While receiving triple therapy, major bleeding occurred in 4.7% of patients; one-half of the events were lethal, and most occurred within the first month.

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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.

Early complete revascularization based only on angiographic findings in patients with STEMI and MVD is associated with an excess of periprocedural/re-MI and with a significantly higher incidence of MACE at follow-up.

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Lipid‐lowering therapy is a mainstay for the management of coronary and carotid disease. Actually, progression of atherosclerosis and adverse events are reduced in proportion to the achieved levels of LDL cholesterol (LDL‐C). A 67‐year‐old patient underwent two hospitalizations 6 months apart due to acute coronary syndromes. In the first, PCI with drug‐eluting stents (DES) was performed to treat ulcerated stenoses in the left anterior descending artery. In the second, lipid‐rich critical disease was found on the right coronary artery and treated with PCI + DES. Later, carotid duplex ultra‐sonography (DU) was done due to some episodes of dizziness. It showed an 80% critical stenosis (peak systolic velocity, PSV 239 cm/s) of the left internal carotid artery (LICA) with high‐risk features (hypoechogenic and irregular plaque with “fluffy” components). In consideration of the plaque morphology and the unmet LDL‐C targets, evolocumab was added to the ongoing statin therapy. In the following months, we observed a parallel trend between carotid plaque regression and LDL‐C lowering. Initial plaque remodeling was seen after 5 months: the atheroma appeared fibrotic, with no more fluffy components. At 10 months, in conjunction with the achievement of LDL‐C goal (23 mg/dl), a fibrocalcific atheroma was observed; PSV, after an initial rise, fell to 229 cm/s. No further cardiovascular event occurred at 46 months. Last DUS showed a 60% fibrocalcific mid LICA stenosis with PSV of 180 cm/s. Our experience highlights the important role of proprotein convertase subtilisin kexin type 9 (PCSK9) inhibitors in promoting remodeling and hopefully regression of atherosclerotic plaques.