension, prevalent risk factors in onset and progression of heart failure with preserved ejection fraction. J Cell Mol Med 2019; 23(10): 6666-78.
[http://dx.doi.org/10.1111/jcmm.14542] [PMID: 31368189]
[30]
Park C, Fraser A, Howe LD, et al. Elevated blood pressure in adolescence is attributable to a combination of elevated cardiac output and total peripheral resistance. Hypertension 2018; 72(5): 1103-8.
[http://dx.doi.org/10.1161/HYPERTENSIONAHA.118.11925] [PMID: 30354820]
[31]
Sheriff DD. Role of mechanical factors in governing muscle blood flow. Acta Physiol (Oxf) 2010; 199(4): 385-91.
[http://dx.doi.org/10.1111/j.1748-1716.2010.02120.x] [PMID: 20345413]
[32]
Parameswaran K, Todd DC, Soth M. Altered respiratory physiology in obesity. Can Respir J 2006; 13(4): 203-10.
[http://dx.doi.org/10.1155/2006/834786] [PMID: 16779465]
[33]
Burke RM, Lighthouse JK, Mickelsen DM, Small EM. Sacubitril/valsartan decreases cardiac fibrosis in left ventricle pressure overload by restoring pkg signaling in cardiac fibroblasts. Circ Heart Fail 2019; 12(4): e005565.
[http://dx.doi.org/10.1161/CIRCHEARTFAILURE.118.005565] [PMID: 30998392]
[34]
Albert CL. Morbid obesity as a therapeutic target for heart failure. Curr Treat Options Cardiovasc Med 2019; 21(10): 52.
[http://dx.doi.org/10.1007/s11936-019-0754-z] [PMID: 31486922]
[35]
Yigla M, Abassi Z, Reisner SA, Nakhoul F. Pulmonary hypertension in hemodialysis patients: An unrecognized threat. Semin Dial 2006; 19(5): 353-7.
[http://dx.doi.org/10.1111/j.1525-139X.2006.00186.x] [PMID: 16970730]
[36]
Ghio S, Fortuni F, Greco A, et al. Dobutamine stress echocardiography in pulmonary arterial hypertension. Int J Cardiol 2018; 270: 331-5.
[http://dx.doi.org/10.1016/j.ijcard.2018.06.032] [PMID: 29903514]
[37]
Aitken E, Kerr D, Geddes C, Berry C, Kingsmore D. Cardiovascular changes occurring with occlusion of a mature arteriovenous fistula. J Vasc Access 2015; 16(6): 459-66.
[http://dx.doi.org/10.5301/jva.5000336] [PMID: 25634156]
[38]
Sikole A, Polenakovic M, Spiroska V, Polenakovic B, Klinkmann H, Scigalla P. Recurrence of left ventricular hypertrophy following cessation of erythropoietin therapy. Artif Organs 2002; 26(2): 98-102.
[http://dx.doi.org/10.1046/j.1525-1594.2002.06839.x] [PMID: 11879236]
[39]
Tamás P. Early and late preeclampsia are characterized by high cardiac output, but in the presence of fetal growth restriction, cardiac output is low: Insights from a prospective study. Am J Obstet Gynecol 2018; 219(6): 627.
[http://dx.doi.org/10.1016/j.ajog.2018.07.029] [PMID: 30096323]
[40]
Lees C, Ferrazzi E. Relevance of haemodynamics in treating pre-eclampsia. Curr Hypertens Rep 2017; 19(9): 76.
[http://dx.doi.org/10.1007/s11906-017-0766-6] [PMID: 28836157]
[41]
Tamás P, Hantosi E, Farkas B, Ifi Z, Betlehem J, Bódis J. Preliminary study of the effects of furosemide on blood pressure during late-onset pre-eclampsia in patients with high cardiac output. Int J Gynaecol Obstet 2017; 136(1): 87-90.
[http://dx.doi.org/10.1002/ijgo.12019] [PMID: 28099709]
[42]
Licata A, Mazzola A, Ingrassia D, Calvaruso V, Cammà C, Craxì A. Clinical implications of the hyperdynamic syndrome in cirrhosis. Eur J Intern Med 2014; 25(9): 795-802.
[http://dx.doi.org/10.1016/j.ejim.2014.09.004] [PMID: 25245607]
[43]
La Villa G, Gentilini P. Hemodynamic alterations in liver cirrhosis. Mol Aspects Med 2008; 29(1-2): 112-8.
[http://dx.doi.org/10.1016/j.mam.2007.09.010] [PMID: 18177931]
[44]
McAvoy NC, Semple S, Richards JM, et al. Differential visceral blood flow in the hyperdynamic circulation of patients with liver cirrhosis. Aliment Pharmacol Ther 2016; 43(9): 947-54.
[http://dx.doi.org/10.1111/apt.13571] [PMID: 26947424]
[45]
Acou WJ, De Buyzere M, De Pauw M. Pulmonary hypertension is not a diagnosis. Acta Cardiol 2010; 65(5): 575-9.
[http://dx.doi.org/10.1080/AC.65.5.2056246] [PMID: 21125981]
[46]
Kawamura Y, Yamazaki J, Okuzumi I, et al. Evaluation of myocardial blood flow and cardiac functional change in acromegaly. Kaku Igaku 1991; 28(1): 19-25.
[PMID: 2020133]
[47]
Fazio S, Cittadini A, Biondi B, et al. Cardiovascular effects of short-term growth hormone hypersecretion. J Clin Endocrinol Metab 2000; 85(1): 179-82.
[http://dx.doi.org/10.1210/jcem.85.1.6313] [PMID: 10634384]

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