Patterns Of Bnp Synthesis And Release In Cardiac Ischemia

Natriuretic peptide levels are elevated both in animal models and in patients with coronary ischemia. In rats that underwent coronary artery ligation, BNP concentration in the left ventricle increased twofold at 12 h and fivefold at 24 h postinfarction, whereas atrial natriuretic peptide (ANP) levels were unchanged (8). Elevated levels of BNP were found in noninfarcted as well as in infarcted areas of the myocardium, suggesting that increased

Table 2 Prognostic Factors in ACSs

Demographic characteristics Age

African-American race Female gender Comorbidities CHF

Hypertension Diabetes

Chronic kidney disease Peripheral vascular disease Physical examination Killip class Elevated heart rate Low blood pressure Biomarkers

Cardiac troponin I or T C-reactive protein BNP and NT-proBNP Other

Angiographic or ECG evidence of more extensive disease

Reduced LVSF

Aggressive pace of symptoms plasma levels of BNP are not simply a "spillover" from infarcted tissue but, rather, a reflection of increased active synthesis by viable myocardial cells. Increased expression of BNP mRNA in the left ventricle further supports this argument.

The plasma concentration of BNP rises in patients with acute myocardial infarction (AMI) more rapidly and to a much greater extent than does the concentration of ANP (9). Both BNP and NT-proBNP levels are higher in patients with anterior MI than in those with inferior MI (9,10). In addition, the time course of the rise in inferior STEMI may be characterized by a single peak during the first day, whereas in anterior STEMI, a biphasic pattern of BNP secretion is common, with the first peak occurring between 1 and 2 d and the second between 4 and 6 d after infarction.

The rise in BNP and NT-proBNP concentration may be sustained over several weeks after ACS and correlates with infarct size, as measured by cardiac enzyme release (11), by thallium-201 single-photon emission computed tomography (SPECT), or contrast-enhanced MRI (12,13). In patients with non-ST-elevation ACS (NSTEACS) with preserved LVSF, NT-proBNP levels also correlate with the extent of regional wall motion abnormalities as assessed by echocardiography (14).

When compared with healthy control subjects and those with stable angina, patients with unstable angina have higher BNP and NT-proBNP levels during the acute phase of illness, with return to near baseline levels following medical stabilization (10,15). In patients with stable coronary artery disease (CAD), BNP and NT-proBNP concentrations rise after exercise (or with dobutamine stress) in proportion to the size of the ischemic territory as measured by nuclear scintigraphy or echocardiography (16,17). In this setting, BNP rises to a greater extent than does NT-proBNP, probably owing to the rapid release of the fully processed active hormone from storage granules (16,17). BNP levels may also

Angiography Thallium Scintigraphy

Fig. 1. Resting NT-proBNP levels in patients without (white bars) and with (slashed bars) either CAD detected on angiography (A) or inducible changes seen on thallium scintigraphy (B). (Adapted from ref. 19.)

Angiography Thallium Scintigraphy

Fig. 1. Resting NT-proBNP levels in patients without (white bars) and with (slashed bars) either CAD detected on angiography (A) or inducible changes seen on thallium scintigraphy (B). (Adapted from ref. 19.)

Fig. 2. Proposed mechanisms of BNP release in coronary ischemic disease.

be elevated at rest in patients with stable angina. The resting plasma concentration of BNP in patients with CAD correlates with inducible ischemia seen on exercise echocardiography and SPECT imaging. Similarly, resting plasma NT-proBNP levels are independently associated with inducible changes on thallium-201 SPECT and with the number of stenotic vessels detected by angiography (Fig. 1) (16-19).

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