Although there are a number of studies on vasospastic angina, the structural changes at the cellular level that occur in the coronary arterial wall during spasm are not well known. Coronary spasm was induced by brushing the coronary adventitia in nine anesthetized beagles, and structural changes in the spastic coronary segments were examined by light and electron microscopy, making comparisons with the adjacent nonspastic segments. The % diameter stenosis of the spastic segments as measured angiographically was 79.4 Ϯ 12% (mean Ϯ SD). Light microscopic changes in the spastic and nonspastic segments were as follows: medial thickness 1,512 vs. 392 m (P Ͻ 0.0001) and % diameter and % area stenoses of spastic segment 81.0% and 96.5%, respectively, indicating that spasm was induced by medial thickening. Circular smooth muscle cells (SMCs) in the media were arranged in parallel with the internal (IEL) and external (EEL) elastic lamina in nonspastic segments but radially rearranged in spastic segments. SMCs were classified by their patterns of connection to IEL into six types by electron microscopy. Of these, three contracted and pulled the IEL toward the EEL, causing folding of the IEL and waving of EEL resulting in thickening of the media and narrowing of the lumen. We conclude that coronary spasm was elicited by radial rearrangement of the medial SMCs due to their own contraction and resultant medial thickening and folding of IEL, creating a piston effect to narrow the lumen, i.e., spasm. smooth muscle cell rearrangement CORONARY SPASM IS THE CAUSE of vasospastic angina. Coronary spasm is thought to be provoked by excessive contraction of circular smooth muscle cells (SMCs) present in the media of the coronary artery.Since medial SMCs can shorten their length by contraction by 30% at most, to attain a luminal narrowing of Ն75% is theoretically difficult without the existence of a thickened intima if their circular arrangement is not altered during contraction. Two concepts have been proposed as to the structural (morphological) mechanisms underlying coronary spasm: concentric narrowing of the coronary lumen in the presence of diffuse intimal thickening (6, 9, 12) and eccentric narrowing of the lumen in the presence of eccentric intimal thickening (2). However, no definitive evidence has emerged to support whether either of these mechanisms actually occurs clinically.There are a number of studies on humoral factors that participate in coronary spasm (7,15). Structural changes at the cellular level that occur in the coronary media during spasm, however, have not been clarified, probably because of the difficulty in analyzing coronary arterial architecture during spasm in patients and the lack of appropriate animal models of coronary spasm.Coronary spasm occurs not only in the large epicardial coronary arteries, often the site of atherosclerotic intimal thickening, but also in arterioles in which intimal thickening infrequently occurs (13). It is therefore necessary to elucidate the mechanisms of coronary spasm that oc...

Background: Approximately 15% of acute coronary syndrome (ACS) cases have no significant coronary stenosis. Mechanisms underlying the attacks are, however, unknown. Methods and Results:The clinical study had 254 patients with ACS; 38 patients (31 females and 7 males; aged 51.0±8.0 years) had no significant coronary stenosis on angiography. They underwent a dye-staining angioscopy of the suspected culprit coronary artery using Evans blue, which selectively stains fibrin and damaged endothelial cells. A fluffy coronary luminal surface was observed in the suspected culprit artery in all 38 patients. The fluffy luminal surface was stained blue with Evans blue. In animal experiments involving 5 beagles, 10% hydrogen peroxide solution was injected into the iliac arteries to damage endothelial cells, which was then followed by blood reperfusion, and then the artery was examined by intravascular microscopy and histology. In the beagles, the arterial segment, where the thrombus had been formed, exhibited a fluffy luminal surface after a washout of the thrombus, and the surface was stained blue. Histologically, the fluffy surfaces were composed of damaged endothelial cells attached by multiple fibrin threads and platelets. Conclusions:It was considered that the coronary segment exhibiting a fluffy luminal surface was the culprit lesion and that the fluffy surface was caused by residual thrombi after dispersion of an occlusive thrombus, which had formed on the damaged endothelial cells. (Circ J 2010; 74: 2379 - 2385

No abstract

SummaryThe mechanism(s) underlying formation of coronary stent thrombus (ST) in chronic phase is yet unclear. Endothelial cells are highly antithrombotic, therefore, it is conceivable that neoendothelial cells (NECs) covering stent struts are damaged and cause ST. This study was performed to examine the role of damaged NECs covering coronary stent struts in the genesis of occlusive or nonocclusive ST in chronic phase.(1) Forty-four patients with acute coronary syndrome (17 females and 27 males) underwent dye-staining coronary angioscopy, using Evans blue which selectively stains damaged endothelial cells, 6 months after bare-metal stent (BMS) deployment. Neointimal coverage was classified into not covered (grade 0), covered by a thin layer (grade 1), and buried under neointima (grade 2) groups. (2) In 7 beagles, the relationships between neointimal thickness and ST were examined 6 months after BMS deployment. (3) The NECs on the struts were stained blue in 4 of 25 patients with grade 2 and in 11 of 20 patients with grade 0/1 (P < 0.05). ST was observed in none of the former and in 5 of the latter (P < 0.05). (4) In beagles, neointimal coverage was grade 0/1 when neointimal thickness was 80.2 ± 40.0 μm, whereas grade 2 when thickness was 184 ± 59.4 μm. ST was observed in 9 of 15 struts with neointimal thickness within 100 μm and in one of 17 struts with thickness over 100 μm (P < 0.05). ST arose from damaged NECs covering the stent struts. NECs may have been damaged due to friction between them and struts due to thin interposed neointima which might have acted as a cushion, resulting in ST. (Int Heart J 2011; 52: 12-16)

No abstract