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Native Coronary Artery and Bypass Graft Atherosclerosis

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PanVascular Medicine

Abstract

Patients with acute coronary syndrome (ACS) classically present with unstable angina, acute myocardial infarction, or sudden coronary death. In approximately 50–60 % of sudden coronary death cases, the culprit lesion exhibits an acute coronary thrombus, whereas the remainder of these cases includes stable coronary plaques with greater than 75 % cross-sectional area luminal narrowing. The most common cause of coronary thrombus is plaque rupture, which is characterized by a large necrotic core and a disrupted cap that allows blood to come in contact with highly thrombogenic necrotic core inducing luminal thrombosis. It is now increasingly recognized that the preexisting thin-cap fibroatheroma (TCFA) (vulnerable plaque) characterized by a necrotic core with an overlying thin fibrous cap (≤65μm) is observed in approximately 50 % of patients dying suddenly with thrombotic occlusion and occurs often in hemodynamically insignificant lesions. The onset of symptoms and life-threatening complications therefore depends not only on the severity of narrowing in stable chronic coronary artery disease but also on the underlying plaque morphology. Intraplaque hemorrhage is a major contributor for the enlargement of the necrotic core. Hemorrhage is thought to occur from leaky vasa vasorum that invade the intima from the adventitia as the intima enlarges. The atherosclerotic plaque progresses from pathologic intimal thickening to a fibroatheroma likely as a result of macrophage infiltration into the lipid pool. The conversion of the lipid pool to necrotic core occurs as a result of macrophage infiltration, which releases matrix metalloproteinase (MMPs) that destroy proteoglycans. The necrotic core is also constituted of apoptotic macrophages and smooth muscle cells that constitute an acellular component of necrotic core. The fibroatheroma has a thick fibrous cap that pinches overtime through macrophage infiltration, MMP release, and apoptotic death of smooth muscle cells converting the fibroatheroma into a TCFA.

Other causes of thrombosis include plaque erosion, which occurs primarily in young patients (<50 years) and represents the majority of acute coronary thrombi in premenopausal women. The underlying lesion morphology in plaque erosion shows PIT or a thick cap fibroatheroma. Calcified nodule is the least frequent cause of thrombosis, which occurs in older individuals with heavily calcified and tortuous arteries.

Coronary artery bypass grafting (CABG) is the preferred therapeutic option for complex multivessel coronary artery disease and is associated with reduced morbidity and mortality compared to percutaneous interventional approaches. The internal mammary artery (IMA) grafts have been associated with long-term patency and improved survival as compared to saphenous vein grafts (SVGs). However, the IMA is predominantly used to bypass the LAD, while in the other beds saphenous vein graft is frequently used. The latter is associated with accelerated atherosclerosis development and has a very high rate of failure.

Structurally, the IMA endothelial layer shows fewer fenestrations, lower intercellular junction permeability, greater antithrombotic molecules such as heparin sulfate and tissue plasminogen activator, and higher endothelial nitric oxide production, which are some of the unique ways that make the IMA impervious to the transfer of lipoproteins. This basic understanding is crucial to championing the use of IMA as the first line of defense for the treatment of coronary artery disease.

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Abbreviations

Endoplasmic reticulum (ER):

Organelle of eukaryotic cells that forms an interconnected network of flattened, membrane-enclosed sacs or tubes termed cisternae. ER fulfills multiple cellular functions including the transport of synthesized proteins from vesicles to the Golgi apparatus.

Lp(a):

Lipoprotein(a) [Lp(a)] contains an LDL-like particle and the specific apolipoprotein(a) [apo(a)], which is covalently bound to the apolipoprotein B of the LDL like particle; Lp(a) is structurally related to plasminogen and tissue plasminogen activator and represents an independent risk factor for the development and progression of atherosclerosis.

Lipoprotein-associated phospholipase A2 (Lp-PLA2):

Enzyme that catalyzes the degradation of platelet activating factor (PAF) to inactive products by hydrolysis of the acetyl group at the sn-2 position, producing the biologically inactive products LYSO-PAF and acetate; Lp-PLA2 represents a risk factor for atherosclerosis.

Rosuvastatin:

Blocker of HMG-CoA-reductase, a catalyst of the reaction of 3-hydroxy-3-methylglutaryl-Coenzyme A (HMG-CoA) to mevalonate, a rate limiting step of cholesterol synthesis in the liver.

CABG:

Coronary artery bypass grafting

CAD:

Coronary artery disease

CTO:

Chronic total occlusion

HPR:

Healed plaque rupture

IMA:

Internal mammary artery

LAD:

Left anterior descending coronary artery

PIT:

Pathologic intimal thickening

SMC:

Smooth muscle cell

SVG:

Saphenous vein graft

TCFA:

Thin-cap fibroatheroma

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Authors and Affiliations

  1. CVPath Institute, Inc., 19 Firstfield Road, Gaithersburg, MD, 20878, USA

    Kazuyuki Yahagi, Fumiyuki Otsuka, Kenichi Sakakura, Michael Joner & Renu Virmani

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  1. Kazuyuki Yahagi
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  2. Fumiyuki Otsuka
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  3. Kenichi Sakakura
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  4. Michael Joner
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  5. Renu Virmani
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Correspondence to Renu Virmani .

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  1. Division of Cardiovascular Disease Department of Internal Medicine, Health Care Center Bitterfeld, Bitterfeld-Wolfen, Germany

    Peter Lanzer

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Yahagi, K., Otsuka, F., Sakakura, K., Joner, M., Virmani, R. (2015). Native Coronary Artery and Bypass Graft Atherosclerosis. In: Lanzer, P. (eds) PanVascular Medicine. Springer, Berlin, Heidelberg. https://doi.org/10.1007/978-3-642-37078-6_15

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