Objectives The aim of this study was to determine the safety and efficacy of a novel pimecrolimus-eluting stent in a porcine coronary model and in a phase I clinical trial.Background Rapamycin- and paclitaxel-eluting stents reduce the need for repeat intervention by limiting neointimal hyperplasia but might cause delayed healing, pre-disposing patients to late stent thrombosis. Because inflammation plays a key role in restenosis, pimecrolimus, an anti-inflammatory drug, might reduce restenosis without adversely affecting re-endothelialization.Methods We evaluated a novel polymeric pimecrolimus-eluting stent covered with a thin parylene C diffusion barrier in a porcine coronary model and in a phase I human clinical trial. The clinical study was a prospective, nonrandomized, first-in-human hypothesis-generating study that enrolled 15 patients who had a single de novo native coronary stenosis.Results At 28 days and 3 months in the porcine model, histopathologic indicators predicted safety and biocompatibility when stents coated with polymer only, drug only, and 2 drug-polymer formulations were compared with bare-metal stents (BMS). In the phase I clinical trial, 15 patients had successful implantation of pimecrolimus-eluting stents. By 6 months, no patient suffered death, myocardial infarction, or stent thrombosis. However, the angiographic restenosis (61%), mean late loss (1.44 mm), and repeat target lesion revascularization (53%) were significantly higher than historical BMS controls. Whereas the primary end point was percent volume obstruction, restenosis was so severe that operators performed intravascular ultrasound examination in only 6 patients.Conclusions Pimecrolimus-eluting stents induced an exaggerated neointimal hyperplasia at 6 months in comparison with historical controls. (J Am Coll Cardiol Intv 2009;2:1017-24) (c) 2009 by the American College of Cardiology Foundation

A young male presented 22 h following onset of symptoms with an anterior ST-elevation myocardial infarction. He was transferred for rescue angioplasty after failing to reperfuse with thrombolytic therapy. On arrival, his symptoms had settled. Following administration of intracoronary abciximab and passage of an angioplasty wire into the distal LAD, extensive thrombus was demonstrated in the left anterior descending artery extending from the ostium to the distal vessel Figure 1(a). Further intervention with attempted thrombectomy was considered but it was postponed pending a viability study because of the risks of displacing thrombus down the circumflex. A cardiac MRI scan with delayed gadolinium hyper-enhancement demonstrated the classical appearance of full-thickness infarction in the LAD territory Figure 1(b). No further intervention was therefore indicated. At one-year follow-up, the patient remains free of angina with NYHA Class 1 symptoms of heart failure.

AIMS Limited data are available on the changes that occur at the dilated site many years after coronary balloon angioplasty. The development of bioabsorbable stents may increase the importance of understanding the long term changes that occur in an unscaffolded coronary artery following balloon-mediated injury. METHODS AND RESULTS This study evaluated, by serial quantitative angiography, the natural history of changes that occurred in the dilated segment between early (mean seven months), late (mean 4.5 years) and very late (mean 17 years) follow-up after balloon angioplasty. Of 127 consecutive patients (174 lesions) with successful coronary angioplasty, 125 underwent early, 84 late and 47 very late angiographic follow-up (75% of eligible survivors). The mean lesion diameter stenosis decreased from 36+/-11% at early to 26+/-15% at late follow-up (p<0.0001), and then increased again to 35+/-25% by very late follow-up (p=0.003). Although stenosis severity at early follow-up angiography predicted lesion regression at late follow-up, there was no significant correlation between late and very late follow-up lesion severity. CONCLUSIONS After coronary angioplasty, lesion regression at the dilated site from 7 months to 4.5 years is followed by slow lesion progression over the next 12 years.

Objectives This study provides insights into "crush" coronary bifurcation stenting through imaging of bench deployments.Background Although the strategy of provisional side-branch stenting is widely accepted for suitable bifurcation lesions, there is no consensus on the best option for elective stenting with 2 stents. The crush technique has the potential to scaffold and apply the drug to the side-branch ostium where restenosis is most common.Methods Sequential steps of crush stent deployment and post-dilation were undertaken in silicone phantoms and recorded on cine angiography and microcomputed tomography. We assessed the effect of deployment strategies, post-dilation strategies, and cell size on side-branch ostial area.Results Side-branch ostial coverage by metal struts was 53% (95% confidence interval [CI]: 46 to 59) after 1-step kissing post-dilation and was reduced by 2-step kissing post-dilation to 33% (95% CI: 28 to 37; p < 0.0001). Although the residual stenosis after the classical crush strategy was 47% (95% CI: 39 to 53), it was 36% (95% CI: 31 to 40; p = 0.002) after mini-crush deployment. Stents with larger cell size (>3.5 mm diameter) had a residual stenosis of 37% (95% CI: 32 to 42) after crush deployment that was less than the residual stenosis for stents with smaller cell size (52%; 95% CI: 44 to 60; p < 0.0001).Conclusions Side-branch ostial stenosis after crush stenting was minimized by mini-crush deployment, 2-step kissing post-dilation, and the use of stents with larger cell size. It is unknown if optimizing stent deployment at bifurcation lesions will reduce clinical stent thrombosis and restenosis. (J Am Coll Cardiol Intv 2008;1:351-7) (C) 2008 by the American College of Cardiology Foundation

Exercise tolerance testing (ETT) is the commonest non-invasive method for investigating stable patients presenting with cardiac-sounding chest pain. The sensitivity and specificity of the ETT for the detection of myocardial ischaemia are approximately 70% in men (1). However, this test is less sensitive for large patient sub-groups including women and patients with abnormal resting ECG’s (2,3). Myocardial Perfusion Scintigraphy has a higher sensitivity and specificity than ETT (4) and its use is less dependent on the functional capacity of the patient. Nevertheless, it remains a relatively expensive test with limited availability. PRIME ECG (manufactured by Meridian Medical Technologies, Belfast, Northern Ireland) is a Body Surface Mapping (BSM) system that utilizes an 80electrode ECG ‘vest’ to detect electro cardiac activity over a much wider distribution of the thorax than the conventional 12-lead ECG electrodes. Electrocardiac data is recorded for all 80 electrodes. A beat marker is manually positioned at the end of the QRS complex. Isopotential map recordings are then taken at 60 ms after the beat marker (ST60) for all leads. The ST 60 data acquired at baseline can be subtracted, for each electrode, from the data derived from subsequent acquisitions taken during exercise or pharmacological stress. The PRIME software allocates a colour scale proportional to the degree of ST segment shift and displays this on a diagramatic torso corresponding to the position of the leads detecting the ST shift (ST elevation—red scale, ST depression—blue scale). Only the ST60 change from baseline for a given electrode is therefore displayed as a colour. This is the visually intuitive ‘Delta Map’. This novel technique has been used to demonstrate transient regional myocardial ischaemia following balloon inflation during percutaneous coronary angioplasty in patients with single vessel coronary artery disease (5). We report, for the first time, a case in which transient regional ischaemia induced during stress nuclear perfusion imaging is also accurately displayed using the PRIME Delta Map, and correlates with a significant stenosis in the epicardial coronary artery perfusing this territory.