Diagnosis of Heart Failure in Patients after COVID-19: Comparison
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Please note this is a comparison between Version 1 by Katarzyna Gryglewska-Wawrzak and Version 3 by Dean Liu.

Coronavirus disease 2019 (COVID-19) is caused by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2). It can lead to myocardial damage. Heart failure (HF) is a significant global health concern and is characterized as a clinical syndrome with symptoms caused by structural and/or functional abnormalities of the heart, confirmed by elevated natriuretic peptide levels and evidence of pulmonary or systemic congestion. The relationship between COVID-19 and heart failure is complex. SARS-CoV-2 can cause cardiac damage through the activation of pro-inflammatory cytokines. Understanding the interactions between the disease and viruses is crucial for optimal patient care. However, the validity of screening for cardiovascular complications after COVID-19 remains unconfirmed, and individualized diagnosis procedures are necessary based on the patient's clinical symptoms.

  • COVID-19
  • heart failure
  • inflammation
  • cardiopulmonary exercise testing

1. Clinical Examination

Thorough subjective and physical examinations allow one to raise suspicion of the disease and plan further diagnostic procedures. The subjective examination is the first examination that, when properly conducted, allows one to propose a correct initial diagnosis of the disease in many patients. For patients who present symptoms of heart failure for the first time to a primary care physician or cardiology clinic, the physician first assesses the likelihood of a disease based on the history of coronary artery disease, high blood pressure, and other diseases and conditions that can cause heart failure. The doctor then examines the patient for signs of heart failure [1][2].

2. Laboratory Tests

The following parameters are of particular importance in the diagnosis of heart failure [3]:
  • concentration of natriuretic peptides in plasma—to exclude HF: in a patient without acute worsening of symptoms, HF is unlikely when BNP < 35 pg/mL (<105 pg/mL in atrial fibrillation), NT-proBNP < 125 pg/mL (<365 pg/mL in atrial fibrillation);
  • arterial blood gas analysis for detection of respiratory failure;
  • serum troponin for detection of acute coronary syndrome (ACS);
  • blood urea nitrogen, serum creatinine, electrolytes—for the detection of renal dysfunction;
  • full blood count—anemia may exacerbate or cause CHF;
  • transferrin, ferritin, signs of iron deficiency, most often of a functional nature—reduced transferrin iron saturation; a decrease in ferritin usually occurs only with absolute iron deficiency (it may not occur in the presence of inflammation);
  • inflammatory cytokines (C-reactive protein, procalcitonin)—for the diagnosis of infection;
  • increased activity of aminotransferases and lactate dehydrogenase (LDH), increased concentrations of bilirubin in plasma—in patients with venous stasis in the systemic circulation, with hepatomegaly;
  • the concentration of thyroid stimulating hormone (TSH), because thyroid disease can mimic or worsen the symptoms of HF;
  • D-dimer—when pulmonary embolism (PE) is suspected.
There are established guidelines for managing outpatients with suspicion of PE [4], based on clinical probability assessment and D-dimer dosage. Outcome studies have shown that the 3-month thromboembolic risk is <1% in patients with low or intermediate clinical probability and D-dimer < 500 ng·mL−1 who are left untreated [5]. The adjust-PE study has demonstrated that the D-dimer level adjusted to patient age, with higher thresholds in older patients (age × 10 ng·mL−1), can safely rule out PE [6]. Hypercoagulability and the need to prioritise coagulation markers for prognostic abilities have been highlighted in COVID-19. In a meta-analysis, the authors included 113 studies (n = 38,310) and showed that higher D-dimer levels provide prognostic information useful for clinicians to assess early COVID-19 patients at risk for disease progression and mortality outcomes [7].

3. Electrocardiogram (ECG)

The ECG usually reveals features of the underlying disease—ischemic heart disease, arrhythmias or conduction disorders, hypertrophy, or overload [8].

4. Chest Radiograph

The chest radiograph generally reveals enlargement of the heart (except in most cases of hyperkinetic states and diastolic insufficiency), signs of venous congestion in the pulmonary circulation [9].

