Correspondence: Other strategies for validating the diagnosis of heart failure

Dear Sirs,

Given the fact that we are now practising medicine in an era where the standard of care is the optimisation of evidence-based treatments – both for heart failure with reduced ejection fraction (HFrEF) and for heart failure with preserved ejection fraction (HFpEF) – it is imperative that strategies should also be optimised both for identification of congestive heart failure (CHF) and for establishing a distinction between HFrEF and HFpEF.

The requirement to distinguish between HFrEF and HFpEF is partly met by the use of transthoracic echocardiography (TTE) for measuring left ventricular ejection fraction (LVEF), but this only serves to allocate the patient either to a category of an LVEF <50% or ≥50%. What TTE fails to do is to validate or refute the diagnosis of CHF in patients in either of these LVEF categories.

The requirement to validate a diagnosis of CHF can be met partly by measuring levels of N-terminal pro B-type natriuretic peptide (NT-pro BNP) in the blood. The drawback to this is the suboptimal sensitivity and specificity of this test,¹ which has suboptimal sensitivity even in HFpEF patients who have a pulmonary capillary wedge pressure >15 mmHg.² Accordingly, instead of relying solely on NT pro-BNP for the purpose of confirming or refuting the diagnosis of CHF, we should  pursue other strategies to confirm or refute the diagnosis in patients with suspected CHF, irrespective of whether the LVEF is <50% or ≥50%.

I propose the following strategies:

• Evaluation of jugular venous pressure (JVP) by bedside clinical examination – a raised JVP is indicative of a raised right atrial pressure and, hence, CHF-related fluid overload. Accordingly, jugular venous distension is associated with a likelihood ratio of 5.1 (95% confidence interval [CI], 3.2 to 7.9) in favour of a diagnosis of CHF.³ In Drazner et al., a JVP of >12 mmHg (≥16.32 cm H₂O) was associated with a positive predictive value of 75% for identifying a pulmonary capillary wedge pressure of >22 mmHg.⁴
• Internal jugular venous ultrasound – this is an alternative strategy for evaluation of raised right atrial pressure (RAP) and, hence, CHF-related fluid overload. One technique is to measure RAP through the combination of atrial depth, using point of care ultrasound (POCUS), which also measures jugular venous collapse point. RAP is the sum of right atrial depth and the jugular venous collapse point i.e. the point where the venous wall collapses completely in a patient who has been identified as having jugular venous distension.⁵ RAP obtained by ultrasound and measured by right atrial catheterisation was found to have a correlation coefficient of +75.⁵ Alternatively, the cross-sectional area of the right internal jugular vein (RIJ) during normal breathing can be measured with patients either reclining at 90 or 45 degrees. RIJ is indexed by height, hence the abbreviation RIJI. In one study,⁶ an RIJI of 10, measured at a 45 degrees recline, was associated with a positive predictive value of 76.74% for a RAP >10 mmHg.
• Evaluating response before and after loop diuretic treatment through the following:
  • Chest radiography which can show radiographic stigmata of CHF, such as vascular opacity redistribution towards the upper lobes and distension of upper pulmonary veins, septal lines in the lower lung, peribronchial cuffing, and bilateral parenchymal opacities.⁷ Usefulness of chest radiography is limited by its suboptimal sensitivity,⁷ interobserver variability, and risk of radiation exposure.
  • Lung ultrasound which can document the presence of ‘B’ lines (indicative of fluid overload in the interstitial spaces of the lung).⁸ In one study of 81 subjects (mean LVEF 45.04% [standard deviation 14.3%]), 96% of the patients had diuretics included in their treatment regimen.⁸ All 81 subjects presented with breathlessness, and all 81 showed diffuse B line patterns on admission. All the areas with B line patterns showed significant (P<0.001) clearing of B lines after treatment.⁸ The use of lung ultrasound in the work up of suspected CHF is now also endorsed in the European Society of Cardiology guidelines for diagnosis of CHF.⁹
  • Serial measurement of forced vital capacity (FVC) and/or total lung capacity (TLC). A reduction in TLC and FVC, respectively, is typical of CHF, attributable to pulmonary fluid overload.¹⁰ This reduction in TLC and/or FVC can be reversed in CHF patients responding to treatment for CHF, probably due to a reduction in pulmonary fluid overload.¹¹

