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Background Intracoronary ultrasound (ICUS) imaging is potentially suitable to identify lesions at high risk of restenosis after percutaneous transluminal coronary angioplasty (PTCA), but it has not been studied systematically. Methods and Results We recruited 200 patients in whom ICUS studies were performed after successful PTCA and related their ICUS parameters to 6-month follow-up quantitative coronary angiography. This was performed in 164 patients (82%), yielding 170 lesions for analysis. The overall incidence of a ≥50% diameter stenosis at follow-up (categorical restenosis) was 29.4%. Quantitative ICUS parameters were weakly but significantly related to follow-up minimal luminal diameter on quantitative coronary angiography (lumen area: R 2 =.36, P =.0001; vessel area: R 2 =.29, P =.0002; plaque area: R 2 =−.18, P =.021; percent obstruction: R 2 =−.15, P =.05), but categorical restenosis was not significantly related to these parameters ( P =.63, .77, .38, and .08, respectively). There were no significant predictors of restenosis in ICUS parameters of plaque morphology: eccentric versus concentric ( P =1.0), plaque type (hard, soft, or calcific, P =.98), or the number of calcified quadrants ( P =.41). There were no significant predictors of restenosis in two predefined types of vessel-wall disruptions: (1) rupture: presence ( P =.79), depth (partial versus complete, P =.85), or extent in quadrants ( P =.6), and (2) dissection: presence ( P =.31), depth ( P =.82), or extent ( P =.38). Conclusions Qualitative ICUS parameters after PTCA did not predict restenosis. A larger lumen and vessel area and a smaller plaque area by ICUS were associated with a larger angiographic minimal lumen diameter at follow-up, but these parameters were not significantly related to categorical restenosis.

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Evidence from the first prospective studies of coronary atherosclerosis demonstrated that intravascular imaging has limited accuracy in detecting lesions that are likely to progress and cause future events, and divided the scientific community into experts who advocate abandoning this quest and others who suggest intensifying our efforts improve and optimise the available imaging techniques. Although the current evidence may not justify the use of invasive or non-invasive imaging in the clinical setting for the detection of vulnerable, high-risk lesions, it is apparent that imaging has provided unique insights about plaque pathophysiology and evolution. Recent evidence indicates that both invasive and non-invasive imaging also provides useful prognostic information in patients with established coronary artery disease and in asymptomatic individuals and is likely to enable more accurate risk stratification. Future studies are anticipated to provide further insights about the value of novel hybrid imaging techniques, which are expected to enable complete assessment of plaque pathophysiology, in detecting vulnerable lesions and identifying high-risk patients that would benefit from new aggressive treatments targeting coronary atherosclerosis.

Both quantitative flow ratio (QFR) and fractional flow reserve derived from computed tomography (FFRCT) have shown significant correlations with invasive wire-based fractional flow reserve. However, the correlation between QFR and FFRCT is not fully investigated in patients with complex coronary artery disease (CAD). The aim of this study is to investigate the correlation and agreement between QFR and FFRCT in patients with de novo three-vessel disease and/or left main CAD. This is a post-hoc sub-analysis of the international, multicenter, and randomized SYNTAX III REVOLUTION trial, in which both invasive coronary angiography and coronary computed tomography angiography were prospectively obtained prior to the heart team discussion. QFR was performed in an independent core laboratory and compared with FFRCT analyzed by HeartFlow™. The correlation and agreement between QFR and FFRCT were assessed per vessel. Furthermore, independent factors of diagnostic discordance between QFR and FFRCT were evaluated. Out of 223 patients, 40 patients were excluded from this analysis due to the unavailability of FFRCT and/or QFR, and a total of 469 vessels (183 patients) were analyzed. There was a strong correlation between QFR and FFRCT (R ​= ​0.759; p ​< ​0.001), and the Bland-Altman analysis demonstrated a mean difference of -0.005 and a standard deviation of 0.116. An independent predictor of diagnostic concordance between QFR and FFRCT was the lesion location in right coronary artery (RCA) (odds ratio 0.395; 95% confidence interval 0.174-0.894; P ​= ​0.026). In patients with complex CAD, QFR and FFRCT were strongly correlated. The location of the lesion in RCA was associated with the highest diagnostic concordance between QFR and FFRCT.

