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Hartmann, J. Mid-regional pro-atrial natriuretic peptide and pro-adrenomedullin testing for the diagnostic and prognostic evaluation of patients with acute dyspnoea. Masson, R. Latini, E. Carbonieri, L. Moretti, M. Rossi, S. Ciricugno, et al. Eur J Heart Fail. Rehman, A. Martinez-Rumayor, T. Mueller, J. Clin Chim Acta. Lassus, E. Gayat, C. Mueller, W. Spinar, V. Harjola, et al. Incremental value of biomarkers to clinical variables for mortality prediction in acutely decompensated heart failure: the Multinational Observational Cohort on Acute Heart Failure MOCA study.

Int J Cardiol. Salah, W. Kok, L. Eurlings, P. Bettencourt, J. Pimenta, M. Metra, et al. Maisel, M. Silver, Y. Xue, C. Natriuretic peptide testing for predicting adverse events following heart failure hospitalization. Congest Heart Fail. Bhardwaj, J. Natriuretic peptide-guided management of acutely destabilized heart failure: rationale and treatment algorithm. Crit Pathw Cardiol. Surfing the biomarker tsunami at JACC: heart failure.

Weinberg, M. Shimpo, G. De Keulenaer, C. MacGillivray, S. Tominaga, S. Solomon, et al. Expression and regulation of ST2, an interleukin-1 receptor family member, in cardiomyocytes and myocardial infarction. Ho, M. Larson, A. Ghorbani, S. Cheng, R. Vasan, T. Wang, et al. J Hypertens.


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Coglianese, M. Larson, R. Vasan, J. Ho, A. Ghorbani, E. McCabe, et al. Distribution and clinical correlates of the interleukin receptor family member soluble ST2 in the Framingham Heart Study. Peacock, A. Jesse, A. Rehman, T. Characteristics of the novel interleukin family biomarker ST2 in patients with acute heart failure. Mueller, D.

Pascual-Figal, Q. Truong, J. Usefulness of soluble concentrations of interleukin family member ST2 as predictor of mortality in patients with acutely decompensated heart failure relative to left ventricular ejection fraction.

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Pascual-Figal, S. Boronat, T. Casas, I. Garrido, J. Bonaque, et al. Soluble ST2, high-sensitivity troponin T- and N-terminal pro-B-type natriuretic peptide: complementary role for risk stratification in acutely decompensated heart failure. Boisot, J. Beede, S. Isakson, A. Chiu, P. Januzzi, et al. Serial sampling of ST2 predicts day mortality following destabilized heart failure. Zilinski, R. Shah, H. Gaggin, M. Gantzer, T.

Wang, J. Measurement of multiple biomarkers in advanced stage heart failure patients treated with pulmonary artery catheter guided therapy. Crit Care. Januzzi, F. Boronat-Garcia, D. Pascual-Figal, et al. Serial monitoring of soluble interleukin family member ST2 in patients with acutely decompensated heart failure.

Breidthardt, C. Balmelli, R. Twerenbold, T. Mosimann, J. Espinola, P. Haaf, et al. Heart failure therapy-induced early ST2 changes may offer long-term therapy guidance. Gaggin, S. Motiwala, A. Bhardwaj, K. Parks, J. Circ Heart Fail. Maisel, Y. Xue, D. Van Veldhuisen, A. Voors, T. Jaarsma, P. Pang, et al. Dieplinger, J. Steinmair, C. Gabriel, W. Poelz, M. Haltmayer, et al. Analytical and clinical evaluation of a novel high-sensitivity assay for measurement of soluble ST2 in human plasma—the Presage ST2 assay. Creemers, Y. Molecular mechanisms that control interstitial fibrosis in the pressure-overloaded heart.

Cardiovasc Res. Sharma, S. Pokharel, T. Van Brakel, J. Van Berlo, J. Cleutjens, B. Schroen, et al. Galectin-3 marks activated macrophages in failure-prone hypertrophied hearts and contributes to cardiac dysfunction. Ellinor, U. Sharma, J. Low, et al. Utility of amino-terminal pro-brain natriuretic peptide, galectin-3, and apelin for the evaluation of patients with acute heart failure.

Shah, A. Chen-Tournoux, M. Picard, R. Galectin-3, cardiac structure and function, and long-term mortality in patients with acutely decompensated heart failure. De Berardinis, L. Magrini, G. Zampini, B. Zancla, G. Salerno, P. Cardelli, et al. Usefulness of combining galectin-3 and BIVA assessments in predicting short- and long-term events in patients admitted for acute heart failure. Biomed Res Int. Aramburu-Bodas, P.

