The role of septal perforators and "myocardial bridging effect" in atherosclerotic plaque distribution in the coronary artery disease

The distribution of atherosclerotic plaque burden in the human coronary arteries is not uniform. Plaques are located mostly in the left anterior descending artery (LAD), then in the right coronary artery (RCA), circumflex branch (LCx) and the left main coronary artery (LM) in a decreasing order of frequency. In the LAD and LCx, plaques tend to cluster within the proximal segment, while in the RCA their distribution is more uniform. Several factors have been involved in this phenomenon, particularly flow patterns in the left and right coronary artery. Nevertheless, it does not explain the difference in lesion frequency between the LAD and the LCx as these are both parts of the left coronary artery. Branching points are considered to be the risk points of atherosclerosis. In the LCx, the number of side branches is lower than in the LAD or RCA and there are no septal perforators with intramuscular courses like in the proximal third of the LAD and the posterior descending artery (PDA). We hypothesized that septal branches generate disturbed flow in the LAD and PDA in a similar fashion to the myocardial bridge (myocardial bridging effect). This coronary architecture determines the non-uniform plaque distribution in coronary arteries and LAD predisposition to plaque formation

The noise of many needles: Jerky domain wall propagation in PbZrO3 and LaAlO3

Measurements of the sample length of PbZrO3 and LaAlO3 under slowly increasing force (3-30 mN/min) yield a superposition of a continuous decrease interrupted by discontinuous drops. This strain intermittency is induced by the jerky movement of ferroelastic domain walls through avalanches near the depinning threshold. At temperatures close to the domain freezing regime, the distributions of the calculated squared drop velocity maxima N(υm2) follow a power law behaviour with exponents ε=1.6±0.2. This is in good agreement with the energy exponent ε=1.8±0.2 recently found for the movement of a single needle tip in LaAlO3 [R. J. Harrison and E. K. H. Salje, Appl. Phys. Lett. 97, 021907 (2010)]. With increasing temperature, N(υm2) changes from a power law at low temperatures to an exponential law at elevated temperatures, indicating that thermal fluctuations increasingly enable domain wall segments to unpin even when the driving force is smaller than the corresponding barrier

Small vessel coronary artery disease: How small can we go with myocardial revascularization?

The issue of small coronary artery atherosclerosis represents an intriguing aspect of coronary artery disease, which is related with higher rates of peri- and post-procedural complications and impaired long-term outcome. This problem is further complicated by the unclear definition of small coronary vessel. Recent randomized controlled trials have provided new data on possible novel interventional treatment of small coronary vessels with drug-coated balloons instead of traditional new-generation drug-eluting stent implantation. Also, the conservative management represents a therapeutic option in light of the results of the recent ISCHEMIA trial. The current article provides an overview of the most appropriate definition, interventional management, and prognosis of small coronary artery atherosclerosis

Extracellular Matrix Proteomics Reveals Interplay of Aggrecan and Aggrecanases in Vascular Remodeling of Stented Coronary Arteries.

BACKGROUND: Extracellular matrix (ECM) remodeling contributes to in-stent restenosis and thrombosis. Despite its important clinical implications, little is known about ECM changes post-stent implantation. METHODS: Bare-metal and drug-eluting stents were implanted in pig coronary arteries with an overstretch under optical coherence tomography guidance. Stented segments were harvested 1, 3, 7, 14, and 28 days post-stenting for proteomics analysis of the media and neointima. RESULTS: A total of 151 ECM and ECM-associated proteins were identified by mass spectrometry. After stent implantation, proteins involved in regulating calcification were upregulated in the neointima of drug-eluting stents. The earliest changes in the media were proteins involved in inflammation and thrombosis, followed by changes in regulatory ECM proteins. By day 28, basement membrane proteins were reduced in drug-eluting stents in comparison with bare-metal stents. In contrast, the large aggregating proteoglycan aggrecan was increased. Aggrecanases of the ADAMTS (a disintegrin and metalloproteinase with thrombospondin motifs) family contribute to the catabolism of vascular proteoglycans. An increase in ADAMTS-specific aggrecan fragments was accompanied by a notable shift from ADAMTS1 and ADAMTS5 to ADAMTS4 gene expression after stent implantation. Immunostaining in human stented coronary arteries confirmed the presence of aggrecan and aggrecan fragments, in particular, at the contacts of the stent struts with the artery. Further investigation of aggrecan presence in the human vasculature revealed that aggrecan and aggrecan cleavage were more abundant in human arteries than in human veins. In addition, aggrecan synthesis was induced on grafting a vein into the arterial circulation, suggesting an important role for aggrecan in vascular plasticity. Finally, lack of ADAMTS-5 activity in mice resulted in an accumulation of aggrecan and a dilation of the thoracic aorta, confirming that aggrecanase activity regulates aggrecan abundance in the arterial wall and contributes to vascular remodeling. CONCLUSIONS: Significant differences were identified by proteomics in the ECM of coronary arteries after bare-metal and drug-eluting stent implantation, most notably an upregulation of aggrecan, a major ECM component of cartilaginous tissues that confers resistance to compression. The accumulation of aggrecan coincided with a shift in ADAMTS gene expression. This study provides the first evidence implicating aggrecan and aggrecanases in the vascular injury response after stenting

A neutron diffuse scattering study of PbZrO₃ and Zr-rich PbZr_1-xTi_xO₃

A combined neutron diffuse scattering study and model analysis of the antiferroelectric crystal PbZrO3is described. Following on from earlier X-ray diffuse scattering studies, supporting evidence for disordering of oxygen octahedral tilts and Pb displacements is shown in the high-temperature cubic phase. Excess diffuse scattering intensity is found at theMandRpoints in the Brillouin zone. A shell-model molecular dynamics simulation closely reproduces the neutron diffuse scattering pattern. Both in-phase and antiphase tilts are found in the structural model, with in-phase tilts predominating. The transition between disordered and ordered structure is discussed and compared with that seen in Zr-rich PbZr1−xTixO3.</jats:p