Discussion
The main aim of this study was to apply, in a real-life clinical setting, a previous finding of this group indicating that NTproBNP levels rise to a peak during the 24-h period following onset of AF and then progressively decline over the next 24 h.7 The observation that approximately 85% of patients with AF of recent onset exceeded the age-adjusted International Collaborative of NT-proBNP Study levels during the first 24–36 h after onset of the arrhythmia (declining rapidly after that despite the persistence of AF) may be used to put a time frame on AF of unknown onset. In other words, if a patient presenting with AF of unknown time of onset has markedly raised NTproBNP levels in the absence of heart failure symptoms and signs, it may mean that the arrhythmia is not more than 36–48 h old. In order to test the safety of such a hypothesis, we performed a proof-of-concept study using TEE to ascertain that those patients with NTproBNP levels above the respective cut-off values for their age were much less likely to have a LA/LAA thrombus. Indeed, a raised NTproBNP level was a powerful independent predictor of absence of LA/LAA thrombi, with a negative predictive value of 95.3%. Consequently, the possibility of using NTproBNP levels to assess the time frame of AF onset appears to be plausible.
The findings of this study can be interpreted as confirmation of the temporal association of the rise in NTproBNP with the onset of AF and the subsequent return to lower values (close to baseline). This is also strengthened by the fact that patients in group B had significantly larger atria than patients in group A, an observation also indicative of ‘older’ AF. These assumptions were not only evident in the markedly increased prevalence of atrial thrombi in patients with low NTproBNP levels, but also in the observation of more patients with atrial SEC among them. SEC, although not formally adopted as a stratifier for thrombotic risk and administration of treatment, is a known imaging indicator of thromboembolic risk.11 12
The observation that, among patients with AF of presumably recent onset (group A), LA/LAA thrombi were found in two patients with particular characteristics (large atria and increased thromboembolic risk as indicated by their CHA2DS2VASc score) could mean that a combination of NTproBNP levels (to assess the time frame of AF onset) with LA size and CHA2DS2VASc score might be able to identify correctly almost all patients without thrombi and who are therefore safe for immediate cardioversion. This would, of course, require validation by a large clinical study.
Discussion
The main aim of this study was to apply, in a real-life clinical setting, a previous finding of this group indicating that NTproBNP levels rise to a peak during the 24-h period following onset of AF and then progressively decline over the next 24 h.7 The observation that approximately 85% of patients with AF of recent onset exceeded the age-adjusted International Collaborative of NT-proBNP Study levels during the first 24–36 h after onset of the arrhythmia (declining rapidly after that despite the persistence of AF) may be used to put a time frame on AF of unknown onset. In other words, if a patient presenting with AF of unknown time of onset has markedly raised NTproBNP levels in the absence of heart failure symptoms and signs, it may mean that the arrhythmia is not more than 36–48 h old. In order to test the safety of such a hypothesis, we performed a proof-of-concept study using TEE to ascertain that those patients with NTproBNP levels above the respective cut-off values for their age were much less likely to have a LA/LAA thrombus. Indeed, a raised NTproBNP level was a powerful independent predictor of absence of LA/LAA thrombi, with a negative predictive value of 95.3%. Consequently, the possibility of using NTproBNP levels to assess the time frame of AF onset appears to be plausible.
The findings of this study can be interpreted as confirmation of the temporal association of the rise in NTproBNP with the onset of AF and the subsequent return to lower values (close to baseline). This is also strengthened by the fact that patients in group B had significantly larger atria than patients in group A, an observation also indicative of ‘older’ AF. These assumptions were not only evident in the markedly increased prevalence of atrial thrombi in patients with low NTproBNP levels, but also in the observation of more patients with atrial SEC among them. SEC, although not formally adopted as a stratifier for thrombotic risk and administration of treatment, is a known imaging indicator of thromboembolic risk.11 12
The observation that, among patients with AF of presumably recent onset (group A), LA/LAA thrombi were found in two patients with particular characteristics (large atria and increased thromboembolic risk as indicated by their CHA2DS2VASc score) could mean that a combination of NTproBNP levels (to assess the time frame of AF onset) with LA size and CHA2DS2VASc score might be able to identify correctly almost all patients without thrombi and who are therefore safe for immediate cardioversion. This would, of course, require validation by a large clinical study.
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