Background-Recent studies indicate that T-cell activation may play an important role in the pathophysiology of acute coronary syndromes (ACS). However, although those studies detected T-cell expansion in peripheral blood cells, demonstration of specific T-cell expansion within the plaque of patients with ACS is lacking. The present study aims to address whether a specific, immune-driven T-lymphocyte recruitment occurs within the unstable plaque of patients with ACS. Methods and Results-We simultaneously examined the T-cell repertoire using CDR3 size analysis both in coronary plaques (obtained by directional atherectomy) and in peripheral blood of patients with either ACS (nϭ11) or chronic stable angina (nϭ10). Unstable plaques showed a 10-fold increase in T-cell content by quantitative PCR. Using spectratyping analysis, we found several specific T-cell clonotype expansions only in unstable plaque from each patient with ACS, indicating a specific, antigen-driven recruitment of T cells within unstable lesions. Conclusions-For the first time, T-cell repertoire was investigated directly into coronary plaques; using this approach, we demonstrate that coronary plaque instability in the setting of ACS is associated with immune-driven T-cell recruitment, specifically within the plaque.

A reduced microvascular network may contribute to abnormal cardiovascular reactivity and to exercise-induced rheological abnormalities in hypertension.

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In a nationwide clinical practice, the vast majority of patients older than 75 years presenting with ST-elevation myocardial infarction does not receive any early reperfusion treatment and presents a significant incidence of major clinical events at 30 days.

Rupture of the interventricular septum is a rare and life-threatening complication of acute myocardial infarction. Postmyocardial infarction, ventricular septal defect is associated with very high morbidity and mortality. The therapy of this complication is the surgical closure. The Amplatzer occluder is currently used to close percutaneously atrial septal defect, patent foramen ovale, and selected congenital ventricular septal defect. Few cases are described regarding transcatheter closure of a postinfarction ventricular septal defect. Here we report a case of a large postinfarction ventricular septal defect successfully closed with Amplatzer multifenestrated atrial septal defect occluder device because of its peculiar anatomical characteristics.

Acute myocardial infarction (AMI) is caused by thrombus formation over a disrupted plaque occluding an epicardial coronary artery. Mechanical thrombectomy is effective in removing thrombus burden from native vessels and saphenous vein grafts. Here we report a case of an aneurysmatic dilatation of an infarct-related artery (IRA) referred to our Institute for rescue PCI, after failed fibrinolysis, successfully treated with only rheolytic thrombectomy (AngioJet, Possis Medical, Minneapolis, Minnesota, USA) without the need for adjunctive balloon or stent implantation.