Abstract Aims Post-cardiac injury syndrome (PCIS) is an inflammatory state involving pericardium, epicardium, and myocardium causing a clinical picture in which epicardial and pericardial symptoms are prevalent. It appears mediated by autoimmune mechanisms and may appear as late post myocardial infarction pericarditis (Dressler’s Syndrome) or as a post traumatic pericarditis in the case of spontaneous thoracic trauma or iatrogenic pericarditis. Apart from the acute setting, pericardial effusion can be a manifestation of PCIS after interventional procedures. Methods and results A 57 years old hypertensive woman suffering from recurrent atrial fibrillation episodes underwent a technically difficult radio-frequency catheter ablation because of complex pulmonary veins anatomy and wide scar in the left atrial wall. During the procedure she developed cardiac tamponade and 410 ml of blood were drained by pericardiocentesis and re-infused without recurrent pericardial effusion during further in-hospital stay. She was discharged on apixaban 5 mg b.i.d. with Hb value of 10.2 g/dl. Two weeks later the patient was hospitalized for worsening cough, atypical chest pain, dyspnoea and modest orthopnea. C-reactive protein levels were 8.7 mg/dl, Hb was 9.9 g/dl and platelet count 484 000/ml; blood cultures were negative. An urgent thoracic CT scan showed bilateral pleural effusion and ubiquitous pericardial effusion (2.5–3 cm), without signs of active bleeding from the cardiac chambers into the pericardium. After stopping apixaban, the patient was given colchicine (1 mg/die). A total of 1200 ml of hematic pericardial fluid was drained from the pericardium over a 5-day period. Autoimmune blood tests were negative, as well as antibodies to pericardiotropic viruses. Pericardial fluid was negative for quantiferon and direct BK. On day 9, the drain was removed and steroidal treatment was started (prednisone 25 mg/die with scheduled tapering). Further echocardiographic exams were stable without pericardial effusion; a chest X-ray scan (at day 16) showed reversal of the water bottle shaped heart and of the pleural effusion. Conclusions Early myocardial infarct-associated pericarditis and Dressler’s syndrome account for about 20% of cases of PCIS accompanied by symptoms of epicardial and pericardial origin. PCIS is quite common after cardiac surgery, but it may be also observed even after iatrogenic trauma occurring during cardiac interventions: PCI, pacemaker lead insertion, radiofrequency ablation and Swan–Ganz catheterization. Blood entering the pericardium is thought to play a pivotal etiological role in iatrogenic PCIS, with consequent huge inflammatory reaction in the mesothelial tissue resulting in clinical manifestations of pericarditis. In animal models of PCIS, systemic release of cardiac antigens and self-antigen specific responses has been hypothesized. In our case cardiac tamponade complicating the ablation procedure probably initiated the epicardial and pericardial inflammatory response. Even if based on few data, the patient was treated with colchicine first, avoiding aspirin because of the hemorrhagic pericardial fluid; glucocorticoids were then started when symptoms and signs of PCIS slowly resolved despite colchicine treatment. The pericardial fluid was hemorrhagic (Hb 5.9 g/dl) and treatment with apixaban, in the context of an inflammatory mesothelial response, could have caused this peculiar, hemorrhagic, pericardial reaction.

