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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.

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.

Spontaneous coronary artery dissection (SCAD) is a non-atherosclerotic coronary artery disease, which typically affects women with a low cardiovascular risk profile, and its prevalence as a cause of acute coronary syndrome and sudden death is probably under-recognized. The pathophysiology of SCAD consists essentially in the formation of an intramural hematoma, with or without intimal tear, which causes luminal compression and obstruction. The most used technique for the diagnosis of SCAD is coronary angiography. Intravascular imaging tools, such as intravascular ultrasound and optical coherence tomography, provide a more accurate characterization of the coronary wall, allowing diagnosis when angiography is unclear. We present the case of a young woman admitted with typical chest pain associated with electrocardiographic changes and elevated cardiac troponin I.

Objectives The purpose of this study was to investigate whether post-ischemic left ventricular (LV) remodeling might be induced by regional contractile dysfunction per se (i.e., in the absence of transmural necrosis) and whether this phenomenon is potentially reversible after contractile recovery. Background Formation of extensive scar tissue is thought to be chiefly responsible for post-infarction LV remodeling; however, myocardial necrosis also causes loss of contractility. We investigated LV geometry and shape in a setting in which contractile dysfunction occurs in the presence of preserved myocyte viability, and thus it is potentially reversible. Methods In 42 patients with chronically dysfunctional myocardium, we evaluated (by two-dimensional echocardiography) LV global and regional function, volumes, and sphericity index (SI), at baseline and 8 ± 3 months after coronary revascularization. Myocardial viability before revascularization was evaluated by dobutamine echocardiography. Results At baseline, regional and global function were depressed and LV dilation was present. Revascularization was followed by recovery of ejection fraction (from 33 ± 6% to 45 ± 10%, p Conclusions Hibernating myocardium is associated with major alterations in LV volumes and shape, which significantly revert after revascularization. Thus, chronic dyssynergy per se is sufficient to induce ischemic LV remodeling in patients.

In the last few years, advances have been made in the diagnosis and management of ST-segment elevation myocardial infarction (STEMI). Recent guidelines have been developed to improve outcome of STEMI patients by implementation of the recommendations into clinical practice. In order to assess the disease burden, the treatment modalities and the mid-term outcome of STEMI in the Umbria region, Italy, we performed a prospective observational study of all patients hospitalized with a diagnosis of STEMI from October 14, 2006 to April 14, 2008 (Umbria-STEMI registry).All the medical emergency services (118) and all the emergency, internal medicine and cardiology departments were involved in the project. Three typologies of cardiology departments are operating in our region: a) intensive care units (ICUs) with percutaneous coronary intervention (PCI) facilities fully operating 24 h/day and 7 days/week (1 center), b) ICUs with PCI facilities operating 6 h/day and 5 days/week (2 centers); c) ICUs without PCI facilities (4 centers). The Umbria-STEMI health area includes about 850 000 inhabitants.Overall, 868 patients (70% male, mean age 66.5 +/- 13.3 years) were enrolled. Patients with late presentation (12 h) or non-persistent ST-segment elevation (9.9%) were excluded. 86.7% of patients underwent reperfusion treatment: 45.9% with primary angioplasty and 40.8% with thrombolysis (64 of them had rescue angioplasty). Primary angioplasty was mainly performed in the hospital with PCI facilities operating 24 h/day. 104 patients with STEMI (13.3%) did not receive any type of coronary reperfusion therapy. In a logistic regression analysis, the direct admission to the hospital with fully operating PCI facilities was the strongest positive predictor of reperfusion therapy utilization, whereas the time delay, older age and TIMI risk index were negative predictors. The mean door-to-needle time for lytic therapy was 60 min, and the door-to-balloon time for primary angioplasty was 156 min. In-hospital mortality was 5.9%.The Umbria-STEMI registry disclosed several discrepancies between guidelines-recommended treatments and their utilization in daily practice. Efforts should be made to reduce the delay from symptom onset to intervention.

