See articles on pages 1562 and 1609
Previous studies have shown that recent activation of the inflammatory response in coronary atherosclerotic lesions contributes to rapid progressive plaque destabilisation. Neopterin, a by‐product of the guanosine triphosphate pathway, is produced by activated macrophages and serves as an activation marker for monocytes/macrophages.
To elucidate the role of neopterin in coronary plaque destabilisation by immunohistochemical study of the presence of neopterin in coronary atherectomy specimens obtained from patients with stable angina pectoris (SAP) and unstable angina pectoris (UAP).
Patients and methods
All patients underwent atherectomy of the primary atherosclerotic lesions responsible for SAP (n = 25) and UAP (n = 25). Frozen samples were studied with antibodies against smooth muscle cells, macrophages, T cells, neutrophils and neopterin.
In 22/25 patients with UAP, abundant neopterin‐positive macrophages were found at the sites of coronary culprit lesions. However, in 25 lesions from patients with SAP, only 11 lesions showed neopterin positivity. Quantitatively, the neopterin‐positive macrophage score was significantly higher (p<0.001) in patients with UAP than in patients with SAP. Moreover, the neopterin‐positive macrophage score showed a significant positive correlation with the number of neutrophils or T cells, respectively (neutrophils, r = 0.55, p<0.001; T cells, r = 0.70, p<0.001).
Neopterin can be considered as one of the significant factors in the process of plaque inflammation and destabilisation in human coronary atherosclerotic lesions. Its exact role in the process needs to be investigated further.
atherosclerosis; inflammation; neopterin; angina
Progression of neointimal stent coverage (NSC) and changes in thrombus were evaluated serially by coronary angioscopy for up to 2 years after sirolimus‐eluting stent (SES) implantation.
Serial angioscopic observations were performed in 20 segments of 20 patients at baseline, and at 6 months and 2 years after SES implantation. NSC was classified as follows: 0, uncovered struts; 1, visible struts through thin neointima; or 2, no visible struts. In each patient, maximum and minimum NSC was evaluated. Existence of thrombus was also examined.
The maximum NSC increased from 6 months to 2 years (1.2 (0.4) vs 1.8 (0.4), respectively, p = 0.005), while the minimum NSC did not change (0.7 (0.5) vs 0.8 (0.4), respectively, p = 0.25). The prevalence of patients with uncovered struts did not decrease from 6 months to 2 years (35% vs 20%, respectively, p = 0.29). Although there were no thrombus‐related adverse events, new thrombus formation was found in one patient (5%) at the 6‐month, and in four patients (20%) at the 2‐year follow‐up evaluations. Frequencies of thrombus inside the SES at baseline, 6 months and 2 years did not differ one from another (40%, 40% and 30%, respectively; p = NS).
Neointimal growth inside the SES progressed heterogeneously. Uncovered struts persisted in 20% of the patients for up to 2 years and subclinical thrombus formation was not a rare phenomenon.
To determine if an aggressive approach to coronary revascularisation with oversized balloons is counterproductive, we studied the effect of increasing balloon‐to‐artery (B:A) ratio on neointimal hyperplasia following primary stent placement using a non‐atherosclerotic porcine coronary overstretch model.
60 vessels in 33 Yorkshire swine were randomly assigned to one of five B:A ratios between 1.0:1 and 1.4:1. Intravascular ultrasound (IVUS) imaging was performed before bare‐metal stent placement to accurately determine vessel size, after stent placement, and at 28 days.
The mean prestent vessel diameter was 3.05 (0.31) (SD) mm. In‐stent neointimal volume, in‐stent volume stenosis and cross‐sectional area stenosis at the stent minimum lumen diameter increased significantly with increasing achieved B:A ratio (multilevel regression test for slope, p<0.001, p = 0.002 and p<0.001, respectively) and were independent of vessel size. Even minor vessel overstretch at an achieved B:A ratio of 1.1:1 resulted in significant neointimal hyperplasia. Larger B:A ratios were also associated with more neointima beyond the stent edges (p = 0.008). For vessels from the same animal, neointimal response at a given B:A ratio was dependent upon the animal treated.
In a porcine model of IVUS‐guided coronary primary stent placement, vessel overexpansion is counterproductive. Neointimal hyperplasia at 28 days is strongly associated with increasing B:A ratio. In addition, vessels do not respond independently of each other when multiple stents are placed within the same animal using a range of B:A ratios.
For a number of patients it is difficult to diagnose the cause of cardiac disease. In such patients cardiac magnetic resonance is useful for helping to make a differential diagnosis between ischaemic and dilated cardiomyopathy; identifying patients with myocarditis; diagnosing cardiac involvement in sarcoidosis and Chagas' disease; identifying patients with unusual forms of hypertrophic cardiomyopathy and those with continuing myocardial damage; and defining the sequelae of ablation treatment for hypertrophic obstructive cardiomyopathy.
cardiac magnetic resonance; hypertrophic cardiomyopathy; infiltrative cardiomyopathies; myocarditis; late gadolinium enhancement
The aim of this study was to use late gadolinium hyper‐enhancement cardiac magnetic resonance (LGE‐CMR) imaging to determine if a 72‐h troponin‐I measurement would provide a more accurate estimation of infarct size and microvascular obstruction (MVO) than serial creatine kinase (CK) or early troponin‐I values.
