El C). The risk of death was lower following post-dilatation (RR 0.81 (CI 0.71?.93) P = 0.003). The numbers at risk are for stent thrombosis and restenosis are identical to Figure 1 and 2 while the numbers at risk for death are identical to Figure 3. doi:10.1371/journal.pone.0056348.gAtmospheres ?what is the ideal number?In modern PCI malapposition and underexpansion of stents are considered major risk factors for stent thrombosis [12] and this view has been supported by observational studies using different imaging techniques [13],[14] and confirmed in a case-control study using IVUS [15]. Such findings are probably the main reason for the use of high inflation pressures during stent implantation despite the lack of documentation from prospective trials. However, there is more to a coronary artery than the interaction between stent and intimal layer. We previously demonstrated that atherosclerotic coronary artery distensibility by balloon inflation is a linear function of pressure at low inflation pressures 
only and primarily in arteries with HIF-2��-IN-1 price concentric lesions [16]. At higher pressures, of relevance for PCI, distensibility was unpredictable. It complicates matters even more for the operator that manufacturer stent balloon compliance charts grossly overestimate the final stent dimensions, as these measurements are typically made in water without the vessel constraint that limits balloon expansion [17]. Very high stent inflation pressures may cause stent edge dissection, coronary rupture, media and intima rupture leading to an increased inflammatory response and higher restenosis rate [18] [19] ?factors that may help to explain our findings in the 22 atm pressure group. Our study identified a possible optimal stent inflation pressure of 20?1 atm during PCI, which was associated with a lower risk of stent thrombosis and restenosis ?a finding that fits well with the studies cited above.patients with diabetes. However, all of these factors were forced into our propensity score method and this considerably 
reduces the likelihood that this explains our findings. The lower mortality seen with post-dilatation was almost immediate following PCI and there was no additional separation of curves over time (Figure 4C). It is probable that this reflects factors not directly related to post-dilatation and was due 23727046 to selection bias not accounted for in our Cox proportional hazard regression model. This notion is supported by the finding that early stent thrombosis did not differ between groups (Figure 4A).LimitationsDespite appropriate statistical adjustments it is possible that unknown confounders may have affected the results of this registry study. The definition of stent thrombosis in our material is not identical to the definition set by the Academic Research Consortium (ARC). The SCAAR definition corresponds to definite stent thrombosis but excludes non-occlusive stent thrombosis. The SCAAR does not hold information on the duration of stent inflation, a parameter closely related to proper stent expansion [24]. The ratio between vessel diameter and balloon diameter was not available and neither was the number of postdilatations. Another important parameter for this study, not SC66 registered in SCAAR, is degree of calcification as calcification per se could be a reason to post-dilate a stent. In SCAAR, when an operator indicates post-dilatation in the database there is no option to specify whether an NC or semi-compliant balloon is used. Our impressi.El C). The risk of death was lower following post-dilatation (RR 0.81 (CI 0.71?.93) P = 0.003). The numbers at risk are for stent thrombosis and restenosis are identical to Figure 1 and 2 while the numbers at risk for death are identical to Figure 3. doi:10.1371/journal.pone.0056348.gAtmospheres ?what is the ideal number?In modern PCI malapposition and underexpansion of stents are considered major risk factors for stent thrombosis [12] and this view has been supported by observational studies using different imaging techniques [13],[14] and confirmed in a case-control study using IVUS [15]. Such findings are probably the main reason for the use of high inflation pressures during stent implantation despite the lack of documentation from prospective trials. However, there is more to a coronary artery than the interaction between stent and intimal layer. We previously demonstrated that atherosclerotic coronary artery distensibility by balloon inflation is a linear function of pressure at low inflation pressures only and primarily in arteries with concentric lesions [16]. At higher pressures, of relevance for PCI, distensibility was unpredictable. It complicates matters even more for the operator that manufacturer stent balloon compliance charts grossly overestimate the final stent dimensions, as these measurements are typically made in water without the vessel constraint that limits balloon expansion [17]. Very high stent inflation pressures may cause stent edge dissection, coronary rupture, media and intima rupture leading to an increased inflammatory response and higher restenosis rate [18] [19] ?factors that may help to explain our findings in the 22 atm pressure group. Our study identified a possible optimal stent inflation pressure of 20?1 atm during PCI, which was associated with a lower risk of stent thrombosis and restenosis ?a finding that fits well with the studies cited above.patients with diabetes. However, all of these factors were forced into our propensity score method and this considerably reduces the likelihood that this explains our findings. The lower mortality seen with post-dilatation was almost immediate following PCI and there was no additional separation of curves over time (Figure 4C). It is probable that this reflects factors not directly related to post-dilatation and was due 23727046 to selection bias not accounted for in our Cox proportional hazard regression model. This notion is supported by the finding that early stent thrombosis did not differ between groups (Figure 4A).LimitationsDespite appropriate statistical adjustments it is possible that unknown confounders may have affected the results of this registry study. The definition of stent thrombosis in our material is not identical to the definition set by the Academic Research Consortium (ARC). The SCAAR definition corresponds to definite stent thrombosis but excludes non-occlusive stent thrombosis. The SCAAR does not hold information on the duration of stent inflation, a parameter closely related to proper stent expansion [24]. The ratio between vessel diameter and balloon diameter was not available and neither was the number of postdilatations. Another important parameter for this study, not registered in SCAAR, is degree of calcification as calcification per se could be a reason to post-dilate a stent. In SCAAR, when an operator indicates post-dilatation in the database there is no option to specify whether an NC or semi-compliant balloon is used. Our impressi.
