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Objectives To evaluate the in vivo feasibility of aortography with one accurately timed diastolic low‐volume contrast injection for quantitative assessment of aortic regurgitation (AR) post transcatheter aortic valve replacement (TAVR). Background With the rise of a minimalistic approach for TAVR, aortography (re)emerges as a pragmatic tool for AR assessment. In a mock circulation system, we have validated the accuracy of a single diastolic injection triggered by electrocardiogram (ECG) with low‐contrast volume. Methods Two‐phase experiment: first, a series of aortograms were performed in a porcine model, with 8 mL of contrast using the synchronized (SYNC) and the conventional non‐synchronized (NS) injections. In a second phase, we developed a model of AR by inserting partially unsheathed Wallstents of 6–10 mm of diameter across the pig's aortic valve, performing SYNC injections with 8 mL of contrast and NS injections with 8 mL and 15 mL (rate: 20 mL/sec). Respective accuracies of SYNC vs. NS were assessed using Passing‐Bablock regression. An angiography core laboratory performed quantitative AR assessment with videodensitometry (VD‐AR). Results The SYNC injections produced higher opacification of the aortic root compared with NS injections ( P = 0.04 for density). In the second phase, a regression line for predicting VD‐AR based on the SYNC injection resulted in a lower intercept and a slope closer to the line of identity (y = 11.9 + 0.79x, P < 0.001, r 2 = 0.94) with the NS‐8 mL than with the NS‐15 mL injection (y = 26.5 + 0.55x, P < 0.001, r 2 = 0.81). Conclusion Synchronized diastolic injection with low contrast volume produced denser images in the aortic root and more accurate than the conventional injection; thus, may be an appealing alternative for assessment of AR post TAVR.

Background Despite the frequent use of spectral analysis of intravascular ultrasound radiofrequency data (VH® IVUS) in clinical studies, the assessment for reproducibility using this with high frequency IVUS remains unexplored. Purpose The aim of this study was to examine the reproducibility of VH IVUS using 45-MHz rotational IVUS in ex vivo human coronary arteries. Methods Data were collected using 45-MHz VH IVUS (Revolution®, Volcano Corporation, San Diego, CA, USA) via a series of pullbacks from eight human coronary artery specimens. Imaging data were analyzed by two independent observers. Intraobserver and interobserver reproducibility were assessed using five pullbacks from five vessels. The intercatheter reproducibility was assessed using three different catheters in each of the five vessels. The intracatheter reproducibility was assessed between the two sequential pullbacks from each of the 15 catheters used in the intercatheter assessment. Results Geometrical measurements consistently showed low variability (relative difference <10%) and excellent intraclass correlation coefficients (ICCs), ranging from 0.88 to 1.00. With respect to the compositional measurements, the relative differences were predominantly higher than those of geometrical measurements. In particular, fibrous-fatty area showed a higher relative difference (17.5% in intercatheter assessment) compared to fibrous, necrotic core, and dense calcium areas (6.5%, 8.4%, and 6.4%, respectively). However, each compositional measurement also showed acceptable reproducibility (ICCs ranging from 0.82 to 1.00). Conclusions The 45-MHz rotational VH IVUS technology had acceptable reproducibility with respect to geometrical and compositional assessments in ex vivo human coronary arteries. These data are crucial when designing future longitudinal studies addressing geometrical measurements and plaque characterization by 45-MHz VH IVUS.

Abstract Cold‐working can occur during the production of flat sheet products and the fabrication of structural cross‐sections. In both cases, when the material is cold‐worked, plastic deformations result in material strength enhancements. These strength enhancements are particularly significant for materials such as stainless steel, which exhibit rounded stress‐strain behaviour and pronounced strain hardening, and for hollow cross‐sections, where the strength increases arise in both the corner and flat regions of the cross‐section. Numerous studies have shown the importance of utilising this strength enhancement in design, and expressions to predict the strength enhancements have been established. However, if cold‐worked material is welded, some enhanced strength can be lost due to partial annealing in the heat affected zone (HAZ). The extent of this strength loss is investigated experimentally herein. The experimental programme comprised ten tensile coupon tests, with central welds parallel and transverse to the direction of cold‐rolling, as well as twelve full cross‐section tensile tests. Digital imaging correlation was utilised to determine the local constitutive properties of the base metal, the HAZ, and the weld metal. The microhardness and microstructure of the welded coupons, along with the widths of the weld and HAZ, were also characterised.

