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brain type ( B type, BNP ) natriuretic peptide in the detection of congestive heart failure

 
   

  • there is evidence that in patients presenting to emergency departments with dyspnoea and possible congestive heart failure (1):
    • B type natriuretic peptide levels revealed a diagnostic accuracy of 83.4% for congestive heart failure (at a cutoff of 100 pg per milliliter); negative predictive value of B-type natriuretic peptide at levels of less than 50 pg per milliliter was 96%
      • this is based on evidence from a blinded comparison of BNP levels with a confirmatory diagnosis of congestive heart failure made by 2 cardiologists who reviewed medical records
      • 1586 emergency department patients who had shortness of breath as the most prominent symptom were included in the study. Exclusion criteria included age < 18 years, dyspnoea clearly not secondary to congestive heart failure (e.g. trauma), acute myocardial infarction, renal failure and unstable angina without dyspnoea as the primary symptom
  • data suggest that serial point-of-care testing of BNP will be of immense help in patients presenting to urgent care clinics with dyspnoea. Additionally, BNP might serve as a screen for patients referred for echocardiography, and might also be an effective way to improve the in-hospital management of patients admitted with decompensated CHF. Finally, the role of BNP in the outpatient cardiac or primary care clinic may be one of critical importance in titration of therapies as well as assessment of the state of the patient's neurohormonal compensation (2)
  • the NICE clinical guideline on CHF recommends that those suspected of having heart failure because of their history, signs and symptoms should have a 12-lead ECG and/or BNP, with echocardiography being performed where the result of either is abnormal (3)

Notes:

  • in the emergency department patients with dyspnoea, BNP and amino terminal proBNP concentrations had similar diagnostic accuracy for detecting patients with congestive heart failure (4,5)
  • BNP and proBNP and cardiovascular risk
    • higher concentrations of BNP or proBNP, are consistently associated with increased risk of death and cardiovascular events (6)
      • proBNP concentrations of >= 100 ng/l increased risk of all-cause mortality in patients with or without stable coronary artery disease (7)
    • there is also evidence that pro-BNP is a marker of long-term mortality in patients with stable coronary disease and provides prognostic information above and beyond that provided by conventional cardiovascular risk factors and the degree of left ventricular systolic dysfunction (8)
    • BNP and cardiac toponin in healthy older adults
      • a study investigated the prognostic value of detectable cardiac troponin T (TnT) and elevated N-terminal pro-B-type natriuretic peptide (NT-proBNP) levels in a population of community-dwelling older adults
        • revealed that apparently healthy adults with detectable TnT or elevated NT-proBNP levels are at increased risk of death
        • those with both TnT and NT-proBNP elevations are at even higher risk, and the increased risk persists for years
  • BNP measurement was superior to two-dimensional echocardiographic determination of EF in identifying CHF, regardless of the threshold value, in patients with acute dyspnoea (8)
  • in patients with atrial fibrillation (AF)
    • the presence of AF is associated with higher circulating BNP levels, suggesting that a higher diagnostic threshold should be used in patients with AF (10)
  • patients with both a completely normal ECG and normal BNP are unlikely to have heart failure (11)
  • BNP and management of heart failure (12):
    • low concentrations of BNP make heart failure unlikely
      • a low concentration (< 100pg/ml) makes heart failure unlikely
    • high levels of BNP in heart failure predict a poor prognosis
      • plasma BNP appears to be the most useful single predictor of prognosis. A very high level on optimal drug treatment (above 500 pg/ml) suggests a poor prognosis, and a low level (below 100pg/ml) suggests the patient will do well
    • driving down BNP levels by aggressive treatment improves the clinical outcome
      • treatment with a diuretic, ACE inhibitor or angiotensin receptor blocker (ARB) reduces the concentration, and beta-blockers may initially increase but then decrease the blood concentration. Reduced excretion of BNP in serious kidney dysfunction (creatinine above 200 ìmol/l) can contribute to increased plasma BNP levels
      • patients with heart failure do better if the doctor is aware of the plasma BNP concentration and tries to drive it down to a low level (<100 pg/ml) by more aggressive use of beta-blockers and ACE inhibitors or ARBs
    • BNP is not recommended for screening for cardiac dysfunction in the general population

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