DIAGNOSTIC AND SCREENING TESTS
Several diagnostic studies can identify HF or elucidate underlying causes. However, not all tests yield sufficient information for diagnosis—and commonly held “maxims” about findings that definitively rule in or out the diagnosis have been confounded by the available evidence.
Laboratory tests. The lab parameter most associated with HF is brain natriuretic peptide (BNP). Natriuretic peptides are produced primarily within the heart and released into the circulation in response to increased wall tension.14 In contrast to atrial natriuretic peptide (ANP), BNP is secreted not only from the atria but also from the ventricles, especially in patients with HF.15
Circulating concentrations of several cardiac natriuretic peptides—including ANP, BNP, and the two peptides’ N-terminal pro-hormones (N-terminal pro-atrial natriuretic peptide and N-terminal pro-brain natriuretic peptide, respectively) are elevated in both symptomatic and asymptomatic patients with left ventricular dysfunction.16 These levels are generally elevated for both systolic and diastolic HF. However, in one study, as many as 30% of diastolic HF patients had a low BNP level, despite signs and symptoms of HF and significantly elevated left ventricular filling pressures, as determined by invasive hemodynamic monitoring.17 Comorbid obesity is associated with low levels of natriuretic peptides.18
Additional lab tests can provide information about underlying causes of HF or reveal contraindications to certain treatment options (to be discussed in the Treatment section). A complete blood count (CBC) might reveal anemia, which can cause or aggravate HF, and which is an important consideration in management because of its association with decreased renal function, hemodilution, and proinflammatory cytokines. Leukocytosis can signal underlying infection. A troponin assay is helpful for ruling out acute MI as a cause of worsening HF in acute cases. Thyroid function tests and iron studies can be considered to rule out secondary causes of HF.
A serum electrolyte screen should be ordered; results are usually within normal ranges. Hyponatremia is an indicator of activation of the renin–angiotensin–aldosterone system (RAAS) and may be seen in the context of prolonged salt restriction and diuretic therapy. Hyperkalemia and hypokalemia are also prevalent in HF; both are limiting factors for some treatment options. A low sodium level is often the result of increased congestion and release of vasopressin; a level of ≤ 135 mEq/L predicts a poorer outcome.
Kidney function tests can determine whether HF is associated with impaired kidney function, secondary to poor renal perfusion. Poor renal function may limit treatment options. Patients with severe HF, particularly those receiving a high dosage of a diuretic for a long period, may have elevated levels of blood urea nitrogen and creatinine, indicating renal insufficiency.
Electrocardiography and chest radiography. ECGs and chest radiographs are noninvasive tests that have been used widely in the diagnosis of HF. They might indicate an underlying cause (eg, acute MI, ischemia, secondary arrhythmia) but are often nonspecific—and thus may be unhelpful in the diagnosis and treatment of HF.
The most common ECG findings in HF are nonspecific ST-T wave abnormalities.19 Other findings often consist of low-voltage left ventricular hypertrophy, conduction defects, and repolarization changes. With chest radiography, primary findings in HF include pulmonary edema—seen as perivascular edema, peribronchial cuffing, perihilar haze, interstitial edema (Kerley B, or septal, lines), and alveolar fluid—and pleural effusion.19,20
For both these modalities, however, there are commonly held conceptions that particular findings rule out HF—which has been disproven by Fonseca and colleagues.19 Because most patients with HF have an abnormal ECG, some studies have proposed that a normal ECG virtually rules out left ventricular systolic dysfunction.20 Evaluating the value of ECG in HF diagnosis, Fonseca et al found that about 85% of patients with an abnormal ECG had HF—but so did 30% of patients with a normal ECG. They concluded that, if used alone, ECG could have missed as many as 25% of patients with HF.19
Likewise, it has been suggested that a patient cannot have HF if heart size is normal on a chest radiograph.20 Fonseca et al found that cardiac enlargement, while the most informative radiologic measurement in HF, was present in only half of patients with HF.19 About 57% of patients who had an abnormal chest radiograph had HF, but so did about 40% of those who had a normal chest radiograph.19 Therefore, abnormal chest radiograph for identification of HF had an estimated sensitivity of 57%, a specificity of 78%, positive predictive value of 50%, and negative predictive value of 83%.19 The conclusion: Caution should be taken regarding the use of chest radiography in isolation to make a diagnosis of HF.
Echocardiography. The most useful test in evaluating HF is the echocardiogram, because it can distinguish between HF with and without preserved left ventricular systolic function. This is critical: The most clinically relevant classification of HF differentiates systolic and diastolic HF, based on LVEF.2 This determination has both prognostic and therapeutic implications.21
Echocardiography is widely available, safe, and noninvasive. The “echo” can identify the size of the atria and ventricles, valve function and dysfunction, and any associated shunting. Pericardial effusions and heart wall-motion abnormalities (for example, an old MI) are also easily identified.9
A normal ejection fraction does not rule out HF. Therefore, assessment of LVEF should not be considered until after a clinical diagnosis has been made, because more than half of HF patients have a normal LVEF—evidence that can confound the diagnostic process.2
Continue to: TREATMENT OF HEART FAILURE WITH REDUCED LVEF