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Objectives This study sought to evaluate 30-day safety and efficacy of dual-layer mesh-covered carotid stent systems for carotid artery stenting (CAS) in the clinical practice. Background When compared with carotid endarterectomy, CAS has been associated with a higher rate of post procedural neurologic events; these could be related to plaque’s debris prolapsing through stent’s mesh. Consequently, the need for increased plaque coverage has resulted in the development of dual-layer mesh-covered carotid stent systems. Methods From January 2017 to June 2019, a physician-initiated, prospective, multispecialty registry enrolled 733 consecutive patients undergoing CAS using the CGuard embolic prevention system in 20 centers. The primary endpoint was stroke up to 30 days; secondary endpoints were technical and procedural success; external carotid artery occlusion; and in-hospital and 30-day transient ischemic attack (TIA), acute myocardial infarction (AMI), and death rates. Results Symptoms were present in 131 (17.87%) patients. An embolic protection device was used in 731 (99.72%) patients. Procedural success was 100%, technical success was obtained in all but 1 (99.86%) patient, who died in hospital due to a hemorrhagic stroke. Six TIAs, 2 minor strokes, and 1 AMI occurred during in-hospital stay, and external carotid artery occlusion was evident in 8 (1.09%) patients. Between hospital discharge and 30-day follow-up, 2 TIAs, 1 minor stroke, and 3 AMIs occurred. Therefore, the cumulative stroke rate was 0.54%. Conclusions This real-world registry suggests that use of CGuard embolic prevention system in clinical practice is safe and associated with a minimal occurrence of adverse neurological events up to 30-day follow-up.

Background: Coronary calcified lesions may limit optimal stent deployment resulting in stent underexpansion, increasing the risk of thrombosis. The Shockwave Lithoplasty System, a new technology combining a balloon angioplasty catheter with the use of sound waves, it is able to break calcium deposits without affecting vascular soft tissue. Case Presentation: An 80-year-old Caucasian man with ST elevation myocardial infarction underwent emergent coronary angiography showing complete intrastent thrombosis at the proximal trait of LAD. After thrombus removal, it was evident that stent under-expansion at its proximal edge was caused by vascular calcification. Coronary shockwave lithoplasty was chosen to treat this lesion. After calcium deposits disruption we were able to obtain complete stent expansion. Conclusion: Our case demonstrates the usefulness and safety of the lithoplasty system in the context of ST elevation myocardial infarction.

Anomalies of the coronary arteries represent rare congenital disorders, which are characterized by a wide spectrum of clinical manifestations. Usually, they are asymptomatic, but sometimes they cause myocardial ischemia or sudden cardiac death. Here, we describe the case of a patient who suffered from angina. Coronary angiography revealed an ectopic origin of the left anterior descending coronary artery from the proximal trait of the right coronary artery and the left circumflex artery, originating from the left sinus; the whole coronary tree was free of atherosclerosis. To better define the coronary anatomy, we performed computed tomography angiography with a three-dimensional reconstruction. The patient was discharged from the clinic after 48 h under optimal medical treatment.

The aim of this study was to evaluate the 1-year safety and efficacy of a dual-layered stent (DLS) for carotid artery stenting (CAS) in a multicenter registry.DLS have been proved to be safe and efficient during short-term follow-up. Recent data have raised the concern that the benefit of CAS performed with using a DLS may be hampered by a higher restenosis rate at 1 year.From January 2017 to June 2019, a physician-initiated, prospective, multispecialty registry enrolled 733 consecutive patients undergoing CAS using the CGuard embolic prevention system at 20 centers. The primary endpoint was the occurrence of death and stroke at 1 year. Secondary endpoints were 1-year rates of transient ischemic attack, acute myocardial infarction, internal carotid artery (ICA) restenosis, in-stent thrombosis, and external carotid artery occlusion.At 1 year, follow-up was available in 726 patients (99.04%). Beyond 30 days postprocedure, 1 minor stroke (0.13%), four transient ischemic attacks (0.55%), 2 fatal acute myocardial infarctions (0.27%), and 6 noncardiac deaths (1.10%) occurred. On duplex ultrasound examination, ICA restenosis was found in 6 patients (0.82%): 2 total occlusions and 4 in-stent restenoses. No predictors of target ICA restenosis and/or occlusion could be detected, and dual-antiplatelet therapy duration (90 days vs 30 days) was not found to be related to major adverse cardiovascular event or restenosis occurrence.This real-world registry suggests that DLS use in clinical practice is safe and associated with minimal occurrence of adverse neurologic events up to 12-month follow-up.

