Rapid changes of atrial natriuretic peptide concentration during percutaneous transluminal coronary angioplasty

Use of pro‐atrial natriuretic peptide in the detection of myocardial ischaemia

“…Our findings regarding proANP extend previous studies on the use of this marker [16,18–24,30,31]. Already more than 10 years ago, Burnett and colleagues have shown that plasma proANP concentrations are significantly increased in patients with asymptometic left‐ventricular dysfunction and that this peptide can serve as a marker for diagnosis of such patients [30].…”

“…Fourth, and again in contrast to our expectation, there was no correlation between the exercise-induced change in the proANP level and the extent of myocardial ischaemia. Our findings regarding proANP extend previous studies on the use of this marker [16,[18][19][20][21][22][23][24]30,31]. Already more than 10 years ago, Burnett and colleagues have shown that plasma proANP concentrations are significantly increased in patients with asymptometic left-ventricular dysfunction and that this peptide can serve as a marker for diagnosis of such patients [30].…”

“…Findings from several previous studies in patients with CAD suggest that proANP is secreted rapidly because of the brief increase in intracardiac pressures observed in patients with exercise‐induced myocardial ischaemia and may be a very promising marker for the detection of myocardial ischaemia [16,22–24]. Thus, the aim of this study was to evaluate the utility of mid‐regional proANP levels to detect exercise‐induced myocardial ischaemia.…”

Pathophysiologic Relevance of Measuring the Plasma Levels of Cardiac Natriuretic Peptide Hormones in Humans

“…It is well known that cardiac natriuretic peptides can be secreted or released by cardiomyocytes during ischemia; however, the exact pathophysiological mechanism(s) responsible for this event is (are) not well known, Indeed, hypoxemia per se may stimulate the release of cardiac peptides by cardiomyocytes as suggested by the increased levels of cardiac natriuretic peptides observed in patients with acute exacerbation of chronic obstructive pulmonary disease [101] or acute dyspnoea [102]. The release of cardiac peptide hormones is enhanced during myocardial ischemia induced by percutaneous transluminal coronary angioplasty (PTCA) [103][104][105][106]. However, such event has been related more frequently to left ventricular dysfunction with increased left ventricular and diastolic and increased left atrial pressure (i.e., to atrial stretch secondary to myocardial ischemia and consequent increase in ventricular and atrial pressures) rather than to myocardial ischemia (hypoxia) per se.…”