Documenting of some or all of the above might prove useful in distinguishing between the presence and absence of CHF in subjects with either an LVEF <50% or ≥50%. Furthermore, rather than relying on a ‘sliding scale’ of ‘cut-off’ blood levels to optimise the sensitivity and specificity of natriuretic peptide levels,¹ it might prove more diagnostically advantageous to identify which combination of NT-pro BNP measurements with one or more of the above strategies is most accurate to predict a correct diagnosis of CHF (when the latter is defined as the association of breathlessness and pulmonary capillary wedge pressure of ≥15 mmHg).

The use of the above strategies may also prove to be useful in distinguishing between breathlessness attributable to CHF versus breathlessness attributable to chronic obstructive pulmonary disease (COPD). Lung function tests performed before and after diuretics might also unmask the coexistence of COPD and CHF. Among patients with dual pathology, the coexistence of COPD is optimally ‘unmasked’ when both CHF-related airflow obstruction and CHF-related  pulmonary congestion have resolved. In this post-treatment context, a TLC which is higher than the predicted value is a powerful indicator of thebcoexistence of COPD and CHF independent of FEV1/FVC ratio[13].

Oscar M P Jolobe
Retired geriatrician
Manchester

([email protected])

Conflicts of interest

None declared.

Funding

None declared.

References

1. Birrell H, Fersia O, Anwar M et al. Assessment of the diagnostic value of NT-pro BNP in heart failure with preserved ejection fraction. Br J Cardiol 2024;31:17–22. https://doi.org/10.5837/bjc.2024.002

2. Anjan V, Loftus TM, Burke MA et al. Prevalence, clinical phenotype, and outcomes associated with normal N-type natriuretic peptide levels in heart failure with preserved ejection fraction. Am J Cardiol 2012;110:870–6. https://doi.org/10.1016/j.amjcard.2012.05.014

3. Wang CS, Fitzgerald JM, Schulzer N, Mak E, Sayas NT. Does this dyspneic patient in the emergency department have congestive heart failure? JAMA 2005;294:1944–56.

4. Drazner MH, Hellkamp AS, Leier CV et al. Value of clinician assessment of hemodynamics in advanced heart failure. The ESCAPE trial. Circ Heart Fail 2008;1:170–7. https://doi.org/10.1161/CIRCHEARTFAILURE.108.769778

5. Istrail L, Kiernan J, Stepanova M. A novel method for estimating right atrial pressure with point of care ultrasound. J Am Soc Echocardiogr 2023;36:278–83. https://doi.org/10.1016/j.echo.2022.12.008

6. Thacker P, Amartunga D, Dhah K et al. Internal jugular vein ultrasound inpatients with chronic congestive heart failure. Eur Heart J 2021;42(suppl1):ehab 724.0858. https://doi.org/10.1093/eurheartj/ehab724.0858

7. Cardinale L, Priola AM, Moretti F, Volpicelli G. Effectiveness of chest radiography, lung ultrasound and thoracic computed tomography in the diagnosis of congestive heart failure. World J Radiol 2014;6:230–7. https://doi.org/10.4329/wjr.v6.i6.230

8. Volpicelli G, Caramello V, Cardinale L et al. Bedside ultrasound of the lung for the monitoring of acute decompensated heart failure. Am J Emerg Med 2008;26:585–91. https://doi.org/10.1016/j.ajem.2007.09.014

9. McDonagh TA, Metra M, Adamo M et al. 2021 ESC Guidelines for the diagnosis and treatment of acute and chronic heart failure. Eur Heart J 2021;42:3599–726. https://doi.org/10.1093/eurheartj/ehab368

10. Gehlbach BK, Geppert E. The pulmonary manifestations of left heart failure. Chest 2004;125:669–82. https://doi.org/10.1378/chest.125.2.669

11. Light RW, George RB. Serial pulmonary function in patients with acute heart failure. Arch Intern Med 1983;143:429-33.