5. Echocardiography

  • Left ventricular systolic function—by analysing segmental and global left ventricular contractility and left ventricular ejection fraction (LVEF) measurement (Simpson method; <40% indicates significant left ventricular systolic dysfunction; values 41–49% are considered the so-called grey zone and one of the diagnostic criteria HFmrEF—a complete differential diagnosis of noncardiac causes of symptoms is necessary, as in HFpEF) [3].
  • Left ventricular diastolic function—transmitral E/A ratio and E velocity deceleration time (DT), e’ velocity (average and absolute value of septal and lateral side) of the mitral annulus by pulsed tissue Doppler, E/e’ ratio, and the estimate of systolic pulmonary artery pressure (sPAP) derived from tricuspid regurgitation (TR) velocity [10].
  • Anatomical abnormalities, hypertrophy, dilation of the heart chambers, valvular defects, congenital defects. Additional evaluation of many parameters of cardiac structure and function is of particular importance in differential diagnosis, especially with LVEF <40%. In some cases (e.g., poor imaging conditions on transthoracic examination, suspected prosthetic valve dysfunction, detection of a thrombus in the left ear in patients with atrial fibrillation, diagnosis of bacterial endocarditis or congenital defects), transoesophageal echocardiography is indicated [11].
  • Signs of PE—dilation of the right ventricle (RV), pulmonary ejection acceleration time <60 ms with a peak systolic tricuspid valve gradient < 60 mmHg [4]. Echocardiographic examination is not mandatory as part of the routine diagnostic workup in haemodynamically stable patients with suspected PE. In case of suspected high-risk PE, the absence of echocardiographic signs of RV overload or dysfunction practically excludes PE as the cause of hemodynamic instability [12].

6. Computed Tomographic Pulmonary Angiography (CTPA)

CTPA is the first-line imaging technique in patients with suspected PE and is indicated as a class IC procedure for individuals with a high suspicion of PE, even in cases of hemodynamic instability. In patients with low or moderate clinical probability, a correct CTPA result can be sufficient to rule out the diagnosis of PE without the need for additional testing (class IA) [4].

7. Compression Ultrasonography (CUS)

CUS is a relevant tool for diagnosing deep vein thrombosis (DVP). This condition is a major medical problem that accounts for most cases of pulmonary embolism [13].

8. Cardiopulmonary Exercise Testing (CPET)

CPET is a relevant tool in patients with long-COVID. This examination is helpful in the case of a discrepancy between the severity of symptoms and the objective parameters of the severity of the disease, and when distinguishing between cardiac and pulmonary causes of dyspnea [14]. In one meta-analysis, the authors demonstrated that exercise capacity was reduced more than 3 months after SARS-CoV-2 infection among individuals with long-COVID symptoms compared with individuals without symptoms [15].
Figure 1 demonstrates proposed management in long-COVID patients with suspected heart failure.
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Figure 1. Management in long-COVID patients with suspected heart failure. The figure was partly generated using Servier Medical Art, provided by Servier, licenced under a Creative Commons Attribution 3.0 unported licence; one of the icons was from Flaticom.com (accessed on 18 April 2023).

