Correlation of Plasma Concentrations of B-Type Natriuretic Peptide With Infarct Size Quantified by Tomographic Thallium-201 Myocardial Scintigraphy in Asymptomatic Patients With Previous Myocardial lnfarction

Abstract

-type (atrial) natriuretic peptide (ANP) and B-type (brain) natriuretic peptide (BNP) are hormones with a wide range of potent biological effects, including natriuresis, diuresis, vasodilatation, and inhibition of the renin -angiotensin -aldosterone and sympathetic nervous systems. 1,2 We and others have shown that ANP is mainly synthesized and secreted from the atria in adult mammals, 1,3-5 but it is also synthesized and secreted from the ventricles in patients with congestive heart failure. [3][4][5] BNP is secreted mainly from the ventricles in normal adult humans as well as in patients with congestive heart failure, and the plasma concentrations of BNP are markedly increased in proportion to the severity of left ventricular (LV) dysfunction in patients with myocardial infarction (MI) or congestive heart failure. 4,[6][7][8] Plasma concentrations of ANP and BNP have been used to predict prognosis after MI. 8,9 It is widely accepted that asymptomatic post-MI patients have a high risk of progression to overt heart failure and death, 10 so it is clinically important to prevent their transition to a stage of accelerated progression of LV dysfunction. BNP concentrations are used to assess prognosis and therapeutic effects in asymptomatic MI patients as well as symptomatic patients 8,11 and the expression of both ANP and BNP is increased in the localized myocardial infarct regions relative to the detrimental hemodynamic parameters in patients with MI. 3,4,6,12 The increase in ANP and BNP concentrations precedes the development of symptoms in asymptomatic MI patients, 4,8,11 but it is unknown what determines the plasma concentrations of ANP and BNP in asymptomatic MI patients with relatively preserved LV function. Therefore, the present study was designed to examine whether the plasma concentrations of ANP and BNP serve as a clinical indicator of the extent of MI, an important determinant of mortality. 13 For these purposes we examined the relationship of plasma concentrations of ANP and BNP with the infarct size quantitatively calculated with thallium-201 single photon emission computed tomography (SPECT), a noninvasive and accurate method of assessment during the chronic phase of MI.

N-Terminal Pro-Brain Natriuretic Peptide is a Biomarker of Congestive Heart Failure and Predictive of 30-Day Untoward Clinical Outcomes in Patients With Acute Myocardial Infarction Undergoing Primary Percutaneous Coronary Intervention

“…It has been reported that the plasma level of BNP increases rapidly and markedly immediately after the onset of AMI, 4 and a more recent study has shown that the BNP level is predictive of infarct size in patients following AMI. 20 The present study found that patients with a longer time-to-treatment interval had a markedly higher plasma NT-proBNP level than those with shorter time-to-treatment interval and that the duration of AMI and a low LVEF (<45%) were independent predictors for elevation of NT-proBNP. Additionally, low LVEF, which has been shown to be a poor prognostic risk factor following AMI, 21 was independently associated with 30-day MACO in this study.…”

Time Course and Prognostic Value of Plasma Levels of N-Terminal Pro-Brain Natriuretic Peptide in Patients After Ischemic Stroke

“…13 Therefore, baseline levels of BNP and NTproBNP have recently been identified as new and useful biochemical markers both in the differential diagnosis of CHF and in predicting adverse cardiac outcomes after AMI, 3,10,14 infarction size 15 or acute coronary syndrome. 13,16 Ischemic stroke, which is mostly caused by atherothrombotic changes of the cerebrovascular system, has many similarities with coronary artery disease.…”

Resuscitative Value of B-Type Natriuretic Peptide in Comatose Survivors Treated With Hypothermia After Out-of-Hospital Cardiac Arrest due to Cardiac Causes

“…[1][2][3][4][5][6][7][8][9][10][11][12] In the clinical studies myocardial ischemia augments the synthesis and release of BNP, even in the absence of myocardial necrosis or preexisting left ventricular dysfunction, although the level of expression of the BNP gene in the left ventricle tripled within 4 h of coronary ligation in an animal model. [25][26][27][28] In the present study, we measured the BNP level once, approximately 43 min after cardiac arrest.…”