Objectives: This study sought to evaluate 30-day safety and efficacy of dual-layer mesh-covered carotid stent systems for carotid artery stenting (CAS) in the clinical practice. Background: When compared with carotid endarterectomy, CAS has been associated with a higher rate of post procedural neurologic events; these could be related to plaque's debris prolapsing through stent's mesh. Consequently, the need for increased plaque coverage has resulted in the development of dual-layer mesh-covered carotid stent systems. Methods: From January 2017 to June 2019, a physician-initiated, prospective, multispecialty registry enrolled 733 consecutive patients undergoing CAS using the CGuard embolic prevention system in 20 centers. The primary endpoint was stroke up to 30 days; secondary endpoints were technical and procedural success; external carotid artery occlusion; and in-hospital and 30-day transient ischemic attack (TIA), acute myocardial infarction (AMI), and death rates. Results: Symptoms were present in 131 (17.87%) patients. An embolic protection device was used in 731 (99.72%) patients. Procedural success was 100%, technical success was obtained in all but 1 (99.86%) patient, who died in hospital due to a hemorrhagic stroke. Six TIAs, 2 minor strokes, and 1 AMI occurred during in-hospital stay, and external carotid artery occlusion was evident in 8 (1.09%) patients. Between hospital discharge and 30-day follow-up, 2 TIAs, 1 minor stroke, and 3 AMIs occurred. Therefore, the cumulative stroke rate was 0.54%. Conclusions: This real-world registry suggests that use of CGuard embolic prevention system in clinical practice is safe and associated with a minimal occurrence of adverse neurological events up to 30-day follow-up.

Coronary calcification is a hard challenge for the interventional cardiologist, as it is associated with incomplete stent expansion and frequently stent failure. In recent years, innovative techniques, such as rotational atherectomy, have been developed to treat coronary calcification. However, these are burdened with an increased procedural risk. We report the case of a 60-year-old Caucasian man treated 1 month before at another center with primary coronary angioplasty and stenting of the ramus intermedius for coronary syndrome. Coronary angiography showed a critical stenosis of the left main coronary artery as well as critical calcified stenosis of the left anterior descending artery and the diagonal branch. Coronary calcification was treated with rotational atherectomy that preceded the angioplasty and stenting. Because of persistence of the symptomatology, coronary angiography was repeated 1 month later and showed a critical calcified restenosis of the ramus intermedius at the site of the previous stenting. Considering the high risk of traditional atherectomy, we performed lithotripsy-enhanced disruption of calcium beyond the stents with the Shockwave Coronary Lithoplasty System. The Shockwave Coronary Lithoplasty System has been introduced recently in order to treat calcified coronary lesions with greater safety. The procedure allows most calcified coronary lesions to be treated with simplicity and safety. This system employs sound waves, similar to those used for treating kidney stones, to crush the calcified lesions. We present the first case described to date in whom this technique was successfully used to treat calcified restenosis in a previous stent.

Heavily calcified lesions may limit optimal stent deployment resulting in stent underexpansion, thus increasing the risk of restenosis and thrombosis. We describe the case of overlapping stents underexpansion treated with a shockwave intravasuclar lithoplasty system (Shockwave Medical Inc., Santa Clara, CA, USA). A 65-year-old man with angina, underwent coronary angiography and intravascular ultrasound showing restenosis, in a site of overlapping stents, due to calcified tissue. Shockwave lithoplasty balloon was able to break calcified tissue in a site of overlapping stents, allowing subsequent vessel dilation and repeat stent implantation with optimal final stent expansion. Heavily calcified lesions may limit optimal stent deployment resulting in stent underexpansion. Treating stent underexpansion or restenosis due to calcified tissue is a great challenge. Shockwave lithoplasty is effective in breaking calcified tissue also in a site of overlapping stents. The improved plaque compliance allows to repeat stent implantation with optimal final stent expansion.

