The association between cardiac calcification and coronary artery disease.

OBJECTIVE: The objective of this study was to determine whether there is an association between mitral annular calcification (MAC), aortic valve annulus calcification (AVAC) and aortic valve calcification (AVC) with coronary artery disease (CAD) in subjects < or =65 years. METHODS: 386 patients under 65 years of age underwent transthoracic echocardiography and coronary arteriography at the same time. RESULTS: The following results were obtained: (I) The patients with calcium deposits were older than the patients without calcium deposits (P < 0.01). Hypertension (P < 0.05) and diabetes mellitus (P < 0.001) were significantly associated with MAC. Hypertension (P < 0.01), diabetes mellitus (P < 0.05) and a smoking history (P < 0.05) were significantly more prevalent in patients with AVC than in those without AVC. Hypertension was significantly more frequent in patients with AVAC (P < 0.05). (II) There was a positive correlation between age (P < 0.001), hypertension (P < 0.001), diabetes (P < 0.05) and the number of sites with calcium deposits. (III) Coronary arteriography was more frequently positive in patients with calcium deposits than in those without (P < 0.01). (IV) Multivariable logistic regression analysis identified multiple calcium deposits (P < 0.01), age (P < 0.05), male gender (P < 0.001), diabetes mellitus (P < 0.001), and hypercholesterolaemia (P < 0.05) as significant predictors for a positive coronary arteriography. Multiple calcium deposits (P < 0.001) and diabetes mellitus (P < 0.001) were also significant predictors in female patients. In patients aged < or =55 years, multiple calcium deposits (P < 0.05), diabetes mellitus (P <0.05), smoking history (P < 0.05) and male gender (P < 0.05) were statistically significant predictors of a positive coronary arteriography. CONCLUSION: There is a significant association between the presence of calcium deposits and coronary artery disease. The presence of multiple calcium deposits is an independent predictor of coronary artery disease.

Insulin-like growth factor 1 improves the efficacy of mesenchymal stem cells transplantation in a rat model of myocardial infarction.

BACKGROUND: Previous study demonstrated the improvement of cardiac function was proportional to the number of cells implanted. Therefore, increasing cell survival in the infarcted myocardium might contribute to the improvement of the functional benefit of cell transplantation. METHODS AND RESULTS: MSCs were treated with IGF-1 in vitro and infused into the acute myocardial infarction rats via the tail vein. After treatment of MSCs with IGF-1 for 48 h, flow cytometric analysis showed marked enhancement of expression of CXCR4 in the cell surface. After 4 weeks of transplantation, we found 1) a greater number of engrafted MSCs arrived and survived in the peri-infarct region; 2) TnT protein expression and capillary density were enhanced; 3) LV cavitary dilation, transmural infarct thinning, deposition of total collagen in the peri-infarct region and cardiac dysfunction were attenuated. CONCLUSION: 1) IGF-1 treatment has time-dependent and dose-dependent effects on CXCR4 expression in MSCs in vitro. 2) IGF-1 improves the efficacy of MSCs transplantation in a rat model of myocardial infarction mainly via enhancement of the number of cells attracted into the infarcted heart. These findings provide a novel stem cell therapeutic avenue against ischemic heart disease.

Anti-ischemia/reperfusion of C1 inhibitor in myocardial cell injury via regulation of local myocardial C3 activity.

C3 is common to all pathways of complement activation augmenting ischemia/reperfusion (I/R)-induced myocardial injury and cardiac dysfunction. Complement inhibition with the complement regulatory protein, C1 inhibitor (C1INH), obviously exerts cardioprotective effects. Here, we examine whether C1INH regulates C3 activity in the ischemic myocardial tissue. C1INH markedly suppressed C3 mRNA expression and protein synthesis in both a model of I/R-induced rat acute myocardial infarction (AMI) and the cultured rat H9c2 heart myocytes. At least, this regulation was at the transcriptional level in response to oxygen tension. In vitro, C3 deposition on, and binding to, the surface of rat myocardial cells were significantly blocked by C1INH treatment. C1INH could inhibit classical complement-mediated cell lysis via suppressing the biological activity of C3. Therefore, C1INH, in addition to inhibition of the systemic complement activation, prevents myocardial cell injury via a direct inhibitory role in the local myocardial C3 activity.

[Application of high frequency ultrasound to the diagnosis of varicocele in infertile males].

OBJECTIVE: To investigate the objective index of the diagnosis of varicocele (VC) in infertile males by ultrasonography and the testis volume changes resulting from varicocele. METHODS: Forty-six healthy male volunteers and 178 infertile men with left varicocele were detected by high frequency ultrasound. According to the clinical data and ultrasonographic results, the 178 VC patients were divided into 4 groups, SVC group (45 cases), VC I group (44 cases), VC II group (48 cases), and VC III group (41 cases). RESULTS: (1) The differences in DR, DV, Vmax, TR and testis volume between the right and the left sides were not statistically significant in the control group (P > 0.05). (2) The differences in DR, DV, Vmax and TR between the experimental and control groups as well as among the VC groups were statistically significant (P < 0.001). (3) The left testis volume was smaller than the right among the VC groups (P < 0.01). The right testis volume of the VC II and VC III groups was significantly smaller than that of the control group ( P < 0.05), and the left testis volume in the VC III group was significantly smaller than that of the SVC group (P < 0.05). CONCLUSION: (1) High frequency ultrasound can detect the accurate diameter of the internal spermatic vein, hemodynamic index and testis volume of infertile men with VC, and hence help to screen the causes of male infertility. (2) Unilateral varicocele can cause a volume decrease in both testes, especially in the left. Both unilateral SVC and VC can cause testicular atrophy, and the more serious VC, the higher testicular atrophy.