Congestive heart failure (CHF) is an increasing problem in the aging U.S. population and a common cause of hospitalization. Definitive diagnosis depends on right-heart catheterization or indirect tests such as radionuclide scanning or echocardiography. In emergency situations, history and physical examination commonly are the basis of the diagnosis. Chest radiography and electrocardiography also may point at the diagnosis of CHF. Unfortunately, these diagnostic aids lack sensitivity and specificity. Clinical criteria such as the Framingham Criteria have improved the accuracy of CHF diagnosing based on history and physical examination, but an objective tool is needed for improved accuracy. Collins and associates reviewed the literature about natriuretic peptides in patients with dyspnea.

Left ventricular dysfunction causes activation of several neurohormonal systems to maintain blood pressure and adequate circulation. Natriuretic peptides counterbalance these effects by decreasing the load on the failing heart through diuresis, natriuresis, vasodilation, and inhibition of the reninangiotensin-aldosterone system (see accompanying table). Higher cardiac stress causes increased secretion of these peptides.

B-type natriuretic peptide levels correlate closely with the presence and severity of CHF as the cause of dyspnea. Using a b-type natriuretic peptide level cutoff of 100 pg per mL, physicians have markedly improved the accuracy of pretest predictions of CHF. Elevated b-type natriuretic peptide levels also correlate positively with the risk of a CHF event, cardiac death, and CHF death. A decreasing b-type natriuretic peptide level in response to therapy is a good indicator of decreasing pulmonary artery wedge pressure. Better prognosis has been documented in patients with CHF being treated with diuretics and vasodilators when the b-type natriuretic peptide level decreases. Although the negative predictive value of a low b-type natriuretic peptide level is high, elevated levels can occur in patients with non-CHF causes of dyspnea, including episodes of large pulmonary embolism and chronic obstructive pulmonary disease exacerbations accompanied by cor pulmonale and right-heart strain. Increasing age and female gender also cause slight elevations of b-type natriuretic peptide levels.

Atrial natriuretic peptide and N-terminal atrial natriuretic peptide also are useful markers of left ventricular dysfunction, with the latter marker being more sensitive. Studies are ongoing to look at these peptide quantitations in predicting mortality after myocardial infarction. Comparisons of b-type natriuretic peptide and the atrial natriuretic peptides have demonstrated the greater accuracy of b-type natriuretic peptide levels in differentiating normal and abnormal left ventricular function, especially when negative predictive value for CHF was evaluated.

N-terminal pro–b-type natriuretic peptide is another peptide being studied that has been found useful in monitoring treatment success. C-type natriuretic peptide levels do not appear to increase in CHF but do increase in persons with renal failure and hypoxic patients with cor pulmonale.

The authors conclude that b-type natriuretic peptides and N-terminal pro–b-type natriuretic peptide quantitation correlate well with CHF, although the former has been better studied and found to be a highly sensitive diagnostic tool for CHF, with a high negative predictive value in persons with dyspnea. A level below 100 pg per mL is useful to exclude CHF as a cause of dyspnea, but an elevated value may occur with other diagnoses. B-type natriuretic peptide quantitation is recommended in the evaluation of persons with undifferentiated dyspnea. Increased levels also correlate with a poorer prognosis. Further investigation of the utility of these peptides in the diagnosis of myocardial ischemia is necessary.