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We read with interest the paper by Konigstein et al, and wish to commend the authors for their significant contribution. In the discussion section the authors suggest that the antiischaemic effect of the Coronary Sinus ReducerTM Stent (CSRS) (Neovasc Medical, Inc., Or Yehuda, Israel) is based on the hypothesis described by Camici et al. We would like to point out that, while Camici et al published this hypothesis in the New England Journal of Medicine in 2007, the initial experiments with the CSRS were performed a decade before. Even Banai et al had used the CSRS before Camici et al published their hypothesis, when they implemented the first-in-man study using this stent. Konigstein et al support their rationalisation of the anti-ischaemic effect of the CSRS by quoting Ido et al, a study which examined the effects of coronary sinus occlusion on coronary collateral blood flow and on the distribution of regional myocardial blood flow in dogs. We wish to emphasise that there is a substantial difference between human and dog morphology of veins that drain into the coronary sinus. In the mid 1990s we tested a new strategy supporting the ischaemic myocardium. This strategy included: 1) catheterisation of the coronary venous system rather than catheterisation of the coronary arteries, and 2) reduction of the coronary sinus (CS) effective cross area, as opposed to the expansion of a narrowed coronary artery. At that time, the main concept behind this strategy was to rebuild retrograde coronary pressure that would be attenuated by the atherosclerotic disease. In order to test this strategy, we designed and manufactured the first CSRS. In a preliminary non-ischaemic pig model we succeeded in increasing the mean CS pressure from 7.0 to 24.6 mmHg (p=0.011) after CSRS deployment. Further studies in a non-ischaemic pig model were devoted to macroscopic and histological investigations of the treated hearts, in particular investigating whether any structural or histological damage, such as an infarct, had occurred after CSRS implantation. While looking for such damage, these studies revealed that eight to 12 weeks of coronary sinus narrowing produced macroscopic epicardial and intramyocardial new blood vessels – neovascularisation. Histopathological analysis described these findings as follows: significant proliferation of small to medium-sized vessels, containing smooth muscle representing coronary collaterals. This was evident in almost all specimens, representing various myocardial anatomical areas, including specimens from the anterior and mid-posterior wall. According to these unpredicted neovascularisation findings after CSRS implantation in a non-ischaemic pig model, we created the name “Neovasc” for this novel CSRS device. Backwards pressure elevation in the venules and capillaries starts immediately after CSRS deployment and a few weeks before clinical improvement. However, neovascularisation created by CSRS a few weeks following deployment seems to be the main contributing factor for the anti-ischaemic effect, and correlates well with the report by Konigstein et al, in which clinical improvement was, in most cases, reported to have started a few weeks following the procedure.

Re: “Transcatheter treatment for refractory angina with the coronary sinus Reducer” by Maayan Konigstein et al