Corrigendum to: 2014 ESC Guidelines on the diagnosis and treatment of aortic diseases [Eur Heart Journal (2014) 35, 2873–2926,doi:10.1093/eurheartj/ehu281]. In Table 3, the radiation for MRI is “0” and not “-“. The corrected table is shown below.

In-stent restenosis is a complication which impairs the success of coronary stenting. Recently, it was supposed that a delayed hypersensitivity reaction to nickel and molybdenum might be one of the triggering factors in in-stent restenosis. We have analyzed the data collected in our centre with respect to this hypothesis. Altogether, 34 patients were investigated (24 male, 10 female). Patch tests were performed with the standard series of the German Contact Dermatitis Research Group and a metal series containing the metal components of 316 L stainless steel. A positive patch test reaction to nickel was observed in 4 (11.8%) patients. None of the patients showed sensitization to the other metals. Retrospective analysis was performed in 20 patients: 2 of these patients had a positive patch test reaction to nickel, one of whom had an in-stent restenosis, and the other not. Restenoses were predominantly observed in patients with negative patch test reactions to nickel (6/18 patients). Out of the patients who were investigated prospectively only one showed sensitization to nickel. Restenosis was observed in 2 patients: neither patient had nickel allergy. Although it still cannot be excluded that metal allergy may play a role in the restenosis process in coronary stenting, there is at present little evidence for it.

The aim of this study was to compare the morphology of stable and unstable coronary lesions using intravascular ultrasound in patients undergoing coronary balloon angioplasty and to determine whether lesion morphology had any influence on the mechanism of balloon angioplasty. Thirty three (15 stable and 18 unstable) patients undergoing single lesion percutaneous transluminal coronary angioplasty were studied with intravascular ultrasound before and after intervention. All examinations, recorded on S-VHS video tape, were studied off-line and matched sites from the point of minimum lumen area after the procedure and the corresponding site prior to intervention were compared. The morphology of lesions before intervention was noted and the mechanisms of angioplasty (vessel stretch, lesion remodelling and lesion tears) were determined by comparing pre- and post-interventional morphology and dimensions. The only significant morphological difference between stable and unstable lesions was the presence of a demarcated inner layer in unstable lesions, delimited by a fine circumferential line. This pattern was noted in 77% (14/18) of unstable lesions and in 7% (1/15) of stable lesions (P < 0.01). Unstable lesions tended to have more echolucent zones than stable lesions (72% (13/18) vs 46% (7/15), P = 0.13). The mechanisms of angioplasty were also found to differ. Whereas lesion remodelling (or 'compression') was seen in 77% (14/18) of unstable lesions, it occurred in only 13% (2/15) of stable lesions and mean lesion cross-sectional area reduction was greater in unstable lesions, - 14.8 +/- 8.3% (2.1 +/- 1.3 mm2) compared to stable lesions, - 4.1 +/- 8.4% (0.42 +/- 0.9 mm2), P < 0.01. In contrast, vessel stretch was seen more frequently in stable lesions (73%, 11/15) compared to unstable lesions (22%, 4/18) P < 0.01 and the mean increase in vessel cross-sectional area was + 13.5 +/- 6.8 (1.6 +/- 0.9 mm2) in stable lesions compared to + 5.5 +/- 5.6% (0.8 +/- 0.9 mm2) in unstable lesions, P < 0.01. Lesion tear was present to a similar degree in both groups of patients. In this observational study we found a set of echographic markers that distinguished unstable lesions. The mechanisms of angioplasty differed between stable and unstable angina, with greater lesion remodelling seen in unstable lesions and vessel stretch in stable lesions. Taken together, these findings suggest that the markers we describe may be echographic indicators of mural thrombus.

