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.     

Can flow cytometry detect successful ticlopidine treatment in patients with VVI pacemakers?

An increased platelet activation status is present in patients with VVI pacemakers. With platelet activation, there is modulation of platelet surface molecule expression. In the current study, the expression of platelet surface markers in VVI patients before and after ticlopidine treatment and control subjects was investigated by means of flow cytometry. The study group consisted of 25 patients with VVI pacemaker, and 15 control subjects. CD42b, CD61, and CD62p expression were significantly increased in VVI patients compared with control subjects (CD42b p < 0.001, CD61 p< 0.005 and CD62p p < 0.001). In addition, after ticlopidine treatment, platelets showed a significant fall in expression of all these markers in VVI patients (CD42b p < 0.001, CD61 p < 0.005 and CD62p p< 0.001). Our data suggest an increase of the surface expression of all these markers on platelets and demonstrate the efficacy of ticlopidine in reducing them.     

The Forgotten Variable of Shear Stress in Mitral Annular Calcification: Whole Blood Viscosity

Objective

The aim of this research was to assess the relationship between mitral annular calcification (MAC) and whole blood viscosity (WBV).

Subjects and Methods

A total of 184 patients with MAC and 133 patients without MAC were enrolled in the study. The WBV was calculated with a confirmed formulation using the hematocrit and total plasma protein at a low shear rate (LSR) and high shear rate (HSR). Early diastolic mitral annular velocity (Ea) and late diastolic mitral annular velocity (Aa) were measured using pulse Doppler tissue echocardiography. Pearson''s correlation analysis was performed to assess the relationship between WBV and mitral annular motion velocities. The effects of different variables on the occurrence of MAC were assessed in univariate and multivariate logistic regression analysis.

Results

In patients with MAC, WBV values were significantly higher at HSR (18.04 ± 0.84 vs. 17.25 ± 0.96 208 s^-1, p < 0.001) and at LSR (78.0 ± 14.2 vs. 61.9 ± 17.1 0.5 s^-1, p < 0.001). The WBV at HSR and LSR were significantly correlated with Ea (r = −0.477, p < 0.001; r = −0.385, p < 0.001, respectively) and Aa (r = −0.544, p < 0.001; r = −0.323, p < 0.001, respectively). Multivariate analysis showed that WBV of both shear rates was an independent predictor of MAC. Using the ROC curve, a cut-off value of 70.1 for WBV at LSR had a sensitivity of 83.7% and a specificity of 73.7% (AUC 0.785, p < 0.001) and a WBV cut-off value of 17.5 at HSR had a sensitivity of 79.6% and a specificity of 71.4% (AUC 0.761, p < 0.001) for the prediction of MAC.

Conclusion

Patients with MAC had significantly higher WBV, which independently predicted the presence of MAC. WBV had an inverse correlation with mitral annular motion velocities, indicating that a higher WBV may lead to greater limitation in annular motion and, thus, more calcification.Key Words: Mitral valve calcification, Shear stress, Blood viscosity