In patients with ischaemic left ventricular (LV) dysfunction and viable myocardium, revascularization improves systolic function. Diastolic dysfunction is also present in such patients; however, whether revascularization improves diastolic function also is largely unknown. Methods Twenty-six patients with chronic ischaemic cardiomyopathy (ejection fraction (EF) 32+6%, wall motion score index (WMSI) 2.45+0.33) and viable myocardium (low-dose dobutamine echocardiography) were examined at baseline and � 4 months after revascularization. Diastolic function was assessed by transmitral pulsed-wave Doppler and tissue Doppler imaging (TDI) at the mitral annulus. Results At baseline, 62% of patients showed non-restrictive filling (non-RF) pattern, and 38% restrictive filling (RF) pattern. After revascularization, along with improvement in systolic function (EF 43+10%, WMSI 1.78+0.47, P ¼ 0.0002 for both), diastolic filling improved in most patients, with only three patients still exhibiting RF pattern (P ¼ 0.016); fur- thermore, E 0 velocity increased (32+42%, P ¼ 0.0028) and E/E 0 decreased (219+31%, P ¼ 0.0378) compared with baseline. Left ventricular filling pressure also decreased, from 17.5+6.8 to 13.1+6.5 mmHg (P ¼ 0.005). Improvement of diastolic function by TDI was related to the extent of viability at baseline (P ¼ 0.0098) and to LV reverse remodelling after revascularization (P ¼ 0.0092). Conclusion In patients with ischaemic cardiomyopathy, LV diastolic filling may largely improve after revascularization. Improve- ment of diastolic dysfunction is related to the amount of viable tissue and it may represent an additional advantage of revascularizing dyssinergic but viable myocardium.

Transradial access (TRA) decreased bleeding after coronary interventions compared with femoral access (FA). However, no large study focused on arterial access-related outcomes in patients with acute coronary syndromes, although procedure-related bleeding significantly impaired prognosis. The aim was to evaluate access site-related outcomes of patients who underwent an invasive coronary procedure in the PRESTO-ACS Study. The cumulative primary study end point was death or reinfarction during hospitalization and at 1-year follow-up. Secondary end points were in-hospital bleeding and a net clinical outcome (combination of the primary end point and bleeding). Of 1,170 patients studied, 863 underwent a percutaneous coronary procedure using FA, and 307, using TRA. Compared with FA, TRA was associated with higher glycoprotein IIb/IIIa inhibitor use (52% vs 34%; p

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 (n=11) or chronic stable angina (n=10). 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.

The purpose of this study was to investigate whether post-ischemic left ventricular (LV) remodeling might be induced by regional contractile dysfunction per se (i.e., in the absence of transmural necrosis) and whether this phenomenon is potentially reversible after contractile recovery.Formation of extensive scar tissue is thought to be chiefly responsible for post-infarction LV remodeling; however, myocardial necrosis also causes loss of contractility. We investigated LV geometry and shape in a setting in which contractile dysfunction occurs in the presence of preserved myocyte viability, and thus it is potentially reversible.In 42 patients with chronically dysfunctional myocardium, we evaluated (by two-dimensional echocardiography) LV global and regional function, volumes, and sphericity index (SI), at baseline and 8 +/- 3 months after coronary revascularization. Myocardial viability before revascularization was evaluated by dobutamine echocardiography.At baseline, regional and global function were depressed and LV dilation was present. Revascularization was followed by recovery of ejection fraction (from 33 +/- 6% to 45 +/- 10%, p0.0001) and wall motion score index (from 2.29 +/- 0.31 to 1.74 +/- 0.42, p0.0001). After revascularization, significant improvement of end-systolic volume index (from 78 +/- 23 ml/m2 to 56 +/- 23 ml/m2, p0.0001), end-diastolic volume index (from 118 +/- 26 ml/m2 to 99 +/- 26 ml/m2, p0.0001), and SI (from 0.69 +/- 0.14 to 0.52 +/- 0.11, p0.0001) was also observed. Improvement in LV volumes and SI were significantly correlated to the number of segments recovering function after revascularization.Hibernating myocardium is associated with major alterations in LV volumes and shape, which significantly revert after revascularization. Thus, chronic dyssynergy per se is sufficient to induce ischemic LV remodeling in patients.

Mediastinal irradiation can induce coronary artery disease characterized by fibrous lesions developing in the absence of lipid/foam cell accumulation. We document several consecutive cases of acute coronary artery occlusion developing over radiation-induced lesions in patients who were relatively young, without evidence of classical risk factors for atherosclerosis, and in whom the coronary vasculature was otherwise apparently free of disease. The finding of acute coronary artery occlusion at the site of a fibrous lesion lends further support to the hypothesis that acute coronary syndromes may not necessarily be identifiable with ulceration/disruption of the atherosclerotic plaque as the underlying mechanism of acute thrombus formation.

The presentation of simultaneous severe coarctation of the descending aorta and severe aortic valve disease is uncommon. We describe the management of simultaneous association of aortic coarctation, aortic valve disease, and ischemic cardiomyopathy and describe a one-stage surgical approach for the correction of all pathologies. After performing the aortic valve replacement and myocardial revascularization, coarctation was solved by means of a prosthesis between the ascending aorta and the abdominal aorta. There were no evidence of myocardial ischemia during exercise testing and the blood pressure is normal.