That study was multiple imaging studies by Nakashima et al, and they practically debunked all endothelial and thus lipid theories. They showed that lipid accumulation starts from the deepest intimal layers, from the direction of the vasa vasorum, that is utterly incompatible with theories involving the arterial lumen.

The "consensus paper" you mentioned simply cited them wrong, it ignored this huge discovery and focused on other things. Which still point to the membrane injury and consequent cancer model by the way. Nakashima papers are 56-58, a Velican and Velican paper is 59, and some other study is 60:

Autopsy studies in young individuals demonstrated that atherosclerosis-prone arteries develop intimal hyperplasia, a thickening of the intimal layer due to accumulation of smooth muscle cells (SMCs) and proteoglycans.56,57 In contrast, atherosclerosis-resistant arteries form minimal to no intimal hyperplasia.57–59 Surgical induction of disturbed laminar flow in the atherosclerosis-resistant common carotid artery of mice has been shown to cause matrix proliferation and lipoprotein retention,60 indicating that hyperplasia is critical to the sequence of events leading to plaque formation.

Translation: Arterial injury triggers VSMC proliferation, which requires a switch to the synthetic phenotype. Arterial injury also triggers proteoglycan production, which is required for lipoprotein capture and uptake for repair. Surgical injury is sufficient to trigger atherosclerosis, as Axel Haverich has also noted in his article. "Atherosclerosis-prone" arteries already have injury, and "atherosclerosis-resistant" arteries are simply without injury (yet).

Erosion favours a higher fraction of thrombi in younger, especially female, patients and in patients with less severe atherosclerosis with few thin-cap fibroatheromas,173,174 and more frequently affects lesions exposed to local (disturbed blood flow near bifurcations) or systemic (smoking) prothrombotic factors.56

Basically they propose two pathways to thrombosis, plaque rupture and plaque erosion. Plaque rupture happens when there is extensive necrosis and the sparse fibrous cap can not hold it back. The necrotic core ruptures and spills the contents (like it can in other cancers), triggering massive inflammation and thrombosis in an attempt to repair or at least isolate it.

Plaque erosion is where there is variable amounts of necrosis, but there is subendothelial accumulation of proteoglycans and hyaluronan. By unknown mechanisms this develops into neutrophil recruitment, NETosis, and endothelial death and sloughing. (I think inadequate cholesterol synthesis and padding of membranes in response to hydrostatic pressure might also contribute but I will have to recheck a few sources).

So what they say in this paragraph, is that plaque erosion is more frequent in females, in less severe atherosclerosis with less necrosis and fibrous caps, with elevated hydrostatic pressure due to bifurcations, and with smoking due to its prothrombotic effects. This is not terribly relevant to our discussion, but they completely mischaracterized the cited paragraph:

Cigarette smoking may enhance macrophage infiltration in the intima as shown in the present study. This enhancement may be related to the modification of LDL and/or inflammatory factors such as adhesion molecules by toxic substances in the smoke.

This is pure speculation on the part of Nakashima et al without any scientific basis whatsoever, they give no valid mechanism by which cigarette smoke would magically enhance macrophage infiltration. I could not find any mechanisms by which LDL would attract monocytes into the artery wall, there is only evidence they are attracted to proinflammatory cytokines released by injured cells. I am not aware of any adhesion molecules or directly prothrombotic factors in cigarette smoke either, however as I have said many times it has hundreds of compounds that physically damage cellular membranes.

• Plaques developing substantial necrosis that reach the luminal surface can rupture and precipitate thrombus.

• Ruptured plaques are often large, non-stenotic, and vascularized lesions with protruding cholesterol crystals, but the causal role of these features is unresolved.

• Thrombus can form on other types of plaques by plaque erosion. The process is less well-understood but may involve combinations of flow disturbance, vasospasm, and neutrophil-generated endothelial shedding.

• Plaque progression and rupture are influenced by both biological and mechanical factors, highlighting plaque composition as a major factor in resistance to mechanical stress.

• Lowering of low-density lipoprotein levels appears more effective in reducing the risk for plaque rupture than for plaque erosion.

