Six months of DAPT was not inferior to 18 months of DAPT following implantation of a DES with a biodegradable abluminal coating. However, this result needs to be interpreted with caution given the open-label design and wide noninferiority margin of the present study. (Nobori Dual Antiplatelet Therapy as Appropriate Duration [NIPPON]; NCT01514227).

In patients with an implanted DDD pacemaker (PM), the atrial contribution may be interrupted by too short an atrioventricular (AV) delay, and filling time may be shortened by too long an AV delay. The AV delay at which the end of the A wave on transmitral flow coincides with complete closure of the mitral valve may be optimal. The subjects were 15 patients [70.3+/-12.3 (SD) years old] with an implanted DDD PM. Cardiac output (CO) and pulmonary capillary wedge pressure (PCWP) were measured by Swan-Ganz catheter. Transmitral flow was recorded by pulsed Doppler echocardiography. AV delay was prolonged stepwise by 25 msc. When the AV delay was set at 155+/-26 ms, the end of the A wave coincided with complete closure of the mitral valve. When the AV delay was prolonged 25, 50, 75, and 100 ms from this AV delay, the interval between the end of the A wave and complete closure of mitral the valve was prolonged 16+/-5, 39+/-6, 65+/-4 and 88+/-5 ms, respectively (r = 0.97, P<0.0001) and diastolic mitral regurgitation was observed during this period. Thus, the optimal AV delay may be predicted as follows: the slightly prolonged AV delay minus the interval between the end of the A wave and complete closure of the mitral valve. When the AV delay was set at 215 ms, there was a significant positive correlation between the predicted optimal AV delay (166+/-23 ms) and the optimal AV delay (CO: 161+/-26 msec, r = 0.93, P<0.0001, PCWP: 161+/-28 msec, r = 0.95, P<0.0001). In conclusion, optimal AV delay can be predicted by this simple formula: slightly prolonged AV delay minus the interval between end of A wave and complete closure of mitral valve at the AV delay setting.

The fractional flow reserve (FFR) is considered to be a reliable index for the assessment of clinically relevant coronary artery stenosis. However, mismatch in assessing the severity of coronary stenosis between coronary angiography and the FFR has been pointed out. The cardiovascular intervention therapeutics (CVIT)-DEFER registry is a prospective multicenter registry study that has enrolled 3,228 consecutive patients among 3,804 patients with angiographically moderate coronary artery lesions in whom FFR analysis was clinically indicated. The demographic and angiographic parameters associated with an FFR ≤0.8 were analyzed, and the incidence of discrepancy between the angiographic severity of coronary stenosis and the FFR was assessed. Based on the visual assessment, 1,609 (42.9%) lesions were categorized as showing 50% stenosis, 1,882 lesions (50.2%) as 75% stenosis, and 257 lesions (6.9%) as 90% stenosis. Angiographic-FFR "mismatch," which was defined as visual stenosis ≥75% with FFR >0.80, was found in 43.4% of lesions, while reverse angiographic mismatch (visual stenosis <75% with FFR ≤0.8) was found in 23.2%. The independent predictors for "angiographic-FFR mismatch" were the presence of percutaneous coronary intervention (PCI) history, one-vessel disease, non-left anterior descending artery (LAD) location, non-diffuse lesion, non-ostial lesion, and non-tandem lesion. Conversely, "reverse angiographic mismatch" was independently associated with the multivessel disease, LAD location, and diffuse lesion. The FFR is not only influenced by luminal stenosis but also by coronary artery morphology and the amount of jeopardized myocardium. Angiographic-FFR mismatch is frequent in patients with moderate coronary stenosis, which suggests the clinical importance of using physiological assessment to guide PCI.

lthough success rates of percutaneous coronary intervention (PCI) are high, PCI of bifurcation lesions is associated with a relatively low success rate and a relatively high incidence of procedural complications, including side branch occlusion and myocardial infarction. . [1][2][3][4][5] Meier et al were among the first to identify the risk of side branch occlusion associated with parent vessel angioplasty. 1 They emphasized that side branches involved in vessel narrowing are at high risk for side branch occlusion during PCI. Boxt et al has reported that vessels with angiographic ostial stenosis >50% have a higher risk of occlusion than those without ostial stenosis. 2 Prior studies have demonstrated that intravascular ultrasound (IVUS) provides information not generated by angiography alone, and the use of sonographic measurements of vascular dimensions has improved short-and long-term outcomes. 6-10 Despite several lines of evidence suggesting that IVUS guidance can reduce the need for target lesion revascularization after PCI, 9,10 it remains controversial whether preintervention IVUS findings can help to identify side branches likely to occlude after PCI of bifurcation lesions.We examined whether preintervention IVUS provides information not available by angiography alone and if it can be used to predict side branch occlusion after PCI. Circulation Journal Vol.69, March 2005 Methods Lesions and the Patient PopulationThe study group consisted of 105 bifurcation lesions in 96 patients with coronary artery disease, all of which had undergone preintervention IVUS examination in the native coronary artery. No directional coronary atherectomy, rotational atherectomy, nor thrombectomy were performed. The clinical diagnoses included: acute myocardial infarction (AMI) (57%), stable angina pectoris (17%), unstable angina pectoris (15%), and previous myocardial infarction (11%). We studied bifurcation lesions involving the main branch and the ostium of the side branch. 11 Only side branches with an estimated reference luminal diameter of 1 mm or greater were considered. Twenty-four lesions were excluded for the following reasons: kissing balloon technique or sequential dilatation was performed (n=6) and extensive target lesion calcification or artifacts which precluded accurate cross-sectional evaluation of the vessel involved (n=18). The remaining 81 bifurcation lesions in 72 patients were studied.Side branch occlusion was defined as a thrombolysis in myocardial infarction (TIMI) flow of ≤2 by the final angiogram after PCI procedures. 12 Quantitative Coronary AngiographyAngiograms were reviewed before introduction of coronary guidewire and after balloon dilation or stent deployment. The coronary flow pattern of side branches was graded according to the classification system of the TIMI trial. 12 Angiograms were digitized and analyzed using an automated edge-detection algorithm (QCA-CMS, version 4.0, Medical Imaging Systems, Rotterdam, The Netherlands).

Background: Monocytes and macrophages have been shown to play major roles in the progression of atherosclerosis. This study examined whether the circulating monocyte count can be used to predict coronary plaque progression of non-culprit intermediate lesions in acute myocardial infarction (AMI). Methods and Results:Intravascular ultrasound findings of non-culprit intermediate plaque in 90 patients were analyzed in the acute phase and at a 7-month follow up. A higher peak monocyte count after AMI was associated with a greater plaque volume change (r=0.32, P=0.002). Multivariate analysis showed that a peak monocyte count of ≥800 /mm 3 was an independent predictor of plaque progression (odds ratio 5.02, P=0.005). High monocyte (≥800 /mm 3 ) at baseline had a higher monocyte count at 7-month follow up than did those with a lower count (368±109 vs 263±64 /mm 3 , P<0.0001). Moreover, the monocyte count at the 7-month follow up was also associated with plaque volume change (r=0.29, P=0.006). Conclusions:The results suggest that circulating monocytes play an important role in the progression of coronary plaque in AMI and that the peak monocyte count during hospitalization might be a predictor of plaque progression. (Circ J 2010; 74: 1384 - 1391