The cyclic AMP phosphodiesterases (PDE) expressed by CD4 + and CD8 + T‐lymphocytes purified from the peripheral blood of normal adult subjects were identified and characterized, and their role in modulating proliferation and the biosynthesis of interleukin (IL)‐2 and interferon (IFN)‐γ evaluated. In lysates prepared from both subsets, SK&amp;F 95654 (PDE3 inhibitor) and rolipram (PDE4 inhibitor) suppressed cyclic AMP hydrolysis indicating the presence of PDE3 and PDE4 isoenzymes in these cells. Differential centrifugation and subsequent inhibitor and kinetic studies revealed that the particulate fraction contained, predominantly, a PDE3 isoenzyme. In contrast, the soluble fraction contained a PDE4 (∼65% of total activity) and, in addition, a novel enzyme that had the kinetic characteristics of the recently identified PDE7. Reverse transcription‐polymerase chain reaction (RT‐PCR) studies with primer pairs designed to recognise unique sequences in the human PDE4 and PDE7 genes amplified cDNA fragments that corresponded to the predicted sizes of HSPDE4A, HSPDE4B, HSPDE54D and HSPDE7. No message was detected for HSPDE4C after 35 cycles of amplification. Functionally, rolipram inhibited phytohaemagglutinin‐ (PHA) and anti‐CD3‐induced proliferation of CD4 + and CD8 + T‐lymphocytes, and the elaboration of IL‐2, which was associated with a three to four fold increase in cyclic AMP mass. In all experiments, however, rolipram was approximately 60 fold more potent at suppressing IL‐2 synthesis than at inhibiting mitogenesis. In contrast, SK&amp;F 95654 failed to suppress proliferation and cytokine generation, and did not elevate the cyclic AMP content in T‐cells. Although inactive alone, SK&amp;F 95654 potentiated the ability of rolipram to suppress PHA‐ and anti‐CD3‐induced T‐cell proliferation, and PHA‐induced IL‐2 release. When a combination of phorbol myristate acetate (PMA) and ionomycin were used as a co‐mitogen, rolipram did not affect proliferation but, paradoxically, suppressed IL‐2 release indicating that cyclic AMP can inhibit mitogenesis by acting at, or proximal to, the level of inositol phospholipid hydrolysis. Collectively, these data suggest that PDE3 and PDE4 isoenzymes regulate the cyclic AMP content, IL‐2 biosynthesis and proliferation in human CD4 + and CD8 + T‐lymphocytes. However, the ability of rolipram to suppress markedly mitogen‐induced IL‐2 generation without affecting T‐cell proliferation suggests that growth and division of T‐lymphocytes may be governed by mediators in addition to IL‐2. Finally, T‐cells have the potential to express PDE7, although elucidating the functional role of this enzyme must await the development of selective inhibitors.

In the Providing Regional Observations to Study Predictors of Events in the Coronary Tree (PROSPECT) study, plaque burden, plaque composition, and minimal luminal area were associated with an increased risk of adverse cardiovascular events arising from untreated atherosclerotic lesions (vulnerable plaques) in patients with acute coronary syndromes (ACS). We sought to evaluate the utility of biomarker profiling and clinical risk factors to predict 3-year all-cause and nonculprit lesion-related major adverse cardiac events (MACEs). Of 697 patients who underwent successful percutaneous coronary intervention (PCI) for ACS, an array of 28 baseline biomarkers was analyzed. Median follow-up was 3.4 years. Beta2-microglobulin displayed the strongest predictive power of all variables assessed for all-cause and nonculprit lesion-related MACE. In a classification and regression tree analysis, patients with beta2-microglobulin >1.92 mg/L had an estimated 28.7% 3-year incidence of all-cause MACE; C-peptide <1.32 ng/ml was associated with a further increase in MACE to 51.2%. In a classification and regression tree analysis for untreated nonculprit lesion-related MACE, beta2-microglobulin >1.92 mg/L identified a cohort with a 3-year rate of 18.5%, and C-peptide <2.22 ng/ml was associated with a further increase to 25.5%. By multivariable analysis, beta2-microglobulin was the strongest predictor of all-cause and nonculprit MACE during follow-up. High-density lipoprotein (HDL), transferrin, and history of angina pectoris were also independent predictors of all-cause MACE, and HDL was an independent predictor of nonculprit MACE. In conclusion, in the PROSPECT study, beta2-microglobulin strongly predicted all-cause and nonculprit lesion-related MACE within 3 years after PCI in ACS. C-peptide and HDL provided further risk stratification to identify angiographically mild nonculprit lesions prone to future MACE.

Background: Early conduction abnormalities and need for pacemaking after transcatheter aortic valve implantation (TAVI) is well recognized. It is still unknown, however, if these conduction abnorma...

An intravenous infusion of 40 mg of recombinant tissue-type plasminogen activator (rt-PA) was given intravenously over 90 minutes to 123 patients with acute myocardial infarction (AMI) of less than 4 hours' duration. A coronary angiogram was recorded at the end of the infusion in 119 patients. Central assessment of the angiograms revealed a patent infarct-related artery in 78 patients (patency rate 66%, 95% confidence limits 57 to 74%). Patients with a patent infarct-related artery at the first angiogram were randomized in a double-blind manner to receive a subsequent 6-hour infusion of either 30 mg of rt-PA or placebo. All patients had received an initial bolus of 5,000 IU of heparin and then 1,000 IU/hour until a second angiogram was recorded 6 to 24 hours after the start of the second perfusion. At central assessment of the second coronary angiogram the reocclusion rate was 2 of 36 patients who received rt-PA at the second infusion and 3 of 37 patients not receiving this drug (or the 2 groups combined 7%, 95% confidence limits 2 to 15%). Three of 60 patients (5%, 95% confidence limits 1 to 14%) with patent arteries on both previous angiograms had a later occlusion as judged on the angiogram recorded at hospital discharge. No difference in late reocclusion rates between the 2 treatment groups was observed.

Current three dimensional (3D) vessel reconstruction using intravascular ultrasound (IVUS) pull back is limited by the lack of information on the real vessel curvatures, because the movement of the catheter is assumed to proceed along a straight path. To overcome this limitation a method (ANGUS) has been developed to combine coronary angiography with data obtained by IVUS. The IVUS data represent a cylindrical stack of cross-sections. A least-square-fit approximation is used to reconstruct the 3D path of the catheter axis from two biplane X-ray images, after which the stack of IVUS contours is wrapped around this 3D catheter centerline. In order to establish the correct rotational position of the stack around the centerline, use is made of 'landmark' which are visible in angiograms, as well as in a simulation of these angiograms derived from the reconstructed 3D contour. The combination of ANGiography and intravascular UltraSound (ANGUS) is promising and provides a unique method of three-dimensional reconstruction of coronary geometry.