INTRODUCTION:Atherothrombosis and coronary artery disease affect more than 13 million individuals only in the United States, about 8 millions in Europe and are the major causes of death worldwide. In particular chronic stable angina impairs patient quality of life, is associated with an important health spending and increased patient mortality; it is a prominent symptom of coronary artery disease (CAD), the latter being prevalent worldwide in patients. A key role in pathophysiology of cardiovascular acute events is played by activated platelets. Aspirin and adenosine diphosphate antagonist in addition to it is recommended for 1 year for reduction of cardiovascular events in patients with prior myocardial infarction with a weak recommendation to continue thereafter. P2Y12 receptor antagonists, in addition to aspirin, have been shown in the last years, to reduce ischemic events in patients with acute coronary syndrome but their role in secondary prevention is still new and unclear. The aim of our paper is to review the long-term effect of therapy with ticagrelor on the basis of recent evidence based data.METHODS:We performed an online search on the major search engines. All the randomized controlled trials were summarized in the table.RESULTS:We included in our paper six randomized controlled trials and we mentioned about ten post - hoc analysis, sub studies and registries. All studies included the type the therapy and a mid or long term clinical follow up.CONCLUSIONS:The studies reported in our paper and in particular PEGASUS - TIMI 54 study showed the merit to placing attention of prevention secondary ischemic events after acute coronary syndrome in the context of treatment with dual anti - platelet therapy; it proved a clinical benefit in patients treated with ticagrelor (60 mg x 2) for 3 years. Nevertheless, the effectiveness of these results cannot be generalized to patients with higher bleeding risk or low ischemic risk. In fact prolonged therapy with ticagrelor 60 mg in combination with aspirin could be considered valuable in patients with repeated acute ischemic events or with several coronary revascularizations over time (especially in patients with lower bleeding risk).

Cardiovascular diseases and in particular coronary atherosclerotic disease are the leading cause of mortality and morbidity in the industrialized countries. Coronary atherosclerosis has been recognized for over a century and it was the subject of various studies. Pathophysiological studies have unravelled the interactions of molecular and cellular elements involved in atherogenesis; during the last decades the basic research has focused on the study of the instability of atherosclerotic plaque. Plaque rupture and resulting intracoronary thrombosis are thought to account for most acute coronary syndromes including ST - segment elevation myocardial infarction and non ST - segment elevation myocardial infarction. This is a brief review of the pathophysiology of atherosclerotic plaque development.

Cardiovascular disease and in particular, acute coronary syndromes are one of the principle causes of death in the industrialized countries. In the setting of acute coronary syndromes (both ST - segment or non ST - segment elevation myocardial infarction), platelets aggregation plays a key and central role in their development. Platelets are the mediators of hemostasis at sites of vascular injury, but they also mediate pathologic thrombosis; activated platelets stimulate thrombus formation in response to rupture of an atherosclerotic plaque or endothelial cell erosion promoting atherothrombotic disease. Recent patent relates to the methods and devices for treating atherosclerosis and to prevent in-stent restenosis or thrombosis. Because of the importance of platelets involvement in the initiation and propagation of thrombosis, antiplatelet drugs have a source of research; in the recent past, new antiplatelet drugs (such as ticagrelor) have been studied and placed in the routine therapy. The aim of this paper is to summarize the pharmacological properties and the clinical characteristics of ticagrelor.

Giant cell myocarditis (GCM) is a rare, rapidly progressive and highly lethal disease in young and middle-aged adults. It is attributed to an inflammation of the heart muscle, and mediated by T lymphocytes and anti-myosin autoantibodies. Making diagnosis of GCM with multiple noninvasive imaging modalities is possible in a small percentage of patients, so myocardial tissue diagnosis is often required. An early diagnosis is very important, because immunosuppressive treatment may significantly improve clinical course and survival of these patients. GCM often escapes diagnosis until autopsy or transplantation and has defied proper treatment trials for its rarity and deadly behavior. This review will focus on the diagnostic approach to patients with suspected GCM and currently evidence-based treatment strategy for this disease.

Coronary artery disease is the major cause of mortality and morbidity in the industrialized countries; in the United States of America and in Europe, it is responsible for one of every six deaths per year. In the setting of ischemic heart disease, angina pectoris and chest pain, in particular, are the major causes of emergency department accesses. Angina pectoris is a clinical syndrome characterized by discomfort typically in the chest, neck, chin and left arm induced by physical exertion, emotional stress and cold and is relieved by rest or by taking of nitrates. The main targets of treatment of angina pectoris are to improve quality of life by reducing the frequency and the severity of symptoms, to increase functional capacity and to improve prognosis. Ranolazine is a recent antianginal drug with unique methods of action. It was approved by the US Food and Drug Administration in 2006 as add-on therapy in patients symptomatic for stable angina. With the inhibition of the late sodium current, Ranolazine protects against ion deregulation, prevents cellular calcium overload and the subsequent increase in diastolic tension without impacting heart rate and blood pressure. Short term clinical trials and patent research show that add on therapy with Ranolazine in patients with chronic stable angina significantly improves exercise duration, exercise time to angina and reduces the use of nitro glycerine. Long term clinical trials showed no significant differences in the rate of cardiovascular death and myocardial infarction in patients with non-ST segment elevation acute coronary syndromes but a reduction in terms of recurrent ischemia. Ranolazine is generally well tolerated and even if it increases the duration of QTc interval it is not associated with atrial and ventricular arrhythmias. Therefore Ranolazine represents a good therapeutic approach in patients with chronic stable angina still symptomatic, while on optimal anti-ischemic therapy, or intolerant to traditional anti-ischemic drugs.