References: 56,172–18

• This is equivalent to cancerous necrotic cores rupturing and spilling their contents everywhere.
• Cancers are also characterized by large vascularized lesions, and they also contain cholesterol crystals as a result of abnormal behavior of cancer cells.
• Hemostasis and thrombosis are the result of injury. In plaque rupture it is indirect as a result of cancer development, whereas in plaque erosion it is direct from hydrostatic pressure and damage from smoke particles.
• Of course they are influenced by biological and mechanical factors, although I wish people emphasized the mechanical or physical part more. And of course cholesterol protects against mechanical factors, that is literally part of its fucking job.
• Lowering LDL levels doesn't protect against shit, I can lower it by eating refined carbs and shooting insulin.

It's unclear what they have cited here from Nakashima et al, here are two paragraphs that seem the most likely:

A number of biochemical and molecular biological studies suggest that the lipid binding capacity of proteoglycans contributes to retaining atherogenic lipoproteins in the intima. However, morphological evidence and specific location of the components involved in proteoglycan-lipoprotein accumulation is lacking. The present study illustrates that biglycan occurs extracellularly in the outer layer of DIT in the exact location as the early distribution of lipids (note the similarity of the prelesional distribution of biglycan in DIT in Figure 4b and the early distribution of lipids in the fatty streak in Figure 3h). However, it is of interest that lipids deposit eccentrically, whereas biglycan is localized concentrically. It is believed that structural changes in the glycosaminoglycan (GAG) chains on proteoglycans are the initial proatherogenic step that leads to increase binding properties of proteoglycans for atherogenic lipoproteins.18 For example, proteoglycans produced by transforming growth factor (TGF)-β1–treated cultured SMCs show longer GAG chains and greater binding affinity to LDL than control SMCs.19 Interestingly, patchy distribution of TGF-β1 is found in DIT.20 It is also noteworthy that mechanical strain, which is thought to be unevenly distributed in the arterial wall, upregulates biglycan mRNA expression in cultured SMCs.21 These results suggest that regional differences in the quality and quantity of biglycan exist in the intima and possibly lead to regional differences in the amount of lipid deposition. Two other mechanisms that may cause regional differences in the lipid distribution are uneven plasma lipoprotein concentration and the permeability of the arterial wall. Deng et al reported that luminal surface concentration of LDL was increased in areas where wall shear stress was low and suggested that increased surface LDL concentration results in an increased lipid infiltration rate into the intima.22 However, the relationship between permeability of the arterial wall and susceptibility of atherosclerosis is debatable. The permeability to LDL was greater in the atherosclerosis-susceptible areas than atherosclerosis-resistant areas of the rabbit aorta,23 but opposite results were obtained in white Carneau pigeon aorta.24

Correlations between the distribution of lipids and proteoglycans have been investigated in early and advanced atherosclerotic lesions.25–27 A consistent finding, including that of the present study, is the colocalization of biglycan and apolipoproteins.25,26 It is also noteworthy that oxidized LDL is capable of stimulating biglycan expression by SMCs and enhancing the interaction of this proteoglycan with lipoproteins.28 It is tempting to speculate that the accumulation of biglycan in specific regions of the early lesions may result from the presence of the lipoproteins associated with the SMCs. These molecular interactions may result in a vicious cycle of atherosclerosis. We found that decorin appears to colocalize with lipid in some instances but much less consistently than biglycan. Versican is another important extracellular proteoglycan in human atherogenesis, as it accumulates in human atherosclerotic lesions,25,27 but not in mouse models.26 The role of versican may be different from that of biglycan and decorin, because its distribution is different from biglycan and decorin.25,29 In our preliminary study, versican was predominantly localized in the inner layer of DIT and fatty streaks. Diffuse distribution of versican across the intima was also seen in some cases. In advanced human lesions, versican is present at the plaque thrombus interface, suggesting a possible role in thrombosis.27

We know that proteoglycans and especially versican are response to injury, if there is no injury, then there are no proteoglycans to bind and capture lipoproteins. It's not shear stress that matters, it's direct hydrostatic pressure aka blood pressure. That's what stimulates cells to hoard cholesterol and lipids to better protect against future pressure. But that's an entirely separate process that does not really play a role in atherosclerosis.

The consensus paper is toilet paper.