We report the case of a stent under-expansion due to heavily calcified plaque treated with the shockwave lithoplasty system. A 77-year-old woman underwent coronary angiography, and intravascular ultrasound revealed stent under-expansion due to calcified plaque. Shockwave lithoplasty balloon was used to disrupt calcium deposits around the stent, thereby allowing a correct stent expansion with an excellent angiographic and intravascular ultrasound result.

Kounis syndrome refers to an acute coronary syndrome, consequent to an allergic reaction. It results from mast cell degranulation with subsequent release of numerous inflammatory mediators, leading to coronary vasospasm, atheromatous plaque rupture, or stent thrombosis. Here, we describe the case of a 47-year-old Caucasian man with acute stent thrombosis, as a consequence of allergic reaction to contrast media. .

The prevalence of isolated right ventricular infarction is 0.4-2.4% in autopsy series and may occur by at least three different mechanisms, of which occlusion of a nondominant right coronary artery is reviewed here. Although rare, as oxygen demand/supply of the right is lower than that of the left ventricle, due to the smaller muscular mass, and it has a good prognosis, sudden death and cardiac rupture have been reported. Differential diagnosis with anterior infarction is needed. ECG may help but specific criteria should be adopted: dome-like and decreasing ST segment elevation from V1 to V3 leads; rapid ST segment normalization and no Q wave evolution from V1 to V3 leads, either accompanied or not by modest ST segment elevation in DIII (but not aVF) evolving in no Q wave; ST segment elevation in right-sided leads which should be explored; absence of ST segment depression in aVL; absent concomitant ST segment elevation in all inferior leads (DII, DIII, aVF). Applying these criteria may prevent erroneous management of right ventricular infarction if it is confused with left ventricular infarction. Right ventricular function evaluation should always be performed by echocardiography. Magnetic resonance imaging should be useful. An illustrative case and an ECG flow-chart are presented.

Different morphologic features of arrhythmogenic right ventricular cardiomyopathy (ARVC) have been described. However, it is still unclear whether they correspond to distinct forms of the same disease. A pathologic study was performed on a series of ARVC (15 from heart transplant and 12 from autopsy) from 2 Italian referral university hospitals. Based on both myocellular features and the nature of myocardial replacement, hearts were divided into 2 groups: infiltrative, with a lacelike pattern of transmural fatty infiltration and strands of normal residual cardiomyocytes (n = 11); and cardiomyopathic, with massive myocardial replacement by fibro fatty tissue and cardiomyopathic changes (such as hypertrophy and myofibril loss) of residual cardiomyocytes (n = 16). Hearts from the infiltrative group were mostly obtained at autopsy of patients who died suddenly. Fatty substitution was limited almost exclusively to the right ventricle. Mitral valve dysplasia (prolapse or cleft) was frequently present. Hearts from the cardiomyopathic group came mainly from heart transplants for congestive heart failure. Fibro fatty replacement was more extensive, usually biventricular. Active myocarditis and features suggestive of myocardial transdifferentiation were also observed. Despite these differences in clinical outcome and morphologic features, patients from the 2 groups showed similar mean age, sex distribution, occurrence of threatening ventricular arrhythmias, and prevalence of family history of sudden death, arrhythmias, or cardiomyopathy. Infiltrative and cardiomyopathic patterns represent different clinical and pathologic subsets of ARVC. Myocellular features are an important clue in the distinction between the two entities. The differentiation between the 2 patterns is feasible on endomyocardial biopsy and could give important prognostic information.