Salamanca-Bautista, J. Morales-Rull, L. Galisteo-Almeda, M. Predictive value of serum galectin-3 levels in patients with acute heart failure with preserved ejection fraction. Fermann, C. Lindsell, A. Storrow, K. Hart, M. Sperling, S. Roll, et al. Galectin 3 complements BNP in risk stratification in acute heart failure.

Christenson, S. Duh, A. Wu, A. Smith, G. Abel, C. Multi-center determination of galectin-3 assay performance characteristics: anatomy of a novel assay for use in heart failure. Clin Biochem. Gopal, M. Kommineni, N. Ayalon, C. Koelbl, R. Ayalon, A. Biolo, et al.

What Is the Role of BNP in Diagnosis and Management of Acutely Decompensated Heart Failure?

Relationship of plasma galectin-3 to renal function in patients with heart failure: effects of clinical status, pathophysiology of heart failure, and presence or absence of heart failure. J Am Heart Assoc. Coburn, W. Comprehensive review of the prognostic value of galectin-3 in heart failure. Cardiol Rev. Filippatos, M. Nieminen, M. Pascual-Figal, T.

Casas, J. Ordonez-Llanos, S. Bonaque, M. Boronat, et al. Highly sensitive troponin T for risk stratification of acutely destabilized heart failure. Parissis, J. Papadakis, N. Kadoglou, C. Varounis, P. Psarogiannakopoulos, P. Rafouli-Stergiou, et al. Prognostic value of high sensitivity troponin T in patients with acutely decompensated heart failure and non-detectable conventional troponin T levels.

Ferreira, M. Santos, S. Almeida, I. Marques, P. Bettencourt, H. High-sensitivity troponin T: a biomarker for diuretic response in decompensated heart failure patients. Cardiol Res Pract. Xue, P. Clopton, W. Serial changes in high-sensitive troponin I predict outcome in patients with decompensated heart failure. Metra, G. Cotter, B. Davison, G. Felker, G. Filippatos, B.

Greenberg, et al. Novel biomarkers in acute heart failure: MR-pro-adrenomedullin. Clin Chem Lab Med. Nishikimi, Y. Saito, K. Kitamura, T. Ishimitsu, T. Eto, K. Kangawa, et al. IABP comprises of a balloon inserted into the aorta through the femoral artery. The balloon inflates during diastole and deflates during systole to increase diastolic BP and consequently coronary perfusion, and reduces afterload thereby increasing CO [60].

On the other hand, the use of VAD is uncommon. It can only be used in specialist centres. It is commonly used as a bridge to cardiac transplantation in patients with favourable quality of life or to recovery in patients with acute myocarditis [61]. Some causes of low-output state in patients with LoHF can be reversed with specific therapies. Reversible causes should be identified early during initial clinical evaluation. These causes include acute myocardial infarction, cardiac tamponade, tension pneumothorax, pulmonary embolism, and acute valve failure [16,17].

Table 3. Hemodynamic profiles based on measures of congestion and perfusion have been used to classify acute HF patients into four profiles: dry-warm A , wet-warm B , dry-cold L and wet-cold C and useful in identifying LoHF patients [51,53]. These two hemodynamic profiles have formed the basis for selecting patients with LoHF in clinical trials as well as provide simple bedside assessment to help classify patients at the time of presentation and to guide the selection of initial therapies [51,62].

The goal of the present meta-analysis is to aggregate published evidence of common diagnostic features and treatment outcomes for patients with LoHF. To avoid overlooking studies that did not mention LoHF in the title or abstract, the first relevance-ranked articles retrieved with a full-text Google Scholar search were included. No publication time or language restrictions were applied. Additional studies were identified through a manual search of the list of references from the included studies as well as from relevant review articles, which were then subjected to the inclusion criteria.

The search criteria included population of interest patients with LoHF or LCOS , diagnostic tests of interest echocardiography and hemodynamic profiles , and intervention of interest ventilator strategies, volume adjustment, pharmacological support and device therapy. Studies were included if they met the following criteria: a included patients with LoHF; b diagnosed using echocardiography and hemodynamic profiles; c treated patients for hemodynamic stabilization; and d reported treatment outcomes.

In cases of studies reporting duplicate data, only the study that provided the largest number of patients was included. Conference abstracts, case reports and review articles were excluded. Figure 4 illustrates the search and screening process used to include eligible studies. Two reviewers independently screened all the titles and abstracts retrieved from the systematic online search. Abstracts that included population, intervention and outcomes of interest were included for full-text search. Afterwards, the two reviewers also independently reviewed full-text articles against the inclusion criteria.