12. McNicol MW, Kirby BJ, Bhoola KD et al. Pulmonary function in acute myocardial infarction. BMJ 1965;2:1270–3.

13. Brenner S, Guder G, Berliner D et al. Airway obstruction in systolic heart failure-COPD or congestion? Int J Cardiol 2013;168:1910–16. https://doi.org/10.1016/j.ijcard.2012.12.083

A response from Dr Jim Moore

From Jim Moore

In both UK¹ and international guidelines,² a diagnosis of heart failure requires the presence of symptoms and/or signs of heart failure, in addition to objective evidence of cardiac dysfunction related to a structural and/or functional abnormality of the heart, with echocardiography the key investigation in the diagnostic pathway.

The measurement of left ventricular ejection fraction (LVEF) is central to the widely accepted classification of heart failure as seen in the current European Society of Cardiology Guidelines:²

heart failure with reduced ejection fraction (HFrEF) is based on the presence of an LVEF ≤40% alone.

Heart failure with mildly reduced ejection fraction (HFmrEF) is based on an LVEF 41–49% with no additional evidence required unless there is uncertainty regarding the measurement of LVEF, where additional echocardiographic evidence of underlying structural abnormality and elevated natriuretic peptides may be used to support the diagnosis.

Heart failure with preserved ejection fraction (HFpEF) based on an LVEF ≥50% is frequently challenging to diagnose and requires additional objective echocardiographic evidence of cardiac structural and/or functional abnormalities consistent with the presence of LV diastolic dysfunction/raised LV filling pressures, including elevated natriuretic peptides. Additional investigations may be required where there remains diagnostic uncertainty.

The author identifies several investigations which may support a diagnosis of congestive heart failure including the use of ultrasound to assess jugular venous/right atrial pressure or to identify the presence of ‘B’ lines indicative of fluid retention on assessment of the lungs. Such assessments by appropriately trained health care professionals are uncommon in current practice but may be helpful in managing fluid retention associated with heart failure though not in determining the underlying heart failure phenotype which is central to providing appropriate evidence-based treatment.

Diagnostic guidelines with a high degree of utility are ideally simple and practical, with recommended investigations routinely available and importantly supported by evidence or expert consensus and as a consequence likely to be widely adopted.²

Jim Moore
GPSI Gloucestershire Heart Failure Service; Past President of the Primary Care Cardiovascular Society

Conflicts of interest

JM has received honoraria in the past 12 months from Amgen, AstraZeneca, Bayer, Boehringer Ingelheim, Cuviva, Novarits, Medtronic, Novo Nordisk, Roche and Vifor. JM is also National Co-clinical Primary Care Lead with the NHSE/I Cardiac Transformation Programme; Clinical Lead (Primary Care), West of England Integrated Cardiac Clinical Network; Member of the National (NHSE) Heart Failure/Heart Valve Disease, Atrial Fibrillations, Hypertension and Lipids Expert Advisory Groups; Member of the National Heart Failure Audit Domain Expert Group; National Institute for Health and Care Excellence Guideline Committee Member for Chronic Heart Failure 2018.

Funding

None declared.

References

1. National Institute of Health and Care Excellence. Chronic heart failure in adults: diagnosis and management NICE guidelin [NG106]. London: NICE, September 2018. https://www.nice.org.uk/guidance/ng106/chapter/Recommendations#diagnosing-heart-failure (last accessed 23rd April 2024)

2. McDonagh TA, Metra M, Adamo M et al. 2021 ESC Guidelines for the diagnosis and treatment of acute and chronic heart failure. Eur Heart J 2021;42:3599–726. https://doi.org/10.1093/eurheartj/ehab368