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It was with great interest that I read the elegant work of Billinger et al. [1] which attempted to investigate the haemodynamic effects of metoprolol on the coronary collateral flow index (CFI) immediately after percutaneous transluminal coronary angioplasty (PTCA) in the setting of chronically developed collateral pathways. The authors suggested the hypothesis that the reduction in CFI secondary to metoprolol administration is mostly due to its direct vasoconstrictive effect on collateral vessels. In addition to the authors' conclusions, I would like to point out two supplementary mechanisms leading to post-procedural reduction in collateral flow.
First, the intramyocardial collateral fraction accounts for one major component of the coronary collateral flow [2]. Furthermore, the collateral flow displays a predominant systolic profile which highlights the importance of systolic function as a crucial provider of total coronary collateral flow [3,4]. As the metoprolol reduces the myocardial contractility and as none of the patients had previous contractility anomalies in the area of PTCA, it is therefore not surprising to observe a reduction of CFI following administration of metoprolol.
Second, independent of pharmacologic interventions, a subsequent reduction in collateral flow following the instauration of antegrade coronary flow has been advanced as "functional downregulation of collateral flow" [5]. As the flow measurement subsequent to metoprolol administration is carried out after the third balloon inflation, the participation of this speculated mechanism in CFI reduction cannot be formally excluded.
Finally I like to congratulate the authors once more for their very well structured clinical trial and their consequent contribution to this ongoing field.
Sincerely yours
M.H. Aazami, MD
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