In cases of discrepancy, it was resolved through discussion and consensus. Two reviewers independently extracted data from the included studies and any discrepancy was resolved through consensus. The main data extracted were echocardiographic and hemodynamic profile data, and treatment used and treatment outcome on hemodynamic cardiac index, PCWP and mortality.

Outcomes of interest reported in more than one study are cardiac index, PCWP and mortality. Forest plots were used to visually examine heterogeneity I 2 across studies.

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Twelve 12 randomized controlled trials RCTs satisfied the inclusion criteria. Seven 7 studies [, 69,70] enrolled LoHF patients and the remaining five 5 [68,] enrolled HF patients who have undergone cardiac surgery with low-cardiac output. The majority of published clinical trials 10 investigated medication comparing the effect of different types of inotropes on hemodynamic and prevention of death: dobutamine only [65], dobutamine and dopamine [63]; levosimendan and dobutamine [64,,71], and levosimendan and placebo [].

Of the remaining two clinical trials, each investigated vasodilator nitroprusside and placebo [69], and device therapy IABP and inotrope levosimendan alone or in combination with IAPB [70]. Diagnosis data on LoHF was inconsistent. Across the twelve clinical trials, no common definition of LoHF emerged that would have been useful to guide diagnosis. Cardiogenic shock has been described as a complex syndrome involving a cascade of acute LV dysfunction, decreased CO, hypotension and tissue hypoperfusion [67]. Figures 5 and 6 show forest plots for standardized mean of cardiac index at baseline and following inotrope or vasodilator therapy respectively.

The baseline cardiac index increased from a mean of 1. Figure 7 shows a forest plot for standard mean difference SMD of cardiac index after treatment with levosimendan and dobutamine. Levosimendan achieve higher cardiac index compared to dobutamine SMD: 2. As a prophylactic against LoHF in post-operative patients, levosimendan infusion after anaesthesia achieved a higher cardiac index 2. Figure 8 shows a forest plot of mortality rate between levosimendan and placebo.

Levosimendan had lower mortality rate compared to placebo Odds Ratio [OR]: 0. Final, Figure 9 further shows Levosimendan has a lower mortality rate compared to dobutamine OR: 0. This systematic review and meta-analysis assessed common diagnostic features, and treatment outcomes of medical and device therapy IABP on LoHF patients. The results indicates that LoHF patients lack widely accepted or standardized diagnosis features. Although LoHF patients could exhibit several features including cardiac index, PCWP, systolic BP and SvO 2 to suggest or support clinical diagnosis, all these features have different cut-off values across studies.

Inotropic support emerged as a very common intervention for improving perfusion and normalizing cardiac output in LoHF patients. Inotropic medication such as levosimendan, dobutamine, dopamine, vasodilator nitroprusside and IABP significantly improved CI between baseline and post-treatment.

In terms of inotropes, levosimendan is more effective in improving hemodynamic stability and a better prophylactic against short-term death day mortality than dobutamine. In addition, inotropes can act as prophylactic against the development of post-operative LoHF. On the other hand, while inotropes improve hemodynamic and normalize cardiac output, they do not provide any significantly better protection against mortality irrespective of the type of inotrope used.

The role of inotropes in the treatment of LoHF has been supported by a previous review of inotropic agents and vasodilator strategies for the treatment of cardiogenic shock and LCOS [75]. The review reported inotropes improve hemodynamic, adverse events in post-operative LCOS and reduced mortality. Newer inotropes such as levosimendan a calcium sensitizer and inodilator is a positive inotrope has some vasodilatory properties [67].

It can also be considered as a selective liver vasodilator, which can improve portal venous flow via hepatic artery and portal venous flow compared to dobutamine that can only improve portal venous flow without vasodilating the hepatic artery [71]. Levosimendan also does not increase myocardial oxygen demand and recommended over dobutamine in LoHF patients with acute myocardial ischemic or post cardiac surgery [5].

For post-operative LoHF, the protective effect of inotropes against short-term mortality rate day mortality remains insignificant compared to placebo [75]. The present systematic review and meta-analysis has some important limitations. LoHF may occur in secondary to underlying cardiac disease such as acute myocardial infarction or post-operative.

Most of the studies focused on two inotropes Levosimendan and dobutamine , limiting the understanding of other inotropes as well as other therapies such as device therapies. In some trials, the analysis were at risk of misclassification bias due to a significant number of patients lost to follow-up. Since most of the trials do not report pair-wise pre- and post-intervention difference with associated standard deviation, pre and post-intervention difference with standard deviation, pre- and post-intervention outcomes measures as independent, this obtaining sider confidence intervals for treatment effect with an associated standard deviation.