Cardiovascular disease, in particular acute coronary syndromes (ACS), is still one of the leading causes of death in industrialized countries. ACS including ST-elevation myocardial infarction (STEMI), non-ST-elevation myocardial infarction (NSTEMI) and unstable angina pectoris (UA) are associated with lower mortality if diagnosed early. The diagnosis is based on clinical symptoms, ECG and circulating biomarker-level changes. Recent studies have shown that there are alternatives to the known biomarkers such as ultrasensitive troponin I or T and creatine kinase Mb; there are, in fact, novel biomarkers such as miRNAs. These are 22-nucleotide-long non-coding RNAs that regulate gene expression at post-transcriptional level. Several recent studies have shown that miRNAs play a physiological role in cardiovascular homeostasis and in the pathogenesis of cardiovascular disease. Expression-pattern studies of myocardial tissue reveal that several miRNAs are up- or down-regulated during myocardial infarction. The purpose of the present review is to highlight the state of the art and future views on this topic.

In patients with coronary artery disease, quantitative coronary angiography (QCA) has proved to be a good method for quantification of atherosclerotic plaques since 80’ years. It is used for diagnosis and management in catheterization laboratory of a lot of patients undergoing percutaneous coronary intervention. QCA allows us to assess with dedicated computer software the impact of atherosclerosis on the lumen of the coronary arteries and to establish over time whether an intervention attenuates progression or regression of atherosclerotic disease. Currently, the use of QCA, in catheterization laboratory during percutaneous coronary intervention, is the most used method to investigate precisely the performance of coronary plaque; it, also, allows studying the efficacy of coronary intervention; nevertheless this technique has some limitations and difficulties resulting from the routine use in the evaluation of parameters. This review aims to summarize the principles and the methods used for quantitative coronary angiography with a look on the past and present describing also more recent patents and developments. Keywords: Angiography, atherosclerotic plaque, coronary angioplasty, coronary disease, coronary stenosis.

During the last years an increasing number of patients with high perioperative risk and decreased left ventricular function are referred to cardiac and non-cardiac surgery. In this subgroup of patients, heart failure is the major cause of perioperative morbidity and mortality. In order to prevent and treat this type of complications several therapeutic attempts have been tried involving intra aortic balloon pump and inotropic agents infusion (such as beta-adrenergic agonists and phosphodiesterase inhibitors) Levosimendan is new inotropic agent; it is a calcium-sensitising inotropic agent and a vasodilator used in the treatment of heart failure. In the last ten years several reports have been published on levosimendan. The inotropic efficacy of levosimendan is dose-dependent and equal or even superior to any of the other commercially available inotropic agents. The aim of the present review is to describe experimental and clinical effects of perioperative treatment with levosimendan.

Acute coronary syndromes and, in paticular, ST - segment elevation myocardial infarction are the principle causes or mortality and morbidity in the industrialized countries. The manadgement of acute myocadial infarction is much debated in the literature; primary percutaneous coronary intervention is the treatment of choice. In the recent years there has been an increasing interest in the concept of adjunctive pharmacological therapy to improve outcomes in primary percutaneous coronary intervention. In the literature randomized trials of intravenous or more recently intracoronary injection of glycoprotein IIb/IIIa inhibitors have provided conflicting results with no definitive evidence for efficacy. The aim of the report is to review the evidence to our date on the role of intracoronary injection of abciximab during primary percutaneous intervention in the setting of acute myocardial infarction.