J. Blake

Factors Influencing Local and Systemic Levels of Plasma Myeloperoxidase in ST-Segment Elevation Acute Myocardial Infarction

Myeloperoxidase (MPO) is associated with risk in acute coronary syndromes. However, the precise role it plays in ST-elevation myocardial infarction (STEMI) remains unclear. In this study we tested the hypothesis that levels of MPO in plasma after a myocardial infarction are affected by its ability to bind to the endothelium and there is local release of the enzyme at the culprit lesion. We measured plasma MPO in systemic circulation and throughout the coronary circulation in patients with STEMI undergoing primary percutaneous coronary intervention (PCI). MPO levels at the femoral artery were higher (p <0.001) in patients with STEMI (n = 67, median 45 ng/ml, interquartile range 34 to 83) compared to control patients (n = 12, 25 ng/ml, 19 to 30) with chronic stable angina undergoing elective PCI. After administration of the anticoagulant bivalirudin in 13 patients with STEMI, plasma MPO was increased only at the culprit coronary artery lesion before PCI (178 ng/ml, 91 to 245) versus all other sites (femoral artery 86 ng/ml, 54 to 139, p = 0.019). Administration of heparin caused a marked increase of plasma MPO. Even so, it was still possible to detect an increase of plasma MPO at culprit lesion in patients with STEMI (n = 54, 171 ng/ml, 122 to 230) versus controls (n = 12, 136 ng/ml, 109 to 151, p <0.05) after heparin and before PCI. MPO levels were higher at the culprit lesion in patients with STEMI who presented early and in those with restricted flow (p <0.05). In conclusion, our results demonstrate that, in addition to a systemic increase of MPO in patients presenting early with STEMI, levels of this leukocyte enzyme are increased at the culprit coronary lesion before PCI.

Removal of contrast media from the coronary sinus attenuates renal injury after coronary angiography and intervention.

To the Editor: Acute renal injury after exposure to radiographic contrast media, contrast-induced nephropathy (CIN), accounts for a substantial proportion of all cases of acute renal failure ([1][1]). The incremental presence of predisposing factors including pre-existing chronic renal impairment

Endovascular Repair of a Traumatic Ascending Aortic Tear Injury.

a shorter time, as other authors confirmed (1). In previous reports, EVAS combined with the chimney technique was a preoperatively planned procedure, including elective (1,2) and urgent (3) procedures. All authors agreed that simultaneous ballooning of the chimney stent during endobag filling is essential to avoid compression of the vessel owing to the endobag itself. The cause of the inadvertent left renal artery coverage in this case is uncertain. The most likely cause is a slight upward shift of the device during the polymer injection; this could have determined a proximal migration of the device and almost complete coverage of the vessel ostium. Adu et al (4) summarized the available surgical and endovascular options in case of accidental renal artery coverage during standard EVAR. According to these authors, the chimney technique is the most suitable in cases of partial occlusion of the vessel ostium. In contrast to the cases cited by Adu et al (4), we immediately recognized the complication on completion angiography, and this allowed us to proceed directly to vessel cannulation and stent placement, which occurred 100 minutes later. In conclusion, we demonstrated that inadvertent aortic branch artery coverage after Nellix EVAS when recognized early can be successfully managed by immediate endobag aspiration and chimney placement before endobag refilling.

Saphenous vein graft aneurysm fistula formation causing right heart failure: an unusual presentation.

Saphenous vein graft aneurysm (SVG) formation after coronary artery bypass grafting is a rare complication of the surgery. We present a case of a 68‐year‐old man with an unusual presentation of such an aneurysm. Thirty‐four years after his initial bypass surgery, the patient presented with a fistula formation into his right atrium from a vein graft aneurysm. Late aneurysm formation is thought to occur secondary to atherosclerotic degeneration of the SVG with background hypertension and dyslipidaemia accelerating the process. Diagnostic modalities used to investigate SVG aneurysms include computed tomography, transthoracic echocardiogram, magnetic resonance imaging and cardiac catheterisation. Aneurysms with fistula formation historically require aggressive surgical intervention. Resection of the aneurysm with subsequent revascularisation if required is the surgical norm. SVG aneurysm with fistula formation into a cardiac chamber is a rare complication of coronary artery bypass grafting (CABG), which can occur with atypical presenting symptoms. Physicians should keep in mind the possibility of this occurring in post‐CABG patients presenting with heart failure and a new murmur.

