Can metamizol play a role in nuclear medicine practice?

Abstract

I read with great interest the letter to the editor by Georgoulias et al., published in the January 2009 issue concerning the drug enhancement of myocardial tracer uptake during myocardial perfusion imaging [1]. The authors also focused on our article “Tc sestamibi myocardial perfusion scintigraphy (MPS) with the novel use of metamizol for the detection of perfusion reversibility” published in the August 2008 issue [2]. Metamizol has been in clinical use for more than three quarters of a century, and recent reports have shown that metamizol also has a relaxing activity in vascular smooth muscle as assessed in in vitro tissue bath techniques and in vivo animal models [3–8]. In our above-mentioned study [2], we aimed to investigate whether the vascular smooth muscle relaxing effect of metamizol has the potential to better define myocardial ischaemia during MPS and we found that metamizol rest MPS displayed the defect reversibility better than baseline rest MPS and that metamizol-induced myocardial sestamibi uptake was significantly higher (p<0.001) than stress/baseline rest MPS examinations. Blood pressure remained unaltered after metamizol induction. So, we concluded that metamizol increases the detection of the viable myocardium regions during MPS and helps to make a confident interpretation for defect reversibility. In their letter to the editor, Georgoulias et al. [1] summarized the use of technetium-labelled tracers (sestamibi and tetrofosmin) for the detection of viable myocardium with one or a combination of the approaches such as determining the severity of resting defects according to the percent of the peak myocardial activity, assessing the radiotracer uptake after nitroglycerin administration and assessing the regional myocardial function and thickening by performing gated SPECT. The authors also shared that they had great experience with gated SPECT on this issue and they emphasized the clinical dilemma in the differentiation of viable myocardium from scar in patients without a history of myocardial infarction who had undergone gated SPECT study. In our study [2], we postulated that since metamizol is no longer detectable in the serum soon after its oral administration, its active metabolite 4-MAA may be responsible from the enhancement of perfusion seen on MPS due to its vasorelaxing effect. 4-MAA has a longer elimination half-life (2.7 h) than nitroglycerin (a few minutes). So, Georgoulias et al. indicated that the investigation of metamizol’s influence on cardiac function would be of interest and proposed that studies are needed to increase the information regarding the use of metamizol in combination with MPS. We are of the same opinion as Georgoulias et al. on this issue. Additionally, in our opinion correlative studies comparing the effects of metamizol and nitroglycerin on the myocardial uptake of the radiopharmaceuticals might be undertaken. Metamizol might have an advantage over nitroglycerin since it causes no significant alteration in blood pressure [2], and we did not observe any complaints such as vertigo, dizziness, nausea or vomiting due to metamizol in our patients. In our above-mentioned study [2], baseline rest MPS showed an average perfusion improvement of 7.8% in the regions where stress perfusion defects were seen. On the other hand, metamizol induction displayed an average perfusion improvement of 18.2% in the same myocardial regions when compared to stress MPS. Consequently, the Eur J Nucl Med Mol Imaging (2009) 36:1191–1192 DOI 10.1007/s00259-009-1149-2