Search

COVID-19 infection appeared to be associated with increased risk of thrombotic events, ranging from microvascular thrombosis to venous thromboembolic disease (including deep vein thrombosis and pulmonary embolism), and stroke [1].

In this chapter we will characterize arterial wall calcification into three main types: (1) inflammatory/atherosclerotic (mostly intimal), (2) metabolic (mostly medial), and (3) genetic (mostly medial). Several overlapping mechanisms trigger all three types of calcification. The extent of coronary artery calcification as determined by computed tomography (CT) is being used to predict future cardiovascular events; nevertheless the contribution of coronary calcium in plaque instability is unclear. In pathologic studies, small microcalcification or spotty calcification identified by clinical CT is associated with rupture-prone unstable plaque, whereas advanced or sheet-like calcification is associated with stable plaque. Carotid artery has distinct geometry at bifurcation region that contributes to unique blood flow patterns, which lead to acceleration of atherosclerosis development. In contrast to the coronary vasculature, Monckeberg’s medial calcification, generally observed in the peripheral arteries, leads to arterial stiffness and is accelerated in the presence of type 2 diabetes and end-stage renal disease. Both medium- to small-sized muscular arteries, including arterioles, could calcify without athrosclerotic process.

Acute coronary syndrome includes unstable angina, acute myocardial infarction, and sudden coronary death. In individuals with sudden coronary death, 50–60% displays acute coronary thrombus at the culprit site, while the remaining cases demonstrate a stable coronary plaques with greater than 75% cross-sectional area luminal narrowing, with or without chronic total occlusion or healed myocardial infarction. Three different causes of coronary thrombus have been shown, i.e., plaque rupture, plaque erosion, and calcified nodule. Plaque rupture (PR) is the most common cause of coronary thrombus, which shows a disrupted fibrous cap and an underlying necrotic core in contact with the flowing blood and a luminal thrombus. The second most common cause of thrombosis is plaque erosion. Plaque erosions show an absence of endothelium with an underlying abundance of smooth muscle cells in a proteoglycan-collagen-rich matrix. The least frequent cause of coronary thrombosis is calcified nodule which occurs in highly calcified arteries. Calcified nodule demonstrates a disrupted fibrous cap due to fragments of calcified spicules typically surrounded by fibrin and an overlying platelet-rich thrombus. Calcified nodules are usually eccentric and usually have an overlying nonocclusive thrombus. The precursor lesion of rupture is a vulnerable plaque which demonstrates all the features of rupture, but there is an intact fibrous cap, and the necrotic core is usually smaller than that observed in ruptures. Erosive plaques mostly show an underlying fibroatheroma or pathologic intimal thickening, while calcified nodules demonstrate a highly calcified plaque in a heavily calcified coronary artery.

More than 5 millions stents have been implanted in patients all over the world and it is estimated that the number will increase to 6.6 million by 2020. It has been almost 30 years since the first stent was implanted in man. Initially, stents were mainly used for bail out in patients with acute occlusion due to coronary dissection following balloon angioplasty. The first stents were typically mounted on high profile, rigid delivery platforms and were difficult to deploy, leading to acute/subacute stent thrombosis. Greater understanding of the need for effective antiplatelet therapy and also improvement in delivery and better stent designs helped to overcome early stent thrombosis. The resulting lower rates of restenosis as compared to balloon angioplasty propelled the use of stents in routine practice. However, restenosis was the “Achilles heel” of bare metal stents and the birth of drug eluting stents (DES) helped dramatically reduce restenosis but late stent thrombosis became an issue. Second generation DES have reduced the incidence of late stent thrombosis however, one of the mechanisms of late stent thrombosis is the development of atherosclerosis within the stented segment (“neoatherosclerosis”), which remains an issue because its development is increased in DES compared to BMS. Recently, third generation DES, using bioabsorable polymer rather than permanent polymer to deliver drug and fully biodegradable vascular scaffolds are available. Many believe that these will overcome the drawback of stenting as no permanent metal or polymer will be left behind. Studies in animals show that when bioabsorable polymers are used the endothelial lining is far more competent as compared to permanent polymers that have been shown to induce hypersensitivity reaction. Also, clinical studies have shown that bioabsorable polymers induce less late thrombosis as compared to permanent polymers. Similarly, in fully bioabsorbable scaffolds, the vascular reactivity and lumen enlargement are seen between 1 and 2 years after implantation and the polymers get replaced by proteoglycan matrix and collagen over time and that mild to moderate inflammation is associated with vessel enlargement. Overall what remains unclear is that bulky scaffolds ≥150 μm thickness may be associated again with greater late stent thrombosis. Therefore, we have to remain vigilant that we do not implant these fully bioabsorbable polymeric scaffolds in patients presenting with acute myocardial infarction until clearly clinical trials prove their safety.