RESUMEN
Background: Epidemiological studies suggest an association between periodontal disease and coronary heart disease. It is possible that periodontal disease may contribute to plaque destabilization in patients with acute coronary syndrome. Aim: To assess the association between severity of periodontal disease, the number of acute plaques and extension of coronary artery disease in patients with acute coronary syndrome. Patients and methods: The severity of periodontal disease was assessed by skilled independent observers in patients with acute coronary syndrome subjected to coronary angiography. The periodental disease was classified as mild or severe. Acute plaques were defined on angiography as those with thrombi, ulcers or flow alterations. The extension of coronary disease was analyzed using the Sullivan score. Results: Forty three patients (35 males) aged 41 to 83 years, were studied. Mild and severe periodontal disease was present in 18 (42percent) and 25 (58percent) patients respectively. Seventy six percent of those with severe disease had two or more acute plaques, compared with 17percent of those with mild disease (p<0.001). Median Sullivan score was 80.6 and 57.2 in patients with severe or mild periodontal disease respectively (p=0.001). Conclusions: Severe periodontal disease was associated with a higher number of acute coronary plasques and a higher extension of coronary artery disease, in patients with acute coronary syndromes.
Asunto(s)
Adulto , Masculino , Humanos , Femenino , Persona de Mediana Edad , Angina Inestable/etiología , Enfermedad de la Arteria Coronaria/etiología , Enfermedades Periodontales/complicaciones , Enfermedad Aguda , Enfermedad CrónicaRESUMEN
Background: Restenosis post stenting is due to the deposit of extracellular matrix, mainly collagen in the neointima. Controversy exists regarding if collagen is generated locally or by immigration from the adventitia. Aim: To study the fibrocellular response after stent implantation in rabbit iliac arteries. To observe, by immunohistochemistry and in situ hybridization, if collagen type I mRNA is expressed in the neointima, in the media or in the adventitia. Material and methods: Thirty eight white rabbits (New Zealand) of 4 kg received an hypercholesterolemic diet during 1 month. After this period, in all but 6 of them, an angioplasty with stent implantation was performed via right carotid artery in both iliac arteries, using a 1:1.3 relationship regarding the reference vessel. Angiograms were performed at day 0, 4, 21, and 40, followed by paraffin fixation of the injured segments, immunohistochemistry for a-actin and in situ hybridization to detect procollagen type I (a1R1) mRNA. Results: No hybridization was observed in non injured arteries or at day 0 (n= 6). Expression of a1R1 mRNA was observed in the neointima starting at day 4 after stenting (n= 8). At day 21 (n= 8) hybridization of procollagen type I was not only observed in the neointima, but also in the media, which became equally intense in both areas. At day 40 (n= 6) hybridization was observed similarly in the media and adventitia. Conclusions: In this model, hybridization of procollagen type I started in the neointima, then involved the media and finally the adventitia. This finding might be useful for designing therapies to be delivered locally at the end of an angioplasty to prevent collagen deposition in the neointima