Background: There is some controversy as to whether tirofiban or eptifibatide, two small anti-aggregating drugs (AAD), may reduce the incidence of composite ischemic events within one year in patients undergoing percutaneous coronary intervention (PCI) in the real clinical world. Methods: We compared consecutive patients on oral double AAD (with clopidogrel and aspirin) who underwent PCI (n=207) and patients who were on single AAD and received a second AAD, just prior to PCI, and either high-dose tirofiban or double-bolus eptifibatide (double AAD plus small molecules group, n=666). The primary end point (incidence of composite ischemic events within one year) included death, acute myocardial infarction, unstable angina, stent thrombosis or repeat PCI or coronary bypass surgery (related to the target vessel PCI failure) and was modelled by Cox’s regression. Results: There were 89 composite ischemic events: 24 (11.6%) in double AAD alone and 65 (9.8%) in double AAD plus small molecules groups (log-rank test: p=0.36). Incidences by type of ischemic events were similar between the 2 groups. Based on 21 potential covariates fitted simultaneously, adjusted hazard ratios (HR and 95% confidence intervals) showed that age (HR 1.03, 1.01-1.06, p=0.01), diabetes (HR 1.68, 1.01-2.79, p=0.05) and intra aortic balloon pump (HR 5.12, 2.36-11.10, p=0.0001) were significant risk factors whereas thrombolysis by tenecteplase (HR 0.35, 0.13-0.98, p=0.05) and having had hypertension or anti-hypertensive treatment (HR 0.58, 0.36-0.93, p=0.03) were significant protectors for events. Whether small molecules were present provided a non significant additional benefit as compared to double AAD alone (HR 0.83, 0.51-1.36, p=0.46). Pre-PCI CK-MB were not useful to predict events (HR 1.01, 0.99-1.01, p=0.17). Conclusions: In clinical world patients undergoing PCI (rescue plus primary

Hypersensitivity myocarditis is a well-known complication of pharmaceutical therapy, often requiring heart transplantation. We report the unusual case of pre-transplant hypersensitivity myocarditis with eosinophilic myocardial infiltration in the donor heart, demonstrated by needle biopsy at the time of transplant ('time-zero' biopsy). At first the myocarditic process was temptatively attributed to a pre-transplant pathology in the donor heart, but the close similarity between the pre-transplant and the post-transplant infiltrate and the clinical data of an eosinophilic peak of the recipient during the transplant procedure brought to the diagnosis of early recurrent hypersensitivity myocarditis.

Images are presented of coronary reperfusion that occurred shortly after insertion of an intra-aortic balloon pump for counter-pulsation in 3 patients with acute myocardial infarction refractory to thrombolytic therapy and hemodynamic derangement. It is shown that prophylactic intra-aortic balloon pump use may facilitate percutaneous coronary intervention during acute myocardial infarction and it is useful to provide a visual assessment of myocardial flow restoring.

A 64-year old man who presented with stress angina, carotid atheromatous plaques and high blood pressure was admitted to undergo coronary angiography whose results were grossly normal (Fig. 1) including right and left hemodynamic data. The patient was detected 6 months later with laryngeal carcinoma and he underwent radiotherapy. During 3 successive months he was exposed to 5040 centi-Gray units (cGy) plus a boost dose of 1980 cGy. The overall exposure, also taking the previous coronarographic session (15 sequences totaling 208.6 cGy) into account, was therefore 7228.6 cGy. The patient was also treated by cycles of cisplatin and 5-fluorouracil. He had to stop the second chemotherapeutical cycle because of typical angina, marked bradycardia and widespread abnormalities of ventricular repolarization. He was then referred for a second coronary angiography. Significant stenoses were shown at the ostial level of both left anterior and circumflex coronary arteries (Fig. 2A). A kissing–stenting technique was performed with excellent angiographic results (Fig. 2B). Radiation exposure may induce, especially in the young, ostial coronary lesions [1]. Radiationsmay affect the heart to induce from subclinical histopathological changes to overt clinical diseases including coronary artery disease, pericarditis, conduction abnormalities and valvular injuries [2,3]. The risk is higher when the mediastinal doses exceed 30 Gy [4] and it seems related to irradiated tissue volume and fraction size [5]. Cancer and atherosclerosis share the same stages of initiation, promotion and complication beginning in a single cell mutation, whereas cytokines and growth factors are involved in the atherosclerotic process [6]. Radiation