AimsThe purpose of this part of the INTERVENT project was (1) to redefine and individually predict post-procedural complications associated with coronary interventions, including alternative/adjunctive techniques to PTCA and (2) to employ the prognostic INTERVENT computer model to clarify the structural relationship between (pre)-procedural risk factors and post-procedural outcome. Methods and ResultsIn a multicentre study, 2500 data items of 455 consecutive patients (mean age: 61·1 8·3 years; 33-84 years) undergoing coronary interventions at three university centres were analysed. 80·4% of the patients were male, 16·7% had unstable angina, and 5·1%/10·1% acute/subacute myocardial infarction. There were multiple or multivessel stenoses in 16·0%, vessel bending >90 in 14·5%, irregular vessel contours in 65·0%, moderate calcifications in 20·9%, moderate/severe vessel tortuosity in 53·2% and a diameter stenosis of 90%-99% in 44·4% of cases. The in-lab (out-of-lab) complications were: 0·4% (0·9%) death, 1·8% (0·2%) abrupt vessel closure with myocardial infarction and 5·5% (4·0) haemodynamic disorders. ConclusionComputer algorithms derived from artificial intelligence were able to predict the individual risk of these post-procedural complications with an accuracy of >95% and to explain the structural relationship between risk factors and post-procedural complications. The most important prognostic factors were: heart failure (NYHA class), use of adjunctive/alternative techniques (rotablation, atherectomy, laser), acute coronary ischaemia, pre-existent cardiac medication, stenosis length, stenosis morphology (calcification), gender, age, amount of contrast agent and smoker status. Pre-medication with aspirin or other cardiac medication had a beneficial effect. Techniques, such as laser angioplasty or atherectomy were predictors for postprocedural complications. Single predictors alone were not able to describe the individual outcome completely. (Eur Heart J 1999; 20: 354-363)

Isolated pig hearts (German farm pigs) were characterized after global in-vivo ischaemia as a potential alternative to in-vivo animal studies. Hearts were harvested from adult farm swine at the abattoir 10.3 +/- 2.1 min after incision of the carotid artery. They were immediately perfused and thereafter stored in ice-cold cardioplegic (St Thomas's) solution. After 38 +/- 3 min, retrograde perfusion was started with oxygenated pig blood (37 degrees C; 5000 U Heparin.l-1; pH 7.38 +/- 0.1; 11 mmol glucose.l-1) at a flow rate of 85 ml.min-1 100 g-1 wet weight (gww-1) for 30 min (n = 10). Additionally, shortly after obtaining the hearts, ATP and CP content were measured by enzymatic tests in 10 pigs at the beginning and after 15 and 30 min of reperfusion. Heart rate was 90 +/- 14 min-1 with little variation during 30 min. Perfusion pressure increased from 89 +/- 17 mmHg to 100 +/- 17 mmHg (NS). Wet weight rose from 488 +/- 33 to 548 +/- 45 g (P < 0.002). CK increased from 2180 +/- 558 to 5900 +/- 1018 U.l-1 (P < 0.001). Calcium in the perfusate decreased from 2.45 +/- 0.15 to 2.2 +/- 0.25 mmol.l-1 and magnesium increased from 0.85 +/- 0.2 to 1.79 +/- 0.35 mmol.l-1 (both P < 0.001). The transmural ATP and CP content was 2.8 +/- 0.48 and 5.08 +/- 0.88 mumol.gww-1.ATP fell moderately during reperfusion to 2.6 +/- 0.35 mumol (NS) and CP rose to 6.0 +/- 1.2 mumol (P < 0.04).(ABSTRACT TRUNCATED AT 250 WORDS)

A vascular myxoma which prolapsed into the mitral valve was found in the left atrium of a 47-year old man. Two-dimensional ultrasonic tomography yielded relevant non-invasive diagnostic information on the pattern of movement of the pedunculated tumour. Highly accurate determination of the tumour volume was achieved via angiocardiography and videometry. Coronography of the tumour vessels allowed identification of an unusual point of insertion of the myxoma. The risk of obstruction of the mitral orifice was documented haemodynamically by a steep gradient above the mitral valve when holding breath during the expiratory phase.

No abstract

In-stent restenosis is a complication which impairs the success of coronary stenting. Recently it was supposed that a delayed hypersensitivity reaction to nickel and molybdenum might be one of the triggering factors in in-stent restenosis. We have performed a retrospective analysis of the data collected in our centre with respect to this hypothesis. Altogether 20 patients were investigated (13 male, 7 female). Patch tests were performed with the standard series of the German Contact Dermatitis Research Group and a metal series containing the metal components of the 316 L stainless steel. A positive patch test reaction to nickel was observed in 2 (10.0%) patients, one of these patients had an in-stent restenosis, the other had not. None of the patients showed a sensitization to the other metals. Restenoses were predominantly observed in patients with a negative patch test reaction to nickel (6/18 patients). Although it cannot be excluded that metal allergy may play a role in the restenosis process in coronary stenting there is at the moment little evidence for it.Key words: Coronary stent, in-stent restenosis, metal allergy, delayed hypersensitivity rection, patch test