In-hospital infection (IHI) after transcatheter aortic valve implantation (TAVI) has received little attention, although it may have a significant effect on outcomes and costs because of prolonged hospital stay. Therefore, the aim of this study was to determine the incidence, type, predictors, and prognostic effects of IHI after TAVI. This study included 298 consecutive patients from 2 centers who underwent TAVI from November 2005 to November 2011. IHI during the hospital stay was defined on the basis of symptoms and signs assessed by the attending physician in the cardiac care unit or medium care unit in combination with all technical examinations performed to confirm infection. IHI after TAVI was observed in 58 patients (19.5%): urinary tract infections in 25 patients (43.1%), pneumonia in 12 patients (20.7%), and access-site infections in 7 patients (12.1%). In 12 patients (20.7%), the site of infection could not be determined, and 2 patients (3.4%) had multiple infection sites. Multivariate analysis revealed that surgical access through the femoral artery was the most important determinant of infection (odds ratio [OR] 4.18, 95% confidence interval [CI] 1.02 to 17.19), followed by perioperative major stroke (OR 3.21, 95% CI 1.01 to 9.52) and overweight (body mass index ≥25 kg/m2; OR 2.27, 95% CI 1.12 to 4.59). The length of hospital stay in patients with IHIs was 15.0 days (interquartile range 8.0 to 22.0) compared with 7.0 days (interquartile range 4.0 to 10.0) in patients without infections (p <0.0001). Kaplan-Meier estimates of survival at 1 year were 76.6% and 74.4% (log-rank, p = 0.61), respectively. Unadjusted and adjusted OR analysis revealed that IHI did not predict mortality at 30 days (OR 1.27, 95% CI 0.49 to 3.30) or at 1 year (hazard ratio 1.24, 95% CI 0.68 to 2.25). In conclusion, IHI occurred in 19.5% of the patients. Patient-related and, more important, procedure-related variables play a role in the occurrence of infection, indicating that improvements in the execution of TAVI may lead to a reduction of this complication.

Background Available data on the long-term impact of coronary artery calcification (CAC) after percutaneous coronary intervention (PCI) with drug-eluting stents (DES) are limited. Purpose We evaluated the long-term impact of CAC on outcomes after PCI and the respective performance of first- and second-generation DES. Methods We pooled patient-level data from 18 randomized trials evaluating DES categorized according to the presence of angiographic core lab-confirmed moderate or severe CAC in any target lesion. Outcome measures of interest were the patient-oriented composite endpoint (POCE; death, myocardial infarction [MI], or any revascularization), the device-oriented composite endpoint of target lesion failure (TLF; cardiac death, target vessel MI or ischemia-driven target lesion revascularization), and definite or probable stent thrombosis (ST). Multivariable Cox proportional regression with study as a random effect was used to assess 5-year outcomes. Results A total of 19,833 patients were included. Moderate or severe CAC was present in 6211 (31.3%) patients and associated with increased 5-year risk of the POCE (adjHR 1.12, 95% CI 1.05–1.20, p&lt;0.001), TLF (adjHR 1.21, 95% CI 1.09–1.35, p&lt;0.001), and a trend for greater ST (adjHR 1.24, 95% CI 0.99–1.54, p=0.06). In patients with CAC, second-generation DES were associated with a reduction in the 5-year risk of TLF and ST, and a trend for reduced POCE compared with first-generation DES (Table). Conclusion In this large-scale study, target lesion moderate or severe CAC was associated with adverse patient- and device-related outcomes at 5 years, risks that were reduced but not eliminated with second-generation DES. Acknowledgement/Funding This investigator-sponsored study was funded by Abbott Vascular.

To determine the role of protein kinase C (PKC) in the signal transduction in eosinophil pathways, we have assessed the effects of the phorbol ester phorbol 12-acetate 13-myristate (PMA) on guinea pig peritoneal eosinophils challenged with platelet-activating factor (PAF). Pretreatment with PMA completely inhibited the PAF-induced release of eosinophil peroxidase (EPO) and superoxide anions and the rise in intracellular Ca2+ concentration ([Ca2+]i), with IC50s of 2 to 10 nM. This inhibition was reversed when the cells were preincubated with the PKC inhibitor staurosporine for 5 min before the addition of PMA. Staurosporine also inhibited PAF-induced EPO release but not the rise in [Ca2+]i. The inactive ester 4 alpha-phorbol 12,13-didecanoate had no inhibitory effect on eosinophil activation. Finally, PMA inhibited the binding of the PAF antagonist [3H]WEB 2086 to intact eosinophils. Taken together, these data suggest that PKC may have a physiologic role in regulating PAF-induced eosinophil responses through expression of PAF receptors on the cell surface.

The concentration of nitric oxide (NO) is increased in the exhaled air of patients with inflammatory lung diseases, including asthma, possibly reflecting cytokine-mediated chronic airway inflammation. Endogenous NO is generated from L-arginine by the action of several types of NO synthase (NOS). NOS have structural similarities with cytochrome P450 reductases. Alcohol decreases exhaled NO in animals, but this has not previously been investigated in man. We studied the effect of alcohol ingestion in nine asthmatic and 12 normal subjects, measuring the peak concentration of exhaled NO using a modified chemiluminescence analyser. A significant decrement in NO occurred in asthmatic patients (mean +/- SEM before ethanol 204 +/- 58 to 158 +/- 59 parts per billion (ppb) after ethanol; p &lt; 0.02), without significant change in the normal subjects (122 +/- 14 to 114 +/- 15 ppb). Thus, in our study, alcohol decreased exhaled nitric oxide in asthmatic subjects but not in normal individuals. This may reflect preferential action on inducible nitric oxide synthase which is expressed in asthmatic airways. An inhibitory effect of ethanol on inducible nitric oxide synthase may contribute towards the effect of alcohol in asthma.