Once the diagnosis of heart failure is made, subsequent laboratory studies should be directed toward the identification of an underlying cause of heart failure.
Renal function should be assessed as a rough guide to the patient's intravascular volume status and renal perfusion. A urinalysis is helpful in the assessment of the patient's volume status. Electrolyte assessment and the correction of electrolyte disturbances such as hypokalemia, hyperkalemia and hypomagnesemia is critical in those patients treated with diuretics. Hyponatremia (due to poor stimulation of the baroreceptors and appropriate ADH release and free water retention) is associated with a poor prognosis.
A complete blood count should be obtained to assess for the presence of anemia which may exacerbate heart failure and to assess the patients coagulation status which may be impaired due to hepatic congestion.
The assessment of thyroid function tests is particularly important in the patient who is being treated with concomitant therapy with an agent such as amiodarone.
The upper limits of normal in the non-acute setting are 35 pg/mL for BNP, and 125 pg/mL for NT-proBNP.[1]
The CoDE-HF decision support tool may help diagnose heart failure[2]. The CoDE-HF interprets the N-terminal pro-B-type natriuretic peptide (NT-proBNP) in various settings including obesity.
Causes of elevated concentrations of natriuretic peptides
BNP or its amino-terminal cleavage equivalent (NT-proBNP) is generated by cardiomyocytes in the context of numerous triggers, most notably myocardial stretch.
BNP levels may be useful in the initial establishment of the diagnosis of heart failure in the patient with dyspnea of unclear etiology. In a meta-analysis, BNP was superior N-terminal pro-BNP (NTproBNP) and was associated with a sensitivity of 85% and specificity of 84% in the diagnosis of heart failure in the primary care setting.[4]
Abbreviations:ACC: American College of Cardiology, AHA: American Heart Association, ADHF: acute decompensated
heart failure, BNP: B-type natriuretic peptide, COR: Class of Recommendation, ED: emergency department, HF: heart failure, NT-proBNP: N-terminal pro-B-type natriuretic peptide, NYHA: New York Heart Association, pts: patients
(*)Other biomarkers of injury or fibrosis include soluble ST2 receptor, galectin-3, and high-sensitivity troponin.
Biomarkers of Myocardial Injury: Cardiac Troponin T or I[edit | edit source]
Even without obvious myocardial ischemic injury, troponin level may be increased in heart failure which means undergoing myocyte injury.[12] Elevated levels of troponin is associated with impaired hemodynamics, progressive LV dysfunction and increased mortality rates.[13]
CA-125 is an emerging, highly sensitive biomarker for heart failure.[14] Although it is not yet used in clinical practice, the CHANCE-HF trial has demonstrated utility in using CA-125 to guide diuretic therapy and for determining short-term prognosis.[15] CA-125 is a non-specific antigen that is most strongly associated with ovarian cancer. In patients with acute heart failure, ambulatory follow-up care aimed at titrating diuretic use according to CA-125 levels has demonstrated ~50% reduction in rehospitalizations.[15] CA-125 was first associated with heart failure in 1999 by Nagele et al.[14][16]
↑McDonagh TA, Metra M, Adamo M, Gardner RS, Baumbach A, Böhm M, Burri H, Butler J, Čelutkienė J, Chioncel O, Cleland J, Coats A, Crespo-Leiro MG, Farmakis D, Gilard M, Heymans S, Hoes AW, Jaarsma T, Jankowska EA, Lainscak M, Lam C, Lyon AR, McMurray J, Mebazaa A, Mindham R, Muneretto C, Francesco Piepoli M, Price S, Rosano G, Ruschitzka F, Kathrine Skibelund A (September 2021). "2021 ESC Guidelines for the diagnosis and treatment of acute and chronic heart failure". Eur Heart J. 42 (36): 3599–3726. doi:10.1093/eurheartj/ehab368. PMID34447992Check |pmid= value (help). Vancouver style error: initials (help)
↑Yancy CW, Jessup M, Bozkurt B, Butler J, Casey DE, Drazner MH, Fonarow GC, Geraci SA, Horwich T, Januzzi JL, Johnson MR, Kasper EK, Levy WC, Masoudi FA, McBride PE, McMurray JJ, Mitchell JE, Peterson PN, Riegel B, Sam F, Stevenson LW, Tang WH, Tsai EJ, Wilkoff BL (2013). "2013 ACCF/AHA guideline for the management of heart failure: a report of the American College of Cardiology Foundation/American Heart Association Task Force on Practice Guidelines". J. Am. Coll. Cardiol. 62 (16): e147–239. doi:10.1016/j.jacc.2013.05.019. PMID23747642.
↑Hudson MP, O'Connor CM, Gattis WA, Tasissa G, Hasselblad V, Holleman CM, Gaulden LH, Sedor F, Ohman EM (2004). "Implications of elevated cardiac troponin T in ambulatory patients with heart failure: a prospective analysis". Am. Heart J. 147 (3): 546–52. doi:10.1016/j.ahj.2003.10.014. PMID14999208.
↑Horwich TB, Patel J, MacLellan WR, Fonarow GC (2003). "Cardiac troponin I is associated with impaired hemodynamics, progressive left ventricular dysfunction, and increased mortality rates in advanced heart failure". Circulation. 108 (7): 833–8. doi:10.1161/01.CIR.0000084543.79097.34. PMID12912820.
↑Heidenreich PA, Bozkurt B, Aguilar D, Allen LA, Byun JJ, Colvin MM, Deswal A, Drazner MH, Dunlay SM, Evers LR, Fang JC, Fedson SE, Fonarow GC, Hayek SS, Hernandez AF, Khazanie P, Kittleson MM, Lee CS, Link MS, Milano CA, Nnacheta LC, Sandhu AT, Stevenson LW, Vardeny O, Vest AR, Yancy CW (May 2022). "2022 AHA/ACC/HFSA Guideline for the Management of Heart Failure: A Report of the American College of Cardiology/American Heart Association Joint Committee on Clinical Practice Guidelines". Circulation. 145 (18): e895–e1032. doi:10.1161/CIR.0000000000001063. PMID35363499Check |pmid= value (help).