LGE‐CMR was performed 3.7±1.4 days after medical treatment for acute ST elevation or non‐ST elevation myocardial infarction. Infarct size and MVO were measured and correlated with serum troponin‐I concentrations, which were sampled 12 h and 72 h after admission, in addition to serial CK levels.
Ninety‐three patients, of whom 71 had received thrombolysis for ST elevation myocardial infarction, completed the CMR study. Peak CK, 12‐h troponin‐I, and 72‐h troponin‐I were related to infarct size by LGE‐CMR (r = 0.75, p<0.0001; r = 0.56, p = 0.0003; r = 0.62, p<0.0001 respectively). Serum biomarkers demonstrated higher values in the group with MVO compared with those without MVO (Peak CK 3085±1531 vs 1471±1135, p<0.001; 12‐h troponin‐I 58.3±46.9 vs 33.4±40.0, p = 0.13; 72‐h troponin‐I 11.5±9.9 vs 5.5±4.6, p<0.005). The correlation between the extent of MVO and 12‐h troponin‐I was not significant (r = 0.16), in contrast to the other serum biomarkers (peak CK r = 0.44, p<0.0001; 72‐h troponin‐I r = 0.46, p = 0.0002).
A single measurement of 72‐h troponin‐I is similar to serial CK measurements in the estimation of both myocardial infarct size and extent of MVO, and is superior to 12‐h troponin‐I measurements.
To determine the effect of insulin for the management of hyperglycaemia in non‐diabetic patients presenting with acute coronary syndrome.
An observational study from the MINAP (National Audit of Myocardial Infarction Project) database during 2003–5 in 201 hospitals in England and Wales. Patients were those with a final diagnosis of troponin‐positive acute coronary syndrome who were not previously known to have diabetes mellitus and whose blood glucose on admission was ⩾11 mmol/l. The main outcome measure was death at 7 and 30 days.
Of 38 864 patients who were not previously known to be diabetic, 3835 (9.9%) had an admission glucose ⩾11 mmol/l. Of patients having a clear treatment strategy, 36% received diabetic treatment (31% with insulin). Mortality at 7 and 30 days was 11.6% and 15.8%, respectively, for those receiving insulin, and 16.5% and 22.1%, respectively, for those who did not. Compared with those who received insulin, after adjustment for age, gender, co‐morbidities and admission blood glucose concentration, patients who were not treated with insulin had a relative increased risk of death of 56% at 7 days and 51% at 30 days (HR 1.56, 95% CI 1.22 to 2.0, p<0.001 at 7 days; HR 1.51, 95% CI 1.22 to 1.86, p<0.001 at 30 days).
In non‐diabetic patients with acute coronary syndrome and hyperglycaemia, treatment with insulin was associated with a reduction in the relative risk of death, evident within 7 days of admission, which persists at 30 days.
To compare bleeding complications and results of percutaneous coronary intervention (PCI) between patients treated by radial and femoral approaches for acute myocardial infarction (AMI,) and using abciximab and 5 French guiding‐catheters.
114 consecutive patients with AMI were prospectively randomised. Exclusion criteria were a history of coronary artery bypass graft, cardiogenic shock, atrioventricular block, and contraindication to abciximab or a negative Allen test. Local haemostasis was achieved by manual compression.
Baseline characteristics were similar between the two groups. Peripheral arterial complication rates and delays to patient ambulation were significantly lower in the radial group than in the femoral group, whereas in‐hospital stay was similar between the two groups. A cross over was more often necessary in the radial group than in the femoral group. Coronary angiography duration and fluoroscopy time were significantly longer in the radial group than in the femoral group, whereas PCI duration was similar in both groups.
The FARMI trial showed that the radial route lowered peripheral arterial complication rates and allowed earlier ambulation, despite no significant benefit on the duration of hospitalisation.
GpIIb/IIIa antagonist; percutaneous coronary intervention; acute myocardial infarction; radial
There is a strong inverse relationship between final vessel diameter and subsequent risk of treatment failure after coronary stent deployment. The aim of this study was to investigate the magnitude by which stent delivery balloon underexpansion and stent elastic recoil contributed to suboptimal final vessel geometry.
A prospective angiographic study recruiting 499 lesions (385 patients) undergoing coronary stent implantation was performed. Quantitative coronary angiography (QCA) was used to measure the minimal lumen diameters of the delivery balloon during stent deployment (MLD1) and of the stented segment following balloon deflation (MLD2). The expected balloon diameter for the deployment pressure was determined from the manufacturer's reference chart. Delivery balloon deficit was measured by subtracting the MLD1 from the expected balloon size and stent recoil was calculated by subtracting MLD2 from MLD1. Delivery balloon deficit and stent recoil were examined as a function of reference vessel diameter (RVD) and balloon–vessel (BV) ratio.
The final stent MLD was a mean 27.2% (SD = 7.2) less than the predicted diameter. The mean delivery balloon deficit was 0.65 mm (SD = 0.27) and the mean stent recoil was 0.28 mm (SD = 0.17). Percentage delivery balloon deficit and stent recoil were independent of RVD. Delivery balloon deficit increased with higher BV ratios. Stent recoil was independent of BV ratio and the use of predilatation.
Failure to achieve predicted final stent diameter is a real problem with contribution from delivery balloon underexpansion and stent recoil. On average the final stent MLD is only 73% of the expected diameter, irrespective of vessel size.