Brain natriuretic peptide and other cardiac markers predicting left ventricular remodeling and function two years after myocardial infarction

Abstract

Background. Left ventricular remodeling is a complex pathologic process of progressive left ventricular dilatation, leading to dysfunction and heart failure in patients after myocardial infarction. Objective. To evaluate biochemical markers, reflecting cardiac remodeling process after first myocardial infarction and compare those markers with clinical characteristics of left ventricular remodeling. Material and methods. Brain natriuretic peptide, troponin I, creatine kinase, creatine kinase MB mass, lactate dehydrogenase levels were measured in 30 patients with acute myocardial infarction on days 1, 2, 3–7 . Brain natriuretic peptide was measured at 3 months, 6 months, and 2 years after myocardial infarction. Echocardiographic parameters of left ventricular remodeling were determined in acute phase (day 1–3), at 3 months, 6 months, and 2 years after MI. Results. In acute phase, brain natriuretic peptide level progressively increased according to worsening of left ventricular geometry: in normal left ventricle geometry group, brain natriuretic peptide level was 84.1 (58.7–121) pg/mL, in concentric remodeling group – 125 (69.2–165) pg/mL, in concentric hypertrophy group – 128 (74–368) pg/mL, and in eccentric hypertrophy group – 470 (459–494) pg/mL, P=0.02. Patients who had increased left ventricular end diastolic diameter index during 2-year period had higher brain natriuretic peptide level in the acute phase (584 (249–865) pg/mL vs. 120 (67–202) pg/mL, P=0.04) and also higher peak lactate dehydrogenase and troponin I levels. Conclusions. Brain natriuretic peptide level in acute phase of myocardial infarction is strongly associated with the markers of myocardial injury and related to left ventricular geometry changes and remodeling. Brain natriuretic peptide together with troponin I levels in acute phase of myocardial infarction might be useful in predicting subsequent cardiac function.

Bone marrow mononuclear cells enhance anti-inflammatory effects of pravastatin against isoproterenol-induced myocardial infarction in rats

“…Experimental studies have shown that the level of BNP secretion and BNP mRNA expression are high mainly in the boundary region between the infarcted and non-infarcted regions (Hama et al 1995) that is stimulated by the increased wall stress that directly related to the infarction. Also it was found that BNP level following MI appears to be associated not only with left ventricle ejection fraction (LV-EF) deterioration, but also with the extent of myocardial injury as assessed by cardiac markers, supporting the opinion that elevation of BNP is a general indicator of reduced cardiac performance (Grybauskiene et al 2007). In a previous study, high plasma BNP levels 3 months after optimized treatment for HF are risk factors for morbidity and mortality of patients with HF; moreover, plasma BNP levels 3 months after optimized treatment are more useful predictors than the levels of LV-EF (Maeda et al 2000).…”

“…In addition, BNP is not considered released from the necrotizing myocardium (Grybauskiene et al 2007). Experimental studies have shown that the level of BNP secretion and BNP mRNA expression are high mainly in the boundary region between the infarcted and non-infarcted regions (Hama et al 1995) that is stimulated by the increased wall stress that directly related to the infarction.…”

The evaluation of B-type Natriuretic Peptide and Troponin I in acute myocardial infarction and unstable angina

“…The results are shown in Figure 1. The other researchers have got results of BNP and troponin correlation with correlation coefficient r = 0.273-0.70 (15,19). Necrosis and apoptosis of myocytes in AMI are contributions of progressive left ventricle dysfunction.…”

Natriuretic Peptide Testing in Primary Care

“…Because natriuretic peptides (NPs) are produced in the heart, they may serve as a biological marker of LV remodeling and changes in circulating NPs may parallel the changes in LV structure [6-8]. …”