Intravenous antiplatelet therapy in patients with ST-segment elevation myocardial infarction undergoing primary percutaneous coronary intervention : A report from the INVEST-STEMI group.

The use of intravenous antiplatelet therapy during primary percutaneous coronary intervention (PPCI) is not fully standardized. The aim is to evaluate the effectiveness and safety of periprocedural intravenous administration of cangrelor or tirofiban in a contemporary ST-segment elevation myocardial infarction (STEMI) population undergoing PPCI. This was a multicenter prospective cohort study including consecutive STEMI patients who received cangrelor or tirofiban during PPCI at seven Italian centers. The primary effectiveness measure was the angiographic evidence of thrombolysis in myocardial infarction (TIMI) flow < 3 after PPCI. The primary safety outcome was the in-hospital occurrence of BARC (Bleeding Academic Research Consortium) 2-5 bleedings. The study included 627 patients (median age 63 years, 79% males): 312 received cangrelor, 315 tirofiban. The percentage of history of bleeding, pulmonary edema and cardiogenic shock at admission was comparable between groups. Patients receiving cangrelor had lower ischemia time compared to tirofiban. TIMI flow before PPCI and TIMI thrombus grade were comparable between groups. At propensity score-weighted regression analysis, the risk of TIMI flow < 3 was significantly lower in patients treated with cangrelor compared to tirofiban (adjusted OR: 0.40; 95% CI: 0.30-0.53). The risk of BARC 2-5 bleeding was comparable between groups (adjusted OR:1.35; 95% CI: 0.92-1.98). These results were consistent across multiple prespecified subgroups, including subjects stratified for different total ischemia time, with no statistical interaction. In this real-world multicenter STEMI population, the use of cangrelor was associated with improved myocardial perfusion assessed by coronary angiography after PPCI without increasing clinically-relevant bleedings compared to tirofiban.

Intramyocardial calcification in apical hypertrophic cardiomyopathy assessed using multimodality imaging: a case series.

Apical hypertrophic cardiomyopathy (ApHCM) is an HCM variant, affecting frequently males in midlife. It is characterized by apical obliteration and persistent diastolic contraction, often resulting in microvascular ischaemia. We report five cases of ApHCM, with evidence of intramyocardial calcification on echocardiogram. On cardiac magnetic imaging (MRI), a hypointense component at early gadolinium enhancement (EGE) sequences, compatible with calcium, and a deep layer, with hyperintensity at late gadolinium enhancement (LGE) sequences, referable to fibrosis, suggest an endomyocardial fibrosis (EMF) diagnosis. EMF pathologic hallmark is endocardium and myocardium scarring, evolving to dystrophic calcification. It is found only in few ApHCM patients. Our series is the largest one described until now. Analysing patients' history, coexistent inflammatory triggers were evident in all of them, so their co-morbidities could represent a further cause of small vessel disease, in the context of ischaemic microvascular stress due to hypertrophy, leading to fibrosis and dystrophic calcification. This series could demonstrate the relation between apical fibrosis/calcification and microvascular ischaemia due to hypertrophy and inflammatory triggers.

"No-Reflow" Phenomenon: A Contemporary Review.

Primary percutaneous angioplasty (pPCI), represents the reperfusion strategy of choice for patients with STEMI according to current international guidelines of the European Society of Cardiology. Coronary no-reflow is characterized by angiographic evidence of slow or no anterograde epicardial flow, resulting in inadequate myocardial perfusion in the absence of evidence of mechanical vessel obstruction. No reflow (NR) is related to a functional and structural alteration of the coronary microcirculation and we can list four main pathophysiological mechanisms: distal atherothrombotic embolization, ischemic damage, reperfusion injury, and individual susceptibility to microvascular damage. This review will provide a contemporary overview of the pathogenesis, diagnosis, and treatment of NR.

[Cardiovascular management of patients with chronic myeloid leukemia treated with BCR-ABL tyrosine kinase inhibitors: it is time for a shared management]. / Gestione cardiovascolare dei pazienti affetti da leucemia mieloide cronica in terapia con inibitori delle tirosin-chinasi anti-BCR-ABL: è tempo per un percorso condiviso.

Chronic myeloid leukemia is a rare myeloproliferative disease, characterized by a chromosomal translocation detected in 95% of cases, defined as "Philadelphia chromosome", encoding for the BCR-ABL fusion protein with continuous activation of the tyrosine kinase domain. Over the last 20 years, treatment has been revolutionized by the use of BCR-ABL tyrosine kinase inhibitors (TKI). Imatinib is the first TKI approved with a good cardiovascular safety profile, while some second-generation (nilotinib and dasatinib) and third-generation (ponatinib) drugs, developed to overcame drug resistance, can be associated with cardiovascular adverse events. The major adverse effect of dasatinib is pulmonary hypertension, reversible after treatment discontinuation. Conversely, nilotinib or ponatinib assumption is associated with a higher incidence of ischemic events, including coronary artery disease, cerebral stroke and peripheral arterial disease. Therefore, the management of patients receiving TKI therapy should include an integrated multidisciplinary evaluation and follow-up, involving highly specialized figures such as a cardiologist, hematologist and/or oncologist and the application of dedicated pathways, in order to prevent the onset or manage cardiovascular complications associated with these drugs.