The success of a primary percutaneous intervention (PCI) in the setting of ST elevation myocardial infarction depends on the functional and structural integrity of coronary microcirculation. Coronary microvascular dysfunction and obstruction (CMVO) occurs in up to half of patients submitted to apparently successful primary PCI and is associated to a much worse outcome. The current review summarizes the complex mechanisms responsible for CMVO, including pre-existing coronary microvascular dysfunction, and highlights the current limitations in the assessment of microvascular function. More importantly, at the light of the substantial failure of trials hitherto published on the treatment of CMVO, this review proposes a novel integrated therapeutic approach, which should overcome the limitations of previous studies.

Myocardial infarction (MI) with no obstructive coronary atherosclerosis (MINOCA) is a syndrome with different causes. Its prevalence ranges between 5 and 25% of all MIs. The prognosis is extremely variable, depending on the causes of MINOCA. Clinical history, echocardiography, coronary angiography, and left ventriculography represent the first-level diagnostic investigations. Nevertheless, additional tests are required in order to establish its specific cause, thus allowing an appropriate risk stratification and treatment. We review pathogenesis, diagnosis, prognosis, and therapy of MINOCA and propose an algorithm for its management.

Myocardial infarction with non-obstructive coronary arteries (MINOCA) is a syndrome with different causes, characterised by clinical evidence of myocardial infarction with normal or near-normal coronary arteries on angiography. Its prevalence ranges between 5% and 25% of all myocardial infarction. The prognosis is extremely variable, depending on the cause of MINOCA. The key principle in the management of this syndrome is to clarify the underlying individual mechanisms to achieve patient-specific treatments. Clinical history, electrocardiogram, cardiac enzymes, echocardiography, coronary angiography and left ventricular angiography represent the first level diagnostic investigations to identify the causes of MINOCA. Regional wall motion abnormalities at left ventricular angiography limited to a single epicardial coronary artery territory identify an 'epicardial pattern'whereas regional wall motion abnormalities extended beyond a single epicardial coronary artery territory identify a 'microvascular pattern'. The most common causes of MINOCA are represented by coronary plaque disease, coronary dissection, coronary artery spasm, coronary microvascular spasm, Takotsubo cardiomyopathy, myocarditis, coronary thromboembolism, other forms of type 2 myocardial infarction and MINOCA of uncertain aetiology. This review aims at summarising the diagnosis and management of MINOCA, according to the underlying physiopathology.

Patients with ACS presenting with PR as culprit lesion by OCT have a worse prognosis compared with that of patients with IFC. This finding should be taken into account in risk stratification and management of patients with ACS.

Background-Radiofrequency ablation of atrial fibrillation has been associated with some risk of thromboembolic events.Previous studies showed that preventive short episodes of forearm ischemia (remote ischemic preconditioning [IPC]) reduce exercise-induced platelet reactivity. In this study, we assessed whether remote IPC has any effect on platelet activation induced by radiofrequency ablation of atrial fibrillation. Methods and Results-We randomized 19 patients (age, 54.7±11 years; 17 male) undergoing radiofrequency catheter ablation of paroxysmal atrial fibrillation to receive remote IPC or sham intermittent forearm ischemia (control subjects) before the procedure. Blood venous samples were collected before and after remote IPC/sham ischemia, at the end of the ablation procedure, and 24 hours later. Platelet activation and reactivity were assessed by flow cytometry by measuring monocyte-platelet aggregate formation, platelet CD41 in the monocyte-platelet aggregate gate, and platelet CD41 and CD62 in the platelet gate in the absence and presence of ADP stimulation. At baseline, there were no differences between groups in platelet variables. Radiofrequency ablation induced platelet activation in both groups, which persisted after 24 hours. However, compared with control subjects, remote IPC patients showed a lower increase in all platelet variables, including monocyte-platelet aggregate formation (P<0.0001), CD41 in the monocyte-platelet aggregate gate (P=0.002), and CD41 (P<0.0001) and CD62 (P=0.002) in the platelet gate. Compared with control subjects, remote IPC was also associated with a significantly lower ADP-induced increase in all platelet markers. Conclusions-Our data show that remote IPC before radiofrequency catheter ablation for paroxysmal atrial fibrillation significantly reduces the increased platelet activation and reactivity associated with the procedure. (Circulation. 2014;129:11-17.)Key Words: atrial fibrillation ◼ blood platelets ◼ catheter ablation ◼ ischemic preconditioning ◼ platelet activation.

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At 1-year follow-up, STEMI patients treated with BVS showed similar rates of DOCE compared with STEMI patients treated with EES or BMS, although rate of scaffolds thrombosis, mostly clustered in the early phase, was not negligible. Larger studies with longer follow-up are needed to confirm our findings.

These results show that, in patients with stable CAD, remote ischaemia induces protection against an exercise-related increase in platelet reactivity.