RESUMEN
The 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.
Asunto(s)
Síndrome Coronario Agudo/terapia , Angioscopía , Colorantes , Reestenosis Coronaria/etiología , Reestenosis Coronaria/patología , Neointima/patología , Stents/efectos adversos , Síndrome Coronario Agudo/etiología , Síndrome Coronario Agudo/patología , Anciano , Angioplastia Coronaria con Balón , Reestenosis Coronaria/prevención & control , Stents Liberadores de Fármacos/efectos adversos , Femenino , Humanos , Masculino , Persona de Mediana Edad , Estudios Retrospectivos , Factores de TiempoRESUMEN
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±12% (mean±SD). Light microscopic changes in the spastic and nonspastic segments were as follows: medial thickness 1,512 vs. 392 µm (P<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.
Asunto(s)
Vasos Coronarios/patología , Acalasia del Esófago/patología , Animales , Angiografía Coronaria , Estenosis Coronaria/patología , Vasos Coronarios/ultraestructura , Perros , Microscopía Electrónica , Microscopía Electrónica de Rastreo , Miocitos del Músculo Liso/fisiología , Miocitos del Músculo Liso/ultraestructuraRESUMEN
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.
Asunto(s)
Síndrome Coronario Agudo/patología , Angioscopía , Vasos Coronarios/patología , Células Endoteliales/patología , Síndrome Coronario Agudo/etiología , Factores de Edad , Anciano , Animales , Distribución de Chi-Cuadrado , Colorantes , Oclusión Coronaria/etiología , Oclusión Coronaria/patología , Trombosis Coronaria/complicaciones , Trombosis Coronaria/patología , Modelos Animales de Enfermedad , Perros , Azul de Evans , Femenino , Humanos , Peróxido de Hidrógeno/administración & dosificación , Arteria Ilíaca/patología , Inyecciones Intraarteriales , Japón , Masculino , Persona de Mediana Edad , Medición de Riesgo , Factores de Riesgo , Factores Sexuales , Fumar/efectos adversos , Trombosis/inducido químicamente , Trombosis/patologíaRESUMEN
BACKGROUND: Web-like (W) and membrane-like (M) structures have been observed on coronary stent edges on angioscopy but their incidence and mechanisms remain obscure. METHODS AND RESULTS: First, 26 patients [acute coronary syndromes (ACS) in 10 and stable angina (SA) in 16] underwent angioscopy of the stented coronary artery immediately after, and 32 patients (ACS in 18 and SA in 14) 6 months after insertion of bare-metal stents. Second, angioscopy of the stented coronary artery was performed in 4 beagles 5 h after, and in 9 beagles 1 month after stenting. W and M were observed in patients with ACS and those with SA (80.0% vs 18.7%; P<0.05) immediately after and 6 months after stenting (55.5% vs 28.5%; NS). They were stained with Evans blue that selectively stains fibrin immediately after stent insertion, but not 6 months later. In beagles, W and M were observed in 75.0% at 5 h and in 66.6% 1 month later. Histologically, W and M were composed of fibrin at 5 h, whereas they were composed of collagen fibers at 1 month. CONCLUSIONS: W and M were frequently formed on the edges of coronary stents. They were formed with fibrin in the acute phase, whereas this fibrin was replaced by collagen fibers in the chronic phase.
Asunto(s)
Síndrome Coronario Agudo/cirugía , Angina de Pecho/cirugía , Stents/efectos adversos , Angioscopía , Animales , Colágeno/metabolismo , Vasos Coronarios/cirugía , Perros , Fibrina/metabolismo , Humanos , Factores de TiempoRESUMEN
Pericarditis is a common complication in systemic lupus erythematosus (SLE) patients, however, that causing congestive heart failure (CHF) is a rare initial manifestation of SLE. We treated a patient whose initial manifestation of SLE was pericardial effusion causing CHF, which improved following prednisolone therapy that led to a dramatic decrease in pericardial effusion and improvement in left ventricular diastolic dysfunction as shown in Doppler echocardiography findings. Further, the plasma brain natriuretic peptide level became normalized.