Low-output heart failure LoHF is a clinical syndrome characterized by decreased cardiac output accompanied by end-organ hypoperfusion. It is an uncommon form of heart failure in the general population but prevalent in post-operation HF patients. Its aetiology is heterogeneous, consisting of various conditions causing low-output state and cardiac surgery. General risk factors for LoHF include Chagas disease, depressed ejection fraction, and renal dysfunction while in post-operative patients include impaired LV function, incomplete revascularization, older age, and presence of diabetes and renal dysfunction.

Diagnosis lacks standardized guidelines and dependent on accepted collection of hemodynamic and physiologic aberrations including conditions causing low-output state. Patient history and physical examination help to assess hemodynamic status and recognize low-output state while echocardiography confirms ventricular dysfunction HF and low cardiac output. Other tests to support diagnosis or establish the cause of low-output state include electrocardiogram and basic laboratory tests blood, serum electrolyte, urea and creatinine, liver test, thyroid function and serum natriuretic peptides and cardiac imaging chest x-ray or coronary angiography.

Treatment lacks established guidelines but depends on the assessment of individual pathophysiology to select the most appropriate treatment strategy. Treatment includes ventilator strategies to improve heart rate and rhythm; volume adjustment to optimize preload; pharmacological support inotropes and vasodilators to manipulate afterload and improve contractility; and device therapy intra-aortic balloon pump or ventricular assist device when these strategies do not restore cardiac output. In selected patients, therapies to reverse underlying disease, can restore cardiac output.

This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited. Albakri A Low-output heart failure: A review of clinical status and meta-analysis of diagnosis and clinical management methods.

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Key words low-output cardiac syndrome, low-output heart failure, low-output state Introduction Despite remarkable advancements in medical and surgical therapies, effective management of heart failure HF continues to pose significant challenges to healthcare providers. Epidemiology The exact prevalence and incidence of LoHF in the general population is completely unknown. Aetiology The aetiology of LoHF is multi-factorial. Table 1. RV dysfunction In LoHF, particularly after coronary artery surgery, the principle pathophysiologic mechanisms of RV dysfunction include increased preload, increased afterload, impaired right coronary artery perfusion and decreased contractility [].

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Diagnosis There is no consensus guidelines or proven diagnostic criteria for LoHF patients. Signs and symptoms Low cardiac output as the presenting feature of acute decompensated HF is uncommon, affecting only 8. Clinical management The presence of LoHF represents a very high-risk condition requiring prompt treatment but lacks standardized guidelines for clinical management [16]. Treating underlying causes Some causes of low-output state in patients with LoHF can be reversed with specific therapies.

Study selection Figure 4 illustrates the search and screening process used to include eligible studies. Figure 4. Flow diagram of literature search and inclusion process Data collection Two reviewers independently extracted data from the included studies and any discrepancy was resolved through consensus.

Statistical analysis Outcomes of interest reported in more than one study are cardiac index, PCWP and mortality. Results Study characteristics Twelve 12 randomized controlled trials RCTs satisfied the inclusion criteria. Synthesis of results Diagnosis data on LoHF was inconsistent. Figure 5. Mean baseline cardiac index Figure 6. Mean post-treatment cardiac index Figure 7. Mean difference in cardiac index between levosimendan and dobutamine Figure 8. Mortality rate between levosimendan and placebo Figure 9.

Mortality rate between levosimendan and dobutamine Discussion of findings This systematic review and meta-analysis assessed common diagnostic features, and treatment outcomes of medical and device therapy IABP on LoHF patients. Conclusion Low-output heart failure LoHF is a clinical syndrome characterized by decreased cardiac output accompanied by end-organ hypoperfusion.

The aim of the document is to provide practical, evidence-based guidelines for the diagnosis and treatment of Heart Failure. Essential initial investigations: natriuretic peptides, electrocardiogram, echocardiography. Stress echocardiography. Single-photon emission computed tomography and radionuclide ventriculography. Objectives in the management of heart failure.

Heart Failure - Clinical Presentation

Treatments recommended in all symptomatic patients with heart failure with reduced ejection fraction. Other treatments recommended in selected patients with symptomatic heart failure with reduced ejection fraction. Other treatments with less-certain benefits in patients with symptomatic heart failure with reduced ejection fraction. Treatments not recommended unproven benefit in patients with symptomatic heart failure with reduced ejection fraction. Treatments not recommended believed to cause harm in patients with symptomatic heart failure with reduced ejection fraction. Effect of treatment on symptoms in heart failure with preserved ejection fraction.

Effect of treatment on hospitalization for heart failure in heart failure with preserved ejection fraction.

Additional Reading

Effect of treatment on mortality in heart failure with preserved ejection fraction. Symptomatic bradycardia, pauses and atrio-ventricular block. Central nervous system including depression, stroke and autonomic dysfunction.