Type Natriuretic Peptide

B-type natriuretic peptide (BNP) is released predominantly by the cardiac ventricles in response to myocardial wall stretch (see Chapter 21) (21).

ten Wolde et al. (22) published the first study showing that the plasma concentration of BNP is associated with the risk of adverse outcome in patients with acute PE. They examined 110 consecutive hemodynamically stable patients and divided their BNP results into terciles: 0-2.5, 2.5-21.7, and >21.7 pmol/L. When they followed patients for 3 mo after the diagnosis of PE, there were no deaths in the lowest tercile, two deaths in the middle tercile, and nine deaths in the highest tercile.

In a separate study, Kucher et al. (23) measured the plasma concentration of BNP in 73 consecutive patients with acute PE. They used a prespecified cutoff of <90 pg/mL for predicting the absence of a major adverse cardiovascular event. In 20 patients with adverse clinical events, the median BNP was 194 compared with 39 among patients with a benign clinical course (Fig. 3). In multivariable analysis, the adjusted OR for an adverse clinical

Benign Adverse

Clinical Outcome

Fig. 3. Box plots with BNP levels according to clinical outcome. (A) Median values, 50 and 95% CIs, and outliers for BNP; (B) ROC curve ofBNP for adverse clinical outcome. (Reprinted with permission from ref. 23.)

Benign Adverse

Clinical Outcome

Fig. 3. Box plots with BNP levels according to clinical outcome. (A) Median values, 50 and 95% CIs, and outliers for BNP; (B) ROC curve ofBNP for adverse clinical outcome. (Reprinted with permission from ref. 23.)

Fig. 4. Cumulative rate of adverse clinical outcomes according to proBNP (NTpBNP) levels <500 ® 500 pg/mL (p < 0.0001). (Reprinted with permission from ref. 24.)

event in patients with BNP > 90 pg/mL was 8.0 (95% CI: 1.3-50; p = 0.03). The sensitivity, specificity, and negative and positive predictive value were 85, 75, 93, and 57%, respectively. However, the most sensitive BNP cutoff, identified by receiver operating characteristic (ROC) analysis, was <50 pg/mL. Sensitivity, specificity, and negative and positive predictive value of BNP levels <50 pg/mL were 95, 60, 97, and 48%, respectively.

Although N-terminal proBNP (NT-proBNP) has not been studied as extensively as BNP in patients with PE, the available data suggest similar prognostic relationships. Low levels of NT-proBNP are associated with an uneventful hospital course, whereas elevated levels portend a higher risk of adverse clinical outcomes (24,25) (Fig. 4).

Despite these promising data, the utility of BNP in patients with PE remains less well established than that of troponin. For example, in a study of 50 patients with PE, BNP levels were increased in the presence of right ventricle dysfunction but were not predictive of mortality or in-hospital complications (26). Moreover, the appropriate cutoff level for BNP for risk assessment in patients with PE is not as clear as for troponin, for which any elevation is abnormal and appears to indicate an increased risk of a complicated

Fig. 5. Mechanism of cardiac biomarker level elevation in pulmonary embolism. RV, right ventricular. NP, natriuretic peptides; cTnI, cardiac troponin I. (Reprinted with permission from ref. 10.)
Fig. 6. Pulmonary embolism management strategy. RV, right ventricular; cTn, cardiac troponin. (Reprinted with permission from ref. 10.)

hospital course. Finally, it remains unclear whether the natriuretic peptides will be complementary to or alternative markers for the troponin.

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