13 Neutrophil activation at the culprit lesion in acute ST-segment elevation myocardial infarction with multiple complex coronary plaques

Introduction The activation of neutrophils at the culprit coronary lesion following acute plaque disruption has not been reported. We hypothesised that neutrophil activation occurs in ST elevation myocardial infarction (STEMI) prior to percutaneous intervention (PCI), and that differences in activation may be detectable locally at the culprit lesion, particularly in patients with multiple complex coronary plaques. Methods Forty STEMI patients having primary PCI were compared to 10 controls with chronic stable angina (CSA) undergoing elective PCI. The clinical, demographic and angiographic characteristics of patients and controls are shown in Abstract 13 table 1. The culprit lesion was sampled after passage of a guide wire across the lesion and use of a low profile sampling catheter (Multifunctional probing catheter, Boston Scientific Corporation, Natick, Massachusetts, USA) at the site of occlusion, prior to further mechanical intervention. Neutrophil activation was measured by flow cytometry using neutrophil intracellular myeloperoxidase content (MPO Index) and the expression of the β2- integrin CD11b, a leukocyte adhesion and activation marker at the culprit coronary lesion (CA), the aorta at the coronary ostium (Ao), the coronary sinus (CS), and femoral artery (FA) prior to primary PCI. A lower MPO content indicates the depletion of intracellular MPO and cell activation.Abstract 13 Table 1 Variable STEMI (n=40) Elective PCI (n=10) p Value Age (years) mean±SD 62±12 68±9.1 0.9 Male (%) 28 (70) 7 (70) 1 Culprit coronary artery lesion treated (%)  Left anterior descending 17 (42) 5 (50) 0.73  Diagonal 2 (5) 1 (10) 0.5  Circumflex 1 (3) 2 (20) 0.1  Right coronary 20 (50) 2 (20) 0.15  Time to presentation (mins) mean±SD 222±155 NA  Baseline TIMI flow 0–1 28 (70) 0 <0.001 Results A marked decrease in MPO content occurred at the CA, Ao and FA in STEMI compared to elective controls (p<0.01). Furthermore, MPO content was lower at the CA (−23.1, (−25.6 to −17.1), n=37) compared to Ao (−22.0, (−24.7 to −16.2), n=37), CS (−20.6, (−24.8 to −16.9), n=30) and FA (−20.4, (−24.4 to −13.1), n=40), all p<0.001 (Abstract 13 figure 1). Neutrophil MPO content was correlated with CD11b expression only at the culprit CA in STEMI (r=−0.4, p=0.03, n=31) (Abstract 13 figure 2). Neutrophil MPO content at the CA in patients with multiple complex plaques was similar to those with a single culprit however only in those with multiple complex plaques was a correlation between MPO content and CD11b (r=−0.7, p=0.02) shown. Conclusion: In acute STEMI, neutrophils are activated systemically, regionally and locally at the culprit coronary lesion. In patients with multiple complex plaques, there may be an extended local role for the activated neutrophil following acute plaque destabilisation.Abstract 13 Figure 1 Abstract 13 Figure 2

THE REAL LIFE EXPERIENCE OF EVEROLIMUS ELUTING CORONARY STENT: “THE APPLIANCE OF XIENCE”

involved a 6-month observation period. Phase 2 involved strategies to expedite movement of the patient from the emergency department (ED) to the catheterization laboratory (10 months). Phase 3 involved initiation of a “Code MI” centralized paging system (11 months). We recorded door (D), call (C) and balloon (B) times. Results: Phase 1 (n= 33) Phase 2 (n= 65) Phase 3 (n= 71) DB—median 99 90 71** CB—median 82 59* 50** DB within 90min 33% 49% 75% DB 90th percentile 205min 185min 110min CB 90th percentile 109min 85min 74min ∗ p< 0.01 vs. Phase 1. ∗∗ p< 0.001 vs. Phase 1. Of the 169 consecutive patients, 105 presented outside normal operating hours, 30 were in cardiogenic shock (CS) and/or had required prolonged resuscitation prior to reaching the catheterization laboratory and there were 15 deaths at 30 days (15/30 in CS and 0/139 not in CS). The introduction of simple strategies to reduce DB times benefits all patients, particularly those for whom prolonged delays may remove the treatment advantage of PCI. doi:10.1016/j.hlc.2008.05.392

Stent deployment with distal vascular protection for the culprit vein graft stenosis in a patient with an acute infarct and cardiogenic shock.

A case of emergency stent deployment to a critical vein graft lesion in a patient with an acute myocardial infarction and cardiogenic shock is described. An Angioguard vascular protection device was used, retrieving a large amount of atheromatous debris. Use of filter‐type protection devices to prevent distal atheroembolism may be lifesaving in such patients. Cathet Cardiovasc Intervent 2002;57:234–238.