References

  1. Harada, R.; Mantha, Y.; Hieda, M. Back to Basics: Key Physical Examinations and Theories in Patients with Heart Failure. Heart Fail. Clin. 2020, 16, 139–151.
  2. Thibodeau, J.T.; Drazner, M.H. The Role of the Clinical Examination in Patients with Heart Failure. JACC Heart Fail. 2018, 6, 543–551.
  3. McDonagh, T.A.; Metra, M.; Adamo, M.; Gardner, R.S.; Baumbach, A.; Böhm, M.; Burri, H.; Butler, J.; Čelutkienė, J.; Chioncel, O.; et al. 2021 ESC Guidelines for the diagnosis and treatment of acute and chronic heart failure: Developed by the Task Force for the diagnosis and treatment of acute and chronic heart failure of the European Society of Cardiology (ESC) with the special contribution of the Heart Failure Association (HFA) of the ESC. Eur. Heart J. 2021, 42, 3599–3726.
  4. Konstantinides, S.V.; Meyer, G.; Becattini, C.; Bueno, H.; Geersing, G.-J.; Harjola, V.-P.; Huisman, M.V.; Humbert, M.; Jennings, C.S.; Jimenez, D.; et al. 2019 ESC Guidelines for the diagnosis and management of acute pulmonary embolism developed in collaboration with the European Respiratory Society (ERS): The Task Force for the diagnosis and management of acute pulmonary embolism of the European Society of Cardiology (ESC). Eur. Respir. J. 2019, 54, 1901647.
  5. Carrier, M.; Righini, M.; Djurabi, R.K.; Huisman, M.V.; Perrier, A.; Wells, P.S.; Rodger, M.; Wuillemin, W.A.; Le Gal, G. VIDAS D-dimer in combination with clinical pre-test probability to rule out pulmonary embolism. A systematic review of management outcome studies. Thromb. Haemost. 2009, 101, 886–892.
  6. Righini, M.; Van Es, J.; Exter, P.D. Age-Adjusted D-Dimer Cutoff Levels to Rule Out Pulmonary Embolism: The ADJUST-PE Study. JAMA 2014, 311, 1117.
  7. Varikasuvu, S.R.; Varshney, S.; Dutt, N.; Munikumar, M.; Asfahan, S.; Kulkarni, P.P.; Gupta, P. D-dimer, disease severity, and deaths (3D-study) in patients with COVID-19: A systematic review and meta-analysis of 100 studies. Sci. Rep. 2021, 11, 21888.
  8. Gouda, P.; Brown, P.; Rowe, B.H.; McAlister, F.A.; Ezekowitz, J.A. Insights into the importance of the electrocardiogram in patients with acute heart failure. Eur. J. Heart Fail. 2016, 18, 1032–1040.
  9. Pan, D.; Pellicori, P.; Dobbs, K.; Bulemfu, J.; Sokoreli, I.; Urbinati, A.; Brown, O.; Sze, S.; Rigby, A.S.; Kazmi, S.; et al. Prognostic value of the chest X-ray in patients hospitalised for heart failure. Clin. Res. Cardiol. 2021, 110, 1743–1756.
  10. Galderisi, M.; Cosyns, B.; Edvardsen, T.; Cardim, N.; Delgado, V.; Di Salvo, G.; Donal, E.; Sade, L.E.; Ernande, L.; Garbi, M.; et al. Standardization of adult transthoracic echocardiography reporting in agreement with recent chamber quantification, diastolic function, and heart valve disease recommendations: An expert consensus document of the European association of cardiovascular imaging. Eur. Heart J. Cardiovasc. Imaging 2017, 18, 1301–1310.
  11. Szyszka, A.; Płońska-Gościniak, E. Transesophageal echocardiography. J. Ultrason. 2019, 19, 62–65.
  12. Roy, P.-M.; Colombet, I.; Durieux, P.; Chatellier, G.; Sors, H.; Meyer, G. Systematic review and meta-analysis of strategies for the diagnosis of suspected pulmonary embolism. BMJ 2005, 331, 259.
  13. Kearon, C. Natural History of Venous Thromboembolism. Circulation 2003, 107, I22–I30.
  14. Glaab, T.; Taube, C. Practical guide to cardiopulmonary exercise testing in adults. Respir. Res. 2022, 23, 9.
  15. Durstenfeld, M.S.; Sun, K.; Tahir, P.; Peluso, M.J.; Deeks, S.G.; Aras, M.A.; Grandis, D.J.; Long, C.S.; Beatty, A.; Hsue, P.Y. Use of Cardiopulmonary Exercise Testing to Evaluate Long COVID-19 Symptoms in Adults: A Systematic Review and Meta-analysis. JAMA Netw. Open 2022, 5, e2236057.
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