Acute type A aortic dissection in a patient with ventricular septal defect

We report the case of a 38-year-old man with a long-standing history of a small ventricular septal defect presented with chest pain. Electrocardiography revealed sinus rhythm, ST-segment elevation in leads V1–6. The chest X-ray showed mild cardiomegaly. He underwent cardiac catheterisation laboratory to primary coronary angioplasty. Coronary angiography showed normal coronary arteries. Aortic root angiography revealed type A aortic dissection. Transthoracic and transesophageal echocardiography showed aortic dissection in ascending aorta and a perimembranous ventricular septal defect. Thoracoabdominal CT angiography confirmed the aortic dissection before the surgery.The patient underwent cardiac surgery immediately. The ventricular septal defect and aortic dissection were repaired successfully. The postoperative recovery was uneventful and he has thus far remained asymptomatic at 6 months' follow-up.     

Usefulness of preprocedural soluble CD40 ligand for predicting restenosis after percutaneous coronary intervention in patients with stable coronary artery disease

CD40-CD40 ligand interaction is involved in the inflammatory pathogenesis of atherosclerosis but clinical data about its role in stent restenosis are still limited. We investigated the effect of preprocedural CD40 ligand (sCD40L) on stent restenosis. We enrolled 36 patients (mean age 61.4 +/- 8.5 years) with stable angina who underwent successful stent implantation. Control angiograms were performed in all patients after 6 months. Plasma sCD40L and high-sensitive C-reactive protein levels were measured before stent implantation and at 1 and 6 months after the procedure. Angiographically proven restenosis rate was 27.8%. Plasma sCD40L levels were significantly higher (preprocedural 0.74 +/- 0.79) and more prolonged in patients with stent restenosis compared with patients without stent restenosis (0.02 +/- 0.22 ng/ml, p < 0.001). According to receiver-operator characteristic analysis, sCD40L > 0.41 ng/ml was the best distinguished parameter between patients with and without restenosis. At the multivariate logistic regression analysis, preprocedural sCD40L was an independent predictor (RR 39.4, 95% confidence interval 4.05 to 383.8, p = 0.002) of stent restenosis after adjusting for confounding variables, including diabetes, reference vessel diameter, lesion length, stent diameter, stent length, and baseline high-sensitive C-reactive protein. Sensitivity, specificity, and positive and negative predictive values and likelihood ratio of preprocedural sCD40L levels in stent restenosis were 78%, 92%, 78%, 92%, and 9.37%, respectively. In conclusion, enhanced inflammation of plaque (increased sCD40L) before percutaneous coronary intervention may increase the rate of stent restenosis. Increased preprocedural sCD40L level is an independent predictor of stent restenosis. We can use this marker for the assessment of